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This document discusses the classification of periodontal diseases and conditions affecting the periodontium. It begins with an outline of the topics to be covered, including gingival diseases, periodontitis, necrotizing periodontal diseases, and other conditions. The classification system presented is based on the 1999 International Workshop for a Classification of Periodontal Diseases and Conditions. Key aspects of the classification include distinguishing between gingivitis and periodontitis based on the extent of tissue involvement, and classifying periodontitis based on factors like severity and rate of progression. An updated 2018 classification from the AAP and EFP is also mentioned. The document then discusses the various categories of gingival and periodontal diseases in more detail

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SECTION II Classification and Epidemiology of Periodontal Diseases OUTLINE Chapter 5 Classification of Diseases and Conditions Affecting the Periodontium Chapter 6 Fundamentals in the Methods of Periodontal Disease Epidemiology 325
CHAPTER 5 Classification of Diseases and Conditions Affecting the Periodontium James E. Hinrichs, Georgios A. Kotsakis CHAPTER OUTLINE Gingival Diseases Periodontitis Medication-Related Osteonecrosis of the Jaw Necrotizing Periodontal Diseases Abscesses of the Periodontium Periodontitis Associated With Endodontic Lesions Developmental or Acquired Deformities and Conditions Our understanding of the causes and pathogenesis of oral diseases 326
and conditions changes continually with increased scientific knowledge. In light of this fact, a classification can be most consistently defined by the differences in the clinical manifestations of diseases and conditions: they are clinically consistent and require little (if any) clarification by laboratory testing. The current classification of periodontal diseases is based on their extent (generalized versus localized), severity (slight, moderate, or severe), rate of progression (aggressive versus chronic), and localization (i.e., contained within the gingiva, as in gingivitis, or further involving periodontal bone loss, as in periodontitis). The existing definitions encompass the best available way to universally define a spectrum of diseases affecting the periodontal tissues and to guide therapeutic approaches. Nonetheless, the disease state is dynamic, and the appropriate diagnosis for an individual can change over time. For instance, a patient diagnosed with existing periodontitis who undergoes successful periodontal therapy may be classified as having a healthy but reduced periodontium (with slight, moderate, or severe attachment loss) at the reevaluation. Subsequently, if the same individual presents with gingival inflammation without signs of further attachment loss at a future appointment, the appropriate diagnosis would be “gingivitis on a reduced periodontium.” Depending on their future compliance with home care and maintenance visits, patients may progress to periodontitis or maintain a healthy but reduced periodontium. The case example highlights the importance of conceptualizing the dynamic nature of inflammatory diseases that affect the periodontium, while appreciating the importance of commonly accepted definitions for periodontal diseases. If a case of gingivitis on a reduced periodontium relapses into periodontitis, the prognosis of the affected teeth will depend on the preexisting attachment loss. The classification presented in this chapter is based on the most recent internationally accepted consensus on the diseases and conditions that affect the tissues of the periodontium. Box 5.1 presents the overall classification system that was proposed at the 1999 International Workshop for a Classification of Periodontal Diseases and Conditions. More recent views on the Classification of Periodontal Diseases and Conditions are also discussed. Each disease or condition is explored where clarification is needed. In 327
each case, the reader is referred to pertinent reviews on the subject and specific chapters within this book that discuss the topics in more detail. Box 5.1 Classification of Periodontal Diseases and Conditions Gingival Diseases Plaque-induced gingival diseasesa Non–plaque-induced gingival lesions Chronic Periodontitisb Localized Generalized Aggressive Periodontitis Localized Generalized Periodontitis as a Manifestation of Systemic Diseases Necrotizing Periodontal Diseases Necrotizing ulcerative gingivitis (NUG) Necrotizing ulcerative periodontitis (NUP) Abscesses of the Periodontium Gingival abscess Periodontal abscess Pericoronal abscess 328
Periodontitis Associated With Endodontic Lesions Endodontic–periodontal lesion Periodontal–endodontic lesion Combined lesion Developmental or Acquired Deformities and Conditions Localized tooth-related factors that predispose to plaque- induced gingival diseases or periodontitis Mucogingival deformities and conditions around teeth Mucogingival deformities and conditions on edentulous ridges Occlusal trauma a These diseases may occur on a periodontium with no attachment loss or on a periodontium with attachment loss that is stable and not progressing. b Chronic periodontitis can be further classified based on extent and severity. As a general guide, extent can be characterized as localized (<30% of teeth involved) or generalized (>30% of teeth involved). Severity can be characterized based on the amount of clinical attachment loss (CAL) as follows: slight = 1 or 2 mm CAL, moderate = 3 or 4 mm CAL, and severe ≥5 mm CAL. Data from Armitage GC: Development of a classification system for periodontal diseases and conditions. Ann Periodontol 4:1, 1999. An updated classification system, which is currently being developed jointly by the American Academy of Periodontology (AAP) and the European Federation of Periodontology (EFP), is scheduled to publish around the time of the release of this book. The goal of this effort is to address some of the shortcomings that exist with the current classification system (discussed in this chapter), including diagnostic inaccuracy and significant overlap of disease entities. Several working groups were created to focus on specific disease entities using the currently available scientific evidence, resulting in the most substantial update to the classification system since 1999. To view the updated AAP/EFP 2018 classification system, visit 329
the companion website www.expertconsult.com. Gingival Diseases Dental Plaque–Induced Gingival Diseases Gingivitis that is associated with retained dental plaque is the most common form of gingival disease (Fig. 5.1). Box 5.2 outlines the classifications of gingival diseases. These diseases may occur on a periodontium with no attachment loss or on a periodontium with attachment loss that is stable and not progressing (i.e., reduced periodontium). The epidemiology of periodontal diseases is reviewed in Chapter 6, and its causes are detailed in Chapters 7 through 15 in this textbook.15,23,26,39,40 What separates gingivitis from periodontitis is the containment of the inflammatory lesion within the gingiva in the former. As such, gingivitis is not associated with progressive attachment loss. This is not to say that gingivitis is solely associated with teeth showing no attachment loss (Fig. 5.2). Gingivitis can also be diagnosed in the gingiva of periodontitis- affected teeth that have previously lost attachment but that have been successfully treated with periodontal therapy to prevent any further attachment loss. In these treated cases, where gingival inflammation recurs around teeth with existing attachment loss due to a history of treated periodontitis, the appropriate diagnosis would be gingivitis on a reduced periodontium. This implies that gingivitis may be the diagnosis for inflamed gingival tissues associated with a tooth with no previous attachment loss or with a tooth that has previously undergone attachment and bone loss (i.e., with reduced periodontal support) and is not currently losing attachment or bone, even though gingival inflammation is present. Clinical attachment levels and radiographic records are needed to establish this diagnosis. 330
FIG. 5.1 (A) Plaque-related gingivitis depicts marginal and papillary inflammation, with 1- to 4-mm probing depths and generalized zero clinical attachment loss, except recession in tooth #28. (B) Radiographic images of the patient. Box 5.2 Gingival Diseases Dental Plaque–Induced Gingival Diseases These diseases may occur on a periodontium with no attachment loss or with attachment loss that is stable and not progressing. I. Gingivitis associated with dental plaque only A. Without local contributing factors B. With local contributing factors (see Box 5.4) II. Gingival diseases modified by systemic factors A. Associated with endocrine system 331
1. Puberty-associated gingivitis 2. Menstrual cycle–associated gingivitis 3. Pregnancy associated a. Gingivitis b. Pyogenic granuloma 4. Diabetes mellitus–associated gingivitis B. Associated with blood dyscrasias 1. Leukemia-associated gingivitis 2. Other III. Gingival diseases modified by medications A. Drug-influenced gingival diseases 1. Drug-influenced gingival enlargements 2. Drug-influenced gingivitis a. Oral contraceptive–associated gingivitis b. Other IV. Gingival diseases modified by malnutrition A. Ascorbic acid deficiency gingivitis B. Other Non–Plaque-Induced Gingival Lesions I. Gingival diseases of specific bacterial origin A. Neisseria gonorrhoeae B. Treponema pallidum C. Streptococcus species D. Other II. Gingival diseases of viral origin A. Herpesvirus infections 1. Primary herpetic gingivostomatitis 2. Recurrent oral herpes 3. Varicella zoster B. Other III. Gingival diseases of fungal origin A. Candida species infections: generalized gingival candidiasis B. Linear gingival erythema 332
C. Histoplasmosis D. Other IV. Gingival lesions of genetic origin A. Hereditary gingival fibromatosis B. Other V. Gingival manifestations of systemic conditions A. Mucocutaneous lesions 1. Lichen planus 2. Pemphigoid 3. Pemphigus vulgaris 4. Erythema multiforme 5. Lupus erythematosus 6. Drug induced 7. Other B. Allergic reactions 1. Dental restorative materials a. Mercury b. Nickel c. Acrylic d. Other 2. Reactions attributable to the following: a. Toothpastes or dentifrices b. Mouth rinses or mouthwashes c. Chewing gum additives d. Foods and additives 3. Other VI. Traumatic lesions (factitious, iatrogenic, or accidental) A. Chemical injury B. Physical injury C. Thermal injury VII. Foreign body reactions VIII. Not otherwise specified Data from Holmstrup P: Non–plaque-induced gingival lesions. Ann Periodontol 4:20, 1999; and Mariotti A: Dental plaque-induced gingival diseases. Ann Periodontol 4:7, 1999. 333
FIG. 5.2 Maxillary second molar exhibits mild inflammation at mesial-palatal surface. However, the clinical attachment loss has been stable for 15 years after apical positioned flap and periodontal maintenance, which is consistent with remission. The appropriate diagnosis is gingivitis on a reduced periodontium. Key Fact Gingivitis may be the diagnosis for inflamed gingival tissues associated with a tooth without previous attachment loss or with a tooth that has previously undergone attachment and bone loss (i.e., with reduced periodontal support) but is not currently losing attachment, even though gingival inflammation is present. In the latter case the appropriate definition would be “gingivitis on a reduced periodontium.” Gingivitis Associated With Dental Plaque Only Plaque-induced gingival disease is the result of an interaction between the microorganisms found in the dental plaque biofilm and the inflammatory host response. A cause-and-effect relationship between microbial plaque and gingivitis has been elegantly demonstrated by a classic experiment demonstrating that the cessation of oral hygiene consistently leads to the manifestation of gingivitis within 2 to 3 weeks in healthy adults.25 Clinical 334
gingivitis is histologically characterized by a dense infiltrate of lymphocytes and other mononuclear cells, fibroblast alterations, increased vascular permeability, and continuing loss of collagen in response to the microbial challenge. However, the alveolar bone is not affected. Microbial plaque is thus considered to be the primary etiologic factor for gingivitis. The severity and duration of the inflammatory response interaction can be altered by the modifying local (see Chapter 13) or systemic modifying factors (see Chapters 14 and 15). Gingivitis is fully reversible in otherwise healthy persons within weeks following the removal of local factors and reduction of the microbial load around the teeth. As noted earlier, gingivitis is rapidly established in cases of generalized or localized inefficient plaque removal. Therefore it is crucial that patients are instructed in oral hygiene to maintain long-term gingival health. Gingival Diseases Modified by Systemic Factors Systemic factors that contribute to gingivitis—such as the endocrine changes associated with puberty (Fig. 5.3), the menstrual cycle, pregnancy (Fig. 5.4A), and diabetes—may exacerbate the gingival inflammatory response to plaque.23,39 This altered response appears to result from the effects of systemic conditions on the host's cellular and immunologic functions, but the primary etiologic factor is still considered to be microbial plaque. One example of altered host response due to systemic factors is apparent during pregnancy when the incidence and severity of gingival inflammation may increase even in the presence of low levels of plaque. 335
FIG. 5.3 A 13-year-old female with hormone- exaggerated marginal and papillary inflammation, with 1- to 4-mm probing depths yet minimal clinical attachment loss. (A) Facial view. (B) Lingual view. FIG. 5.4 (A) Clinical image of pyogenic granuloma in a 27-year-old pregnant female. (B) Histologic image depicts dense inflammatory infiltrate and prominent vessels. 336
Clinical Correlation Increased estrogen and progesterone levels in pregnant women during their third trimester have been associated with increased severity of gingivitis via substituting nutrient needs for certain oral bacteria and stimulating their proliferation. One species that has been specifically associated with gingivitis during pregnancy is Prevotella intermedia. In blood dyscrasias (e.g., leukemia), the reduced number of immunocompetent lymphocytes in the periodontal tissues is associated with increased edema, erythema, and bleeding of the gingiva as well as gingival enlargement that may be associated with the swollen, spongy gingival tissues caused by the excessive infiltration of malignant blood cells (Fig. 5.5). FIG. 5.5 A 12-year-old female with a primary medical diagnosis of leukemia that exhibits swollen/spongy gingiva. Gingival Diseases Modified by Medications Gingival diseases that are modified by medications include gingival overgrowth due to anticonvulsant drugs such as phenytoin, immunosuppressive drugs such as cyclosporine (Fig. 5.6), and 337
calcium channel blockers such as nifedipine (Fig. 5.7), verapamil, diltiazem, and sodium valproate.15,26,39 The development and severity of gingival enlargement in response to medications is patient specific and may be influenced by uncontrolled plaque accumulation as well as by elevated hormonal levels. The increased use of oral contraceptives by premenopausal women has also been previously associated with a higher incidence of gingival inflammation and gingival enlargement. Although this fact stood true for earlier contraceptive formulations, existing contraceptives that include more modest doses of active ingredients are not commonly associated with gingival inflammation. FIG. 5.6 Clinical images of a 9-year-old male with severe gingival overgrowth secondary to heart transplant and cyclosporine therapy. 338
FIG. 5.7 Clinical images of gingival overgrowth following use a of calcium channel blocker to control hypertension. Gingival Diseases Modified by Malnutrition Gingival diseases modified by malnutrition have received attention because of clinical descriptions of bright red, swollen, and bleeding gingiva associated with severe ascorbic acid (vitamin C) deficiency or scurvy.26 Various nutrients, such as long chain omega-3 fatty acids, have been found to have immunomodulatory properties, whereas others act to ameliorate the destructive effects of reactive oxygen species (ROS) functioning as ROS scavengers. Nonetheless, the available evidence to support a clinically impactful role for mild nutritional deficiencies in the development or severity of gingival inflammation in humans is limited. Data have shed light on the implication of increased dietary carbohydrate intake on gingivitis, in addition to its known causal role on the occurrence of dental caries.19 Non–Plaque-Induced Gingival Lesions Oral manifestations of systemic conditions that produce lesions in the tissues of the periodontium are less common than plaque- induced gingivitis. This category mainly encompasses lesions of autoimmune or idiopathic etiology that can manifest in the gingiva. Benign mucous membrane pemphigoid is an example of a non– plaque-induced lesion associated with sloughing gingival tissues, which leave painful ulcerations of the gingiva (Fig. 5.8). In pemphigoid, autoimmune antibodies are targeted at the basement membrane, and histologically the destruction resembles a 339
subepithelial blister (Fig. 5.8C–D). Case Scenario 5.2 depicts gingival recession accompanied by a mucosal lesion located on the gingiva manifesting with a white lacy pattern with characteristic striations. FIG. 5.8 A 62-year-old female with benign mucous membrane pemphigoid. (A–B) Clinical image with sloughing epithelial surface. (C) Hematoxylin and eosin (H&E) stain depicting separation of epithelium from connective tissue. (D) Immunofluorescent-labeled antibodies to basement membrane. Gingival Diseases of Specific Bacterial Origin Gingival diseases of this category are attributed to specific bacteria that cause characteristic lesions in the gingiva. Neisseria gonorrhoeae and Treponema pallidum that can be transferred as a result of sexually transmitted diseases such as gonorrhea and syphilis, respectively, cause characteristic lesions in the gingiva.41,46 Refer to the online references for further description. Streptococcal gingivitis or gingivostomatitis is a rare entity that may present as an acute condition with fever, malaise, and pain associated with acutely inflamed, diffuse, red, and swollen gingiva with increased bleeding and occasional gingival abscess formation. The gingival infections 340
are usually preceded by tonsillitis. Gingival Diseases of Viral Origin Gingival diseases of viral origin may be caused by a variety of deoxyribonucleic acid and ribonucleic acid viruses, with the most common being the herpesviruses. A case example of herpetic stomatitis is demonstrated in Fig. 5.9A–B. Herpetic lesions are not uncommon and develop as intraoral blisters, usually grouped together, that quickly burst, leaving minuscule ulcerations. Lesions are frequently related to the reactivation of latent viruses, especially as a result of reduced immune function. The oral manifestations of viral infection have been comprehensively reviewed.20,45 Viral gingival diseases are treated with topical or systemic antiviral drugs (Fig. 5.9C–D). FIG. 5.9 (A–B) A 29-year-old male with primary herpetic infection and severe gingival inflammation. (C–D) Six weeks post systemic acyclovir. 341
Clinical Correlation Unlike other herpetic recurrences, varicella zoster virus (VZV) usually manifests with a prodrome of tingling, itching, burning, or a unilateral numbness at the affected dermatome. These symptoms are followed by moderate to severe pain shortly after initiation and are very important for differential diagnosis. Gingival Diseases of Fungal Origin Gingival diseases of fungal origin are relatively uncommon in immunocompetent individuals, but they occur more frequently in immunocompromised individuals and in those with disturbed microbiota by the long-term use of broad-spectrum antibiotics.20,46,47 The most common oral fungal infection is candidiasis (Candida albicans is often implicated). Candidiasis can also be seen under prosthetic devices, in individuals using topical steroids, and in individuals with decreased salivary flow, increased salivary glucose, or decreased salivary pH. A generalized candidal infection may manifest as white patches on the gingiva, tongue, or oral mucous membrane that can potentially be removed with gauze and leave a red, bleeding surface. In human immunodeficiency virus (HIV) seropositive persons, candidal infection may present as continuous erythematous stripe of the attached gingiva; this has been referred to as linear gingival erythema or HIV-associated gingivitis (see Chapter 30). The diagnosis of candidal infection can be made by culture, smear, or biopsy. Less common fungal infections have also been described.46,47 Gingival Diseases of Genetic Origin Gingival diseases of genetic origin may involve the tissues of the periodontium and have been described in detail.2 One of the most clinically evident conditions is hereditary gingival fibromatosis, which exhibits autosomal-dominant or (rarely) autosomal-recessive modes of inheritance. The gingival enlargement may completely cover the teeth, delay eruption, and present as an isolated finding; alternatively, it may be associated with several more generalized syndromes. 342
Gingival Manifestations of Systemic Conditions Gingival manifestations of systemic conditions may appear as desquamative lesions, ulcerations of the gingiva, or both.20,38,46 Allergic reactions that manifest with gingival changes are uncommon but have been observed in association with several restorative materials (Fig. 5.10A), toothpastes, mouthwashes, chewing gums (Fig. 5.11), and foods (see Box 5.2). The diagnosis of these conditions may prove difficult and may require an extensive history and the selective elimination of potential causes. Conjoint assessment with an allergologist is indicated, and percutaneous tests are often recommended. Histologic traits of biopsies from gingival allergic reactions include a dense infiltrate of eosinophilic cells (Fig. 5.10B–C). FIG. 5.10 (A) Localized pronounced gingival inflammation secondary to nickel allergy. (B–C) Biopsy 343
depicts dense infiltrate of plasma cells. FIG. 5.11 Generalized severe allergic response of gingiva as a result of additive in chewing gum. Traumatic Lesions Traumatic lesions may be self-inflicted and factitious in origin, which means that they are intentionally or unintentionally produced by artificial means (Fig. 5.12). Other examples of traumatic lesions include toothbrush trauma that results in gingival ulceration, recession, or both. FIG. 5.12 Self-inflicted gingival dehiscence induced via 344
patient's fingernail. Clinical Correlation Individuals who perform aggressive horizontal brushing are often found to have gingival recession or cervical abrasion on the teeth quadrants contralateral to their dominant hand. Iatrogenic trauma (i.e., induced by the dentist or health professional) to the gingiva may also lead to a gingival lesion. Such trauma may be caused directly (i.e., via use of dental instruments) or by the induction of cement or preventive or restorative materials (Fig. 5.13A). Peripheral ossifying fibroma may develop in response to the embedment of a foreign body (Fig. 5.13B–C). Self-inflicted accidental damage to the gingiva may also occur as a result of minor burns from hot foods and drinks.20 FIG. 5.13 (A) Proliferative gingival overgrowth secondary to impaction of foreign body. (B) Histology of peripheral ossifying fibroma. (C) Higher magnification of image in part B. (D) Four weeks post 345
excisional biopsy. Foreign-Body Reactions Foreign-body reactions lead to localized inflammatory conditions of the gingiva and are caused by the introduction of foreign material into the gingival connective tissues through breaks in the epithelium.20 Common examples are the introduction of amalgam into the gingiva during the placement of a restoration, the extraction of a tooth, or an endodontic apicoectomy with retrofill leaving an amalgam tattoo (Fig. 5.14A), with resultant metal fragments observed during biopsies (Fig. 5.14B); abrasives may also be introduced during polishing procedures. FIG. 5.14 (A) Gingival pigmentation associated with previous apicoectomy and amalgam retro-fill. (B) Biopsy depicts metal fragments. Periodontitis Periodontitis is defined as “an inflammatory disease of the supporting tissues of the teeth caused by specific microorganisms or groups of specific microorganisms, resulting in progressive destruction of the periodontal ligament and alveolar bone with increased probing depth formation, recession, or both.”51 The clinical feature that distinguishes periodontitis from gingivitis is the presence of clinically detectable attachment loss as a result of 346
inflammatory destruction of the periodontal ligament and alveolar bone. This loss is often accompanied by periodontal pocket formation and changes in the density and height of the subjacent alveolar bone. In some cases, recession of the marginal gingiva may accompany attachment loss, thereby masking ongoing disease progression if only probing depth measurements are taken without measurements of clinical attachment levels. Key Fact Probing depth measurement alone is inadequate for an assessment of periodontitis. Clinical attachment loss is usually assessed by adding the extent of gingival recession to the probing depth measurement to estimate the total extent of tissue loss from the cementoenamel junction (CEJ) of the tooth. However, when recession is not visible, it is essential that height of the marginal gingiva coronal to the CEJ be determined and that measurement subtracted from the probing depth to establish the extent of clinical attachment loss. The measurement of clinical attachment around a tooth provides insights on the history and extent of periodontal destruction around the tooth. One common pitfall of clinical periodontal examination is the direct translation of probing depths as clinical attachment levels when the gingival margin lies above the cementoenamel junction, leading to an overestimation of attachment levels. Clinical signs of inflammation—such as changes in color, contour, and consistency as well as bleeding with probing—may not always be positive indicators of ongoing attachment loss. However, the presence of continued bleeding with probing during sequential visits has proved to be a reliable indicator of the presence of inflammation and an increased risk for subsequent attachment loss at the bleeding site. The attachment loss associated with periodontitis may occur in a cyclic fashion, with attachment loss progressing either continuously or in episodic bursts of disease activity. However, the available clinical instruments for detecting disease are not sensitive enough to capture the cycles of attachment loss and repair that occur during disease activity and remission, 347
respectively (i.e., the periodontal probe is graded in 1-mm increments). Key Fact In the AAP/EFP 2018 classification of periodontal diseases, a multidimensional staging and grading system will be introduced to subclassify periodontitis disease entities. The severity of periodontal disease at the time of presentation and the complexity of disease management will dictate the staging, while grading offers additional information, including the rate of past progression of the disease and the risk for future progression. Although many classifications of the different clinical manifestations of periodontitis have been presented since the late 1990s, consensus workshops in North America in 19898 and in Europe in 19936 identified that periodontitis may present in early- onset, adult-onset, and necrotizing forms (Table 5.1). In addition, the AAP consensus concluded that periodontitis may be associated with systemic conditions (e.g., diabetes, HIV) and that some forms of periodontitis may be refractory to conventional therapy. Early- onset disease was distinguished from adult-onset disease by the age of onset (< 35 years of age was set as an arbitrary separation of diseases), the rate of disease progression, and the presence of alterations in host defenses. The early-onset diseases were more aggressive, occurred in individuals younger than 35 years old, and were associated with defects in host defenses. Adult forms of disease were slowly progressive, became clinically more evident during the fourth decade of life, and were not associated with defects in host defenses. In addition, early-onset periodontitis was subclassified into prepubertal, juvenile, and rapidly progressive forms with localized or generalized disease distributions. TABLE 5.1 Classification of the Various Forms of Periodontitis Classification Forms of Periodontitis Disease Characteristics AAP World Workshop in Adult periodontitis Age of onset >35 years 348
Clinical Periodontics, 19895 Slow rate of disease progression No defects in host defenses Early-onset periodontitis (may be prepubertal, juvenile, or rapidly progressive) Age of onset <35 years Rapid rate of disease progression Defects in host defenses Associated with specific microflora Periodontitis associated with systemic disease Systemic diseases that predispose to rapid rates of periodontitis Diseases: diabetes, Down syndrome, HIV infection, Papillon–Lefèvre syndrome Necrotizing ulcerative periodontitis Similar to acute necrotizing ulcerative gingivitis but with associated clinical attachment loss Refractory periodontitis Recurrent periodontitis that does not respond to treatment European Workshop in Periodontology, 19933 Adult periodontitis Age of onset: fourth decade of life Slow rate of disease progression No defects in host response Early-onset periodontitis Age of onset: before fourth decade of life Rapid rate of disease progression Defects in host defense Necrotizing periodontitis Tissue necrosis with attachment and bone loss AAP International Workshop for Classification of Periodontal Diseases, 19992 Chronic periodontitis Aggressive periodontitis Periodontitis as a manifestation of systemic diseases See Box 5.3 AAP, American Academy of Periodontology; HIV, human immunodeficiency virus. Extensive clinical and basic scientific research involving these disease entities has been performed in many countries, and emerging information has provided support for the unification of many of the preexisting disease categories.13,23,49 In particular, supporting evidence was lacking for the distinct classifications of adult periodontitis, refractory periodontitis, and the various different forms of early-onset periodontitis as outlined by the AAP Workshop for the International Classification of Periodontal Diseases in 19995 (see Table 5.1). It has been observed that chronic periodontal destruction caused by the accumulation of local factors (e.g., plaque, calculus) can occur before the age of 35 years and that the aggressive disease seen in young patients may be independent of age and instead have a familial (genetic) association. With 349
respect to refractory periodontitis, little evidence supports the theory that this condition is indeed a distinct clinical entity. The causes of continued loss of clinical attachment and alveolar bone after periodontal therapy are currently poorly defined and apply to many disease entities. In addition, clinical data from the medical community emerged to support the belief that forms of periodontitis that were collectively referred to as prepubertal periodontitis were in fact representing periodontitis as a manifestation of distinct systemic diseases, such as in leukocyte adhesion deficiency syndromes. As a result, the AAP held an International Workshop for the Classification of Periodontal Diseases in 1999 to further refine the classification system with the use of current clinical and scientific data.5 The resulting classification of the different forms of periodontitis was simplified to describe three general disease forms: chronic periodontitis, aggressive periodontitis, and periodontitis as a manifestation of systemic disease (Table 5.1 and Box 5.3). Box 5.3 Periodontitis The disease periodontitis can be subclassified into the following three major types based on clinical, radiographic, historical, and laboratory characteristics. Chronic Periodontitis The following characteristics are common to patients with chronic periodontitis: • Prevalent in adults but can occur in children • Amount of destruction consistent with local factors • Associated with a variable microbial pattern • Subgingival calculus frequently found • Slow-to-moderate rate of progression with possible periods of rapid progression • Possibly modified by or associated with the following: 350
• Systemic diseases such as diabetes mellitus and human immunodeficiency virus (HIV) infection • Local factors predisposing to periodontitis • Environmental factors such as cigarette smoking and emotional stress Chronic periodontitis may be further subclassified into localized and generalized forms and characterized as mild, moderate, or severe based on the common features described previously and the following specific features: • Localized form: <30% of teeth involved • Generalized form: >30% of teeth involved • Mild: 1 to 2 mm clinical attachment loss (CAL) • Moderate: 3 to 4 mm CAL • Severe: ≥5 mm CAL Aggressive Periodontitis The following characteristics are common to patients with aggressive periodontitis: • Otherwise clinically healthy patient (note the distinction with periodontitis as a manifestation of systemic disease) • Rapid attachment loss and bone destruction • Familial aggregation of diseased individuals The following characteristics are common but not universal: • Amount of microbial deposits inconsistent with disease severity • Increased levels of Actinobacillus actinomycetemcomitans • Abnormalities in phagocyte function • Hyper-responsive macrophages, producing increased prostaglandin E2 (PGE2) and interleukin-1β (IL-1β) • In some cases, self-arresting disease progression 351
Aggressive periodontitis may be further classified into localized and generalized forms based on the common features described here and the following specific features. Localized Form • Circumpubertal onset of disease • Localized first molar or incisor disease with proximal attachment loss on at least two permanent teeth, one of which is a first molar • Robust serum antibody response to infecting agents Generalized Form • Usually affecting persons under 30 years of age (however, may be older) • Generalized proximal attachment loss affecting at least three teeth other than first molars and incisors • Pronounced episodic nature of periodontal destruction • Poor serum antibody response to infecting agents Periodontitis as a Manifestation of Systemic Diseases Periodontitis may be observed as a manifestation of the following systemic diseases: 1. Hematologic disorders a. Acquired neutropenia b. Leukemias c. Other 2. Genetic disorders a. Familial and cyclic neutropenia b. Down syndrome c. Leukocyte adhesion deficiency syndromes d. Papillon–Lefèvre syndrome e. Chédiak–Higashi syndrome f. Histiocytosis syndromes g. Glycogen storage disease 352
h. Infantile genetic agranulocytosis i. Cohen syndrome j. Ehlers-Danlos syndrome (types IV and VIII autosomal dominant [AD]) k. Hypophosphatasia l. Other 3. Not otherwise specified Data from Flemmig TF: Periodontitis. Ann Periodontol 4:32, 1999; Kinane DF: Periodontitis modified by systemic factors. Ann Periodontol 4:54, 1999; and Tonetti MS, Mombelli A: Early-onset periodontitis. Ann Periodontol 4:39, 1999. Since the establishment of the currently accepted 1999 classification, a taskforce commissioned by the AAP proposed an update to the existing classification scheme in 2015.3 The update focused on suggestions to address the challenges in clinical documentation of attachment level changes and the distinction between chronic and aggressive periodontitis. In particular, the AAP task force recommended the consideration of probing depth levels, in addition to attachment levels, in determining the severity of periodontitis to avoid overestimation. The classification of diseases and conditions of the periodontium discussed in this chapter will focus on the currently accepted 1999 classification with references to the AAP update when appropriate. Chronic Periodontitis Chronic periodontitis is the most common form of periodontitis13 ; Box 5.3 includes the characteristics of this form of periodontitis. Chronic periodontitis is most prevalent in adults, but it can also be observed in children. Different classification schemes have confirmed or discarded the age range of more than 35 years to separate chronic versus aggressive periodontitis. According to the existing definition, persons younger than 35 years may exhibit a rate of progression of disease consistent with the definition of chronic periodontitis. Nonetheless, epidemiologic evidence supports the suggestion that persons younger than 25 years at disease onset are likely to exhibit aggressive periodontitis. Intraoral radiographs along with periodontal charting records are of 353
paramount importance to the documentation of disease onset and rate of progression. Chronic periodontitis is associated with the accumulation of plaque and calculus. It generally has a slow to moderate rate of disease progression, but periods of more rapid destruction may also be observed. Increases in the rate of disease progression may be caused by the impact of local, systemic, or environmental factors that may influence the normal host–bacteria interaction. Local factors may influence plaque accumulation (Box 5.4), whereas systemic diseases (e.g., diabetes mellitus, HIV) may influence the host's defenses, and environmental factors (e.g., cigarette smoking, stress) may influence the response of the host to plaque accumulation. Chronic periodontitis may occur as a localized disease in which less than 30% of evaluated teeth demonstrate attachment and bone loss, or it may occur as generalized when more than 30% of teeth are affected. Box 5.4 Developmental or Acquired Deformities and Conditions Localized Tooth-Related Factors That Modify or Predispose to Plaque-Induced Gingival Diseases or Periodontitis 1. Tooth anatomic factors 2. Dental restorations or appliances 3. Root fractures 4. Cervical root resorption and cemental tears Mucogingival Deformities and Conditions Around Teeth 1. Gingival or soft tissue recession a. Facial or lingual surfaces b. Interproximal (papillary) 2. Lack of keratinized gingiva 354
3. Decreased vestibular depth 4. Aberrant frenum or muscle position 5. Gingival excess a. Pseudopocket b. Inconsistent gingival margin c. Excessive gingival display d. Gingival enlargement (see Box 5.2) e. Abnormal color Mucogingival Deformities and Conditions on Edentulous Edges 1. Vertical and/or horizontal ridge deficiency 2. Lack of gingiva or keratinized tissue 3. Gingival or soft tissue enlargements 4. Aberrant frenum or muscle position 5. Decreased vestibular depth 6. Abnormal color Occlusal Trauma 1. Primary occlusal trauma 2. Secondary occlusal trauma Data from Blieden TM: Tooth-related issues. Ann Periodontol 4:91, 1999; Halmon WW: Occlusal trauma: effect and impact on the periodontium. Ann Periodontol 4:102, 1999; and Pini Prato GP: Mucogingival deformities. Ann Periodontol 4:98, 1999. Key Fact Chronic periodontitis is classified by extent and severity of disease, such as generalized (extent), moderate (severity) chronic periodontitis. Chronic periodontitis can be further classified on the basis of its extent and severity. The severity of disease has been traditionally determined as either slight/mild (1 to 2 mm of loss; Fig. 5.15), moderate (3 to 4 mm of loss; Fig. 5.16), or severe (≥5 mm of loss; Fig. 355
5.17) on the basis of the amount of clinical attachment loss (see Box 5.3). Clinical attachment levels provide important benefits over probing depth alone to monitor disease progression using the CEJ as a fixed reference point. In fact, probing depth levels only have poor to moderate sensitivity for predicting attachment level changes overtime. Nonetheless, clinical experience has revealed that oftentimes measurement of clinical attachment levels in practice may prove to be erroneous. The most common error occurs in the case of sites without gingival recession, whereby the location of the gingival margin is coronal to the CEJ. If the clinician in such a case only records the probing depth without charting the location of the CEJ (often charted as “positive recession” in electronic periodontal charts), the resulting attachment levels will be erroneously recorded as being equal to the probing depth. To prevent such an overestimate of disease, it has been suggested that clinicians consider that mild periodontitis be associated with probing depths of <4 mm, moderate periodontitis with probing depths of 5 to 6 mm, and severe periodontitis with probing depths of ≥7 mm. However, probing depths alone should not be used to classify periodontitis without simultaneous consideration of clinical attachment levels and radiographic bone loss. 356
FIG. 5.15 (A) Clinical image of plaque-related slight/early chronic periodontitis with 1- to 2-mm clinical attachment loss in 40-year-old female. (B) Radiographic images of the patient. 357
FIG. 5.16 (A) Clinical image of plaque-related moderate chronic periodontitis with 3- to 4-mm clinical attachment loss in a 53-year-old male smoker. (B) Radiographic images of the patient. FIG. 5.17 (A) Clinical image of plaque-related severe/advanced chronic periodontitis with >5 mm clinical attachment loss in a 47-year-old female. (B) Radiographic images of the patient. Key Fact In the AAP/EFP 2018 classification of periodontal diseases, one of the major changes that will be implemented is avoidance of a separate category of “aggressive periodontitis.” Both chronic and aggressive periodontitis disease entities will be grouped together and will be simply called periodontitis. Aggressive Periodontitis 358
Aggressive periodontitis differs from the chronic form primarily by the rapid rate of disease progression seen in an otherwise healthy individual (Figs. 5.18 and 5.19). The absence of large accumulations of plaque and calculus, with a positive family history of aggressive disease, is suggestive of a genetic trait34,49 (see Box 5.3). This form of periodontitis was previously classified as early-onset periodontitis (see Table 5.1) and therefore still includes many of the characteristics previously identified with the localized and generalized forms of early-onset periodontitis. Although the clinical presentation of aggressive disease appears to be universal, the causative factors involved are not always consistent. Box 5.3 outlines additional clinical, microbiologic, and immunologic characteristics of aggressive disease that may be present. As was previously described for early-onset disease, aggressive forms of periodontitis usually affect young individuals during or shortly after puberty and may be observed during the second and third decades of life (i.e., 10 to 30 years of age). The disease may be localized, as previously described for localized juvenile periodontitis, or generalized, as previously described for generalized juvenile periodontitis and rapidly progressive periodontitis (see Table 5.1). Box 5.3 describes the common features of the localized and generalized forms of aggressive periodontitis. 359
FIG. 5.18 (A) Clinical image of plaque-related aggressive moderate periodontitis with 1- to 7-mm PD and 3- to 4-mm clinical attachment loss in a 31-year- old male. (B) Radiographic images of the patient. 360
FIG. 5.19 (A) Clinical image of plaque-related aggressive severe periodontitis with 3- to 13-mm PD and 7- to 15-mm clinical attachment loss in a 32-year- old male. (B) Radiographic images of the patient. Flash Back Recall that chronic periodontitis is also categorized by the extent of localized or generalized disease according to the percentage of teeth involved with 30% of teeth being the cutoff between the two categories. Importantly, there is a distinct difference in the use of these definitions in the context of aggressive periodontitis. For aggressive periodontitis, the localized form is recognized to have a specific clinical phenotype, which is typically limited to incisor and first molar teeth. Periodontitis as a Manifestation of Systemic Disease Several hematologic and genetic disorders have been associated 361
with the development of periodontitis in affected individuals22,23 (see Box 5.3). The majority of existing publications are case reports, whereas only a few research studies have been performed to investigate the exact nature of the effect of the specific condition on the tissues of the periodontium primarily because of the rare occurrence of many of these diseases. It is speculated that the major effect of these disorders is through alterations in immune response, such as in the case of interleukin-17 overexpression in leukocyte adhesion deficiency30 or due to tissue metabolic disorders such as in some forms of Ehlers–Danlos syndrome.2 The clinical manifestation of many of these disorders appears at an early age and may be confused with aggressive forms of periodontitis depicting rapid attachment loss and the potential for early tooth loss. This was one of the drivers for the transition from the term early-onset periodontitis, which characterized a heterogeneous group of diseases, to the definitions of aggressive periodontitis and periodontitis as a manifestation of systemic diseases. With the introduction of this form of periodontitis (see Table 5.1), the potential exists for overlap and confusion between periodontitis as a manifestation of systemic disease in both the aggressive and the chronic forms of disease when a systemic component is suspected. At present, periodontitis as a manifestation of systemic disease is the diagnosis to be used when the systemic condition is the major predisposing factor and when local factors (e.g., large quantities of plaque and calculus) are not clearly evident or their presence alone does not justify the severity or progression of disease. This definition is reserved for a specific group of diseases and syndromes that have been documented to have a profound destructive effect on the periodontium. The removal of local factors as part of conventional periodontal therapy in such cases is often inadequate to arrest the periodontal destruction due to the systemic effect. When periodontal destruction is clearly the result of local factors but has been exacerbated by the onset of conditions such as diabetes mellitus (Figs. 5.20 and 5.21) or HIV infection, the diagnosis should be chronic periodontitis modified by the systemic condition. 362
FIG. 5.20 (A) Clinical image of plaque-related severe aggressive periodontitis in a 53-year-old male, smoker with diabetes and hemoglobin A1c (HbA1c) = 10.7. (B) Radiographic images of the patient. 363
FIG. 5.21 Selective probing depths of the same 53- year-old diabetic patient shown in Fig. 5.20 with severe aggressive periodontitis. Papillon–Lefèvre syndrome (PLS) is one example of a condition that causes severe periodontitis as one of its manifestations. PLS is an autosomal-recessive disorder caused by mutations in the cathepsin C gene located on chromosome 11q14.17 The clinical manifestations of the syndrome include severe aggressive periodontitis and diffuse keratoderma on the palms, the soles, the knees, or all three16 (Figs. 5.22 and 5.23). The consanguinity of the parents is a common finding in approximately one-third of the cases.31 FIG. 5.22 Panoramic radiograph and clinical photos of a 13-year-old female with Papillon–Lefèvre syndrome (PLS). PLS is an autosomal recessive disorder caused by mutations in the cathepsin C gene located on chromosome 11q14. The clinical manifestations of the syndrome are severe aggressive periodontitis as well as diffuse keratoderma on the palms, soles, or knees. 364
In PLS patients by the age of 4 to 5 years, the primary teeth have typically exfoliated or been extracted due to severe periodontal destruction. Subsequently, an edentulous phase occurs during which a reduction in the oral microbial load is noted and gingival health is restored. Following eruption of the permanent dentition, a similar cycle of severe periodontal inflammation is repeated that generally does not respond to conventional periodontal therapy. An increase in tooth mobility and periodontal abscesses is frequently observed shortly after the eruption of permanent teeth. (Courtesy Dr. Georgios Kotsakis, Seattle, Washington.) FIG. 5.23 Patient with Papillon-Lefèvre (PLS) syndrome exhibiting hyperkeratosis on palms of the hand and soles of the feet. PLS clinically affects both the primary and permanent dentition. Signs of palmoplantar keratoderma usually appear simultaneously with the eruption of the first primary teeth (5–6 months), but may appear as early as 1 month of age. (Courtesy Dr. Georgios Kotsakis, Seattle, Washington.) 365
Clinical Correlation When monogenic diseases are encountered, consanguinity can be a common finding particularly in certain ethnic cultures where it is socially acceptable. Appropriate genetic counseling is advisable. In addition, when the diagnosis for the proband (the first offspring for whom disease is noted) is established, it is crucial that the siblings are carefully examined for prompt diagnosis of additional cases. Impaired neutrophil function is considered to be the primary cause of PLS and to eventually result in the deregulation of the polymorphonuclear leukocyte response to microbial infection.11 Although the subgingival microbiota associated with PLS is diverse, opportunistic periodontal pathogens such as Aggregatibacter actinomycetemcomitans (Aa), Porphyromonas gingivalis, Tannerella forsythia, Fusobacterium nucleatum, and Prevotella intermedia are frequently identified among plaque samples from PLS patients.1,50 Serum immunoglobulin G titers against Aa are typically elevated in individuals with PLS, thereby implicating Aa as a significant causative factor.50 Individuals with PLS are often initially screened by a dermatologist or a pediatrician, and the phenotype of the syndrome may be mistaken for atopic dermatitis (eczema) or palmoplantar keratoderma.35 The case presented in Figs. 5.22 and 5.23 was treated for several years by a dermatologist as atopic dermatitis with occasional cauterization of misdiagnosed “plantar warts.” The diagnosis of PLS was established in a periodontal office. A multidisciplinary treatment approach for these patients including referral to a periodontist cannot be overemphasized. After a diagnosis of PLS has been established, it is important to collect a complete family history and to construct a pedigree to help identify undiagnosed or misdiagnosed siblings (Fig. 5.24). In 1979 Haneke proposed palmoplantar hyperkeratosis, the loss of primary and permanent teeth, and an autosomal- recessive pattern of inheritance as being essential criteria to verify a diagnosis of PLS.16 Secondary manifestations of PLS may include ectopic intracranial calcifications and increased susceptibility to infections, including pyogenic liver abscesses that can be fatal.9 366
FIG. 5.24 No history of consanguinity was reported in this case. However, approximately one-third of the diagnosed Papillon-Lefèvre (PLS) cases descend from same ancestor. Offsprings III1, III3, and III4 display a PLS phenotype. All siblings should be thoroughly examined by a periodontist once a case of PLS has been diagnosed. PLS clinically affects both the primary and permanent dentition. Signs of palmoplantar keratoderma usually appear simultaneously with the eruption of the first primary teeth (i.e., 5 to 6 months of age), but they may appear as early as the age of 1 month. By the age of 4 to 5 years, the primary teeth have typically exfoliated or been extracted as a result of severe periodontal destruction. Subsequently, an edentulous phase occurs during which a reduction in the oral microbial load is noted and gingival health is restored. After the eruption of the permanent dentition, a similar cycle of severe periodontal inflammation is repeated that generally does not respond to conventional periodontal therapy.11 An increase in tooth mobility and periodontal abscesses is frequently observed shortly after the eruption of the permanent teeth. The periodontal prognosis for patients with PLS has significantly improved in response to an increase in the prompt and accurate diagnosis of the syndrome, the better understanding of its pathogenesis, and more efficient professional supervision. There appears to be a consensus among clinicians that the successful treatment of periodontitis among individuals with PLS requires the 367
eradication of Aa.10,12,43 Treatment of the primary dentition includes frequent prophylaxis appointments to ensure that the patient maintains adequate masticatory function and nutrition during early childhood. To create a healthy environment for the permanent teeth to erupt into, it has been advocated that a course of antibiotics effective against Aa be systemically administered along with the extraction of all primary teeth 6 to 12 months before the eruption of the first permanent tooth. However, culture and sensitivity testing of the subgingival plaque may enhance the selection of the most effective antibiotic regimen. De Vree and colleagues described two patients with PLS.10 Aa was eradicated from one individual, who was able to retain most of his teeth over a 15-year period; the second individual's Aa was found to be resistant to the antibiotics combination, and he lost all of his teeth despite intensive treatment. The combination of trimethoprim and sulfamethoxazole (i.e., cotrimoxazole) has also been shown to be effective against Aa and to lead to a significant improvement in neutrophilic function against Aa.24 A stringent periodontal maintenance schedule is of utmost importance to efficaciously monitor the patient's oral hygiene and to be able to intercede promptly if signs of inflammation reoccur.32 Retinoids, which are synthetic analogues of vitamin A, a treatment modality against PLS skin manifestations, have also been considered as immunomodulatory adjuncts for the treatment of PLS-associated periodontitis.12,24 Sarcoidosis is a chronic disease that is expressed as a cell- mediated, delayed-type hypersensitivity that primarily affects the lungs, lymph nodes, skin, eyes, liver, spleen, and small bones of the hands and feet.36 Sarcoidosis rarely affects the oral cavity, with incidence of occurrence in descending order noted in the lymph nodes, lips, soft palate, buccal mucosa, gingiva, tongue, and bone.36 Fig. 5.25 depicts the pretreatment pattern of bone loss and recession associated with sarcoidosis, with pulmonary parenchymal fibrous infiltrate noted in the lungs as depicted by a white lacy pattern on a chest radiograph (Fig. 5.25C). Histologic features of sarcoidosis include the presence of an intense chronic inflammatory infiltrate with focal areas of noncaseating granulomas and a positive Kveim test (Fig. 5.26C). The remineralization of alveolar bone is noted on radiographs obtained 1 year after the systemic administration of 368
steroids (e.g., prednisone) (Fig. 5.26A). FIG. 5.25 Sarcoidosis pretreatment. (A) Intraoral x- rays depict more extensive bone loss for anterior teeth than clinical attachment loss. (B) Extensive recession plus clinical attachment loss. (C) Pulmonary parenchymal fibrous infiltrate. 369
FIG. 5.26 Sarcoidosis after treatment with prednisone. (A) Intraoral x-rays depict remineralization of bone. (B) Reduction in gingival inflammation while extensive recession and clinical attachment loss persist. (C) Pretreatment biopsy. Medication-Related Osteonecrosis of the Jaw Medication-related osteonecrosis of the jaw (MRONJ) is an updated term that has replaced the phrase bisphosphonate-related osteonecrosis of the jaw (BRONJ). Bisphosphonates (BPs) are pyrophosphate analogues with a high affinity for hydroxyapatite crystals. They inhibit osteoclast-mediated bone resorption and play a key role in the management of osteolytic bone disorders, including osteoporosis, Paget disease, bone metastasis, and multiple myeloma.44 However, their prolonged use is associated with MRONJ.18 The American Association of Oral and Maxillofacial Surgeons defined MRONJ as “exposed bone in the maxillofacial area 370
occurring in the absence of head and neck irradiation and showing no evidence of healing for at least 8 weeks after identification in patients treated with BP therapy”4 (Figs. 5.27 and 5.28). To date, the true incidence of, causes of, and risk factors for the development of MRONJ are largely unknown. An overwhelming proportion (i.e., 97%) of the reported cases are related to the high-dose intravenous BP given to patients with cancer. However, a small fraction (i.e., 3%) has been reported in patients with osteoporosis and patients with Paget disease who are receiving oral BP.18 The estimated incidence of MRONJ in patients with osteoporosis who are receiving oral BP is around 0.7 per 100,000 persons/years of exposure.4 The incidence of MRONJ among patients with cancer who are receiving intravenous BP ranges from 0.72% to 7.4%.18 FIG. 5.27 Exposed bone on buccal lower premolar and molar in medication-related osteonecrosis of the jaw (MRONJ) patient following extraction of the first molar. (Courtesy Dr. Vivek Thumbigere Math, Minneapolis.) 371
FIG. 5.28 Medication-related osteonecrosis of the jaw (MRONJ) patient with exposed bone on lingual aspect of lower premolar and molar following root canal treatment. (Courtesy Dr. Vivek Thumbigere Math, Minneapolis.) MRONJ lesions may be asymptomatic, or they may present with pain, purulent discharge, swelling, tooth mobility, and paresthesia, culminating in a reduced ability to eat and speak. MRONJ occurs most frequently in the mandible (65%), followed by the maxilla (26%) and both jaws (95%).52 The frequency of MRONJ is higher in the posterior region of the jaw. Among patients who develop MRONJ, approximately 60% of cases occur after an invasive dental procedure (e.g., tooth extraction), whereas 40% develop spontaneously.48 Radiographic evaluation is usually inconclusive for early lesions. In advanced cases, a poorly defined moth-eaten radiolucency is noted with radiopaque sequestra. Currently, there is no effective treatment for MRONJ. The discontinuance of BP is not helpful because BPs tend to reside in the bone for very long periods of time. Radical surgical intervention often exacerbates the condition, and the merit of hyperbaric oxygen treatment for the management of MRONJ is not conclusive. Patients are typically treated via minimally invasive conservative debridement, antibiotics, and chlorhexidine mouth rinses to limit the extent of the damage and to facilitate wound healing.48 The American Dental Association suggests that an oral health program that consists of sound hygiene practices and regular dental care is a valuable approach to lowering the risk of developing MRONJ.18 372
Practitioners are encouraged to use atraumatic surgical techniques and to minimize the extent of dentoalveolar manipulation. Communication with the patient's physician and proper risk assessment are fundamental to the successful management of patients who are receiving BP therapy. The use of the term MRONJ was introduced to capture the rising number of osteonecrosis cases of the jaw that are associated with new types of medication, such as other antiresorptive (denosumab) and antiangiogenic therapies, by the American Association of Oral and Maxillofacial Surgeons (AAOMS) in their 2014 update. Readers are referred to the position paper by the AAOMS for additional information on MRONJ.4 Necrotizing Periodontal Diseases The clinical characteristics of necrotizing periodontal diseases may include (but are not limited to) ulcerated and necrotic papillary and marginal gingiva that is covered by a yellowish white or grayish slough or pseudomembrane, blunting and cratering of the papillae, bleeding on provocation or spontaneous bleeding, pain, and fetid breath. These diseases may be accompanied by fever, malaise, and lymphadenopathy, although these characteristics are not consistent. Two forms of necrotizing periodontal disease have been described: necrotizing ulcerative gingivitis (NUG) (Fig. 5.29) and necrotizing ulcerative periodontitis (NUP) (Fig. 5.30). NUG was previously classified as “gingival disease” or “gingivitis,” because clinical attachment loss is not a consistent feature. NUP has been classified as a form of “periodontitis,” because attachment loss is present. Nonetheless, NUP cases are almost exclusively reported in immunocompromised persons. Both NUG and NUP have been determined to constitute a separate group of diseases that have tissue necrosis as a primary clinical feature (see Box 5.1). 373
FIG. 5.29 (A) Ulcerative gingivitis illustrating sloughing of marginal gingiva. (B) Phase-contrast microscopy reveals spirochetes in subgingival plaque sample. 374
FIG. 5.30 (A) Necrotizing ulcerative periodontitis with severe clinical attachment loss in a 28-year-old male infected with human immunodeficiency virus (HIV). (B) Spirochetes noted on surface of sloughed epithelial cells. Necrotizing Ulcerative Gingivitis The clinical and causative characteristics of NUG42 are described in detail in Chapter 20. The defining characteristics of NUG are its bacterial cause, necrotic lesion, and predisposing factors, such as psychologic stress, smoking, and immunosuppression. In addition, malnutrition may be a contributing factor in developing countries. NUG is usually seen as an acute lesion that responds well to antimicrobial therapy in combination with professional plaque and calculus removal as well as improved oral hygiene. Necrotizing Ulcerative Periodontitis NUP differs from NUG in that the loss of clinical attachment and alveolar bone is a consistent feature originating from the proximal region.33 The characteristics of NUP are described in detail in Chapter 29. NUP may be observed among HIV seropositive individuals with low CD4 counts. Clinical manifestations include local ulceration and the necrosis of gingival tissue with the exposure and rapid destruction of underlying bone as well as spontaneous bleeding and severe pain. HIV+ persons with NUP are 20.8 times more likely to have CD4+ cell counts of less than 200 cells/mm3 of peripheral blood as compared with those without NUP, which suggests that immunosuppression is a major contributing factor. NUP has also been associated with severe malnutrition in developing countries. More aggressive cases of necrotizing stomatitis exhibit tissue necrosis beyond the confines of the periodontium to include other oral tissues, such as the hard palate. Key Fact 375
Necrotizing stomatitis is a serious inflammatory condition that develops in systemically compromised individuals and is characterized by soft tissue necrosis that extends beyond the gingiva, with potential bony sequestrum formation. This disease entity is now included in the AAP/EFP 2018 classification of periodontal disease. Abscesses of the Periodontium A periodontal abscess is a localized purulent infection of periodontal tissues, and it is classified by its tissue of origin as gingival, periodontal, or pericoronal abscesses.28 The clinical, microbiologic, immunologic, and predisposing characteristics are discussed in Chapters 8, 9, and 13. Periodontitis Associated With Endodontic Lesions The classification of lesions that affect the periodontium and the pulp is based on the sequence of the disease process. Endodontic–Periodontal Lesions Pulpal necrosis precedes periodontal changes in endodontic– periodontal lesions. A periapical lesion that originates with pulpal infection and necrosis may drain to the oral cavity through the periodontal ligament, resulting in the destruction of the periodontal ligament and the adjacent alveolar bone. This may present clinically as a localized, deep, periodontal probing depth that extends to the apex of the tooth (Fig. 5.31A). If the endodontic infection is left untreated in such cases, an extensive alveolar ridge defect may occur (Fig. 5.31B−C), thereby necessitating reconstructive surgery (Fig. 5.31D) before the placement of implants and prostheses (Fig. 5.32) to reestablish a functional and aesthetic outcome. Pulpal infection may also drain through accessory canals, especially in the area of the furcation, which may lead to furcal involvement through the loss of clinical attachment and alveolar bone. 376
FIG. 5.31 (A and C) Clinical images of extensive loss of alveolar ridge secondary to periapical endodontic lesion. (B) CT scan depicts alveolar bone loss. (D) CT image of regenerated ridge via allogenic bone graft, tenting screw, and membrane. 377
FIG. 5.32 Same patient depicted in Fig. 5.31. (A–B) CT scans of regenerated ridge with implants placed in areas 7, 9, and 10. (C–D) Clinical images of implant- supported bridge. Clinical Correlation In early stages of primary endodontic lesions, root canal therapy may be the only treatment necessary to restore the periodontal apparatus. Periodontal–Endodontic Lesions It is more uncommon for periodontal disease to lead to endodontic disease than vice versa. In a periodontal–endodontic lesion, the bacterial infection from a periodontal pocket leads to loss of attachment, and root exposure then spreads to the pulp, resulting in pulpal necrosis. In the case of advanced periodontal disease, the infection may reach the pulp through the apical foramen. Nonetheless, existing studies have shown that although scaling and 378
root planing remove cementum and underlying dentin, they may lead to dentine hypersensitivity but not to irreversible pulpitis. Combined Lesions Combined lesions occur when pulpal necrosis and a periapical lesion occur on a tooth that is also periodontally involved. An intrabony defect that communicates with a periapical lesion of pulpal origin results in a combined periodontal–endodontic lesion. In all cases of periodontitis associated with endodontic lesions, the endodontic infection should be controlled before the definitive management of the periodontal lesion begins, especially when regenerative or bone-grafting techniques are planned.29 Tooth prognosis in combined lesions highly depends on the outcome of the periodontal treatment. Developmental or Acquired Deformities and Conditions Localized Tooth-Related Factors That Modify or Predispose Individuals to Plaque-Induced Gingival Diseases or Periodontitis In general, localized tooth-related factors contribute to the initiation and progression of periodontal disease through the enhancement of plaque accumulation or the prevention of effective plaque removal via normal oral hygiene measures.7 These factors fall into the four subgroups outlined in Box 5.4. Tooth Anatomic Factors Tooth anatomic factors are associated with malformations of tooth development or tooth location. Anatomic factors (e.g., cervical enamel projections, palatal grooves, enamel pearls) have been associated with clinical attachment loss, especially in furcation areas. Cervical enamel projections are found on 15% to 24% of 379
mandibular molars and on 9% to 25% of maxillary molars, and strong associations have been observed with furcation involvement.27 Palatogingival grooves, which are found primarily on maxillary incisors, are observed in 8.5% of the population and are associated with increased plaque accumulation and clinical attachment as well as bone loss. Proximal root grooves on incisors and maxillary premolars also predispose individuals to plaque accumulation, inflammation, and the loss of clinical attachment and bone. Tooth location is considered important for the initiation and development of disease. Misaligned teeth predispose individuals to plaque accumulation with resultant inflammation in children, and they may predispose adults to clinical attachment loss, especially when they are associated with poor oral hygiene habits. Open interproximal contacts that contribute to food impaction have been associated with an increased loss of attachment.21 Dental Restorations and Appliances Dental restorations or appliances are frequently associated with the development of gingival inflammation. Restorations placed deep in the sulcus or within the junctional epithelium may impinge on the biologic width resulting in inflammation and the loss of clinical attachment and bone. Contour of a complete crown restoration can affect plaque retention with flat surfaces being more hygienic as compared to convex restorations exhibiting increased bulk of material at the cervical region. Root Fractures Root fractures may be associated with endodontic or restorative procedures as well as traumatic forces (Fig. 5.33A–C) and may lead to periodontal involvement through the apical migration of plaque along the fracture line (Fig. 5.33D). 380
FIG. 5.33 (A–B) Clinical images of fistula tract. (C) Root fracture. (D) Resultant alveolar ridge defect. Flash Back Vertical root fractures involving both the pulp and PDL are true combined endodontic–periodontal lesions. Cervical Root Resorption and Cemental Tears Invasive cervical root resorption (ICR) (as noted on the cone beam computed tomography scans shown in Fig. 5.34A–B) and cemental tears may lead to periodontal destruction when the lesion communicates with the oral cavity and allows bacteria to migrate subgingivally. The atraumatic removal of teeth with progressed cervical resorption lesions and the reconstruction of resultant ridge defects with bone grafts, dental implants, and prostheses are viable solutions for such defects (Fig. 5.35). Avulsed teeth that are reimplanted frequently develop ankylosis and cervical root resorption many years after reimplantation. If the patient is still in the phase of skeletal growth, decoronation may be the treatment of choice for ridge preservation. In adults with completed skeletal growth, atraumatic removal of such ankylosed teeth, followed by ridge reconstruction and placement of implants and prosthesis, is a 381
viable treatment option in adults (see Fig. 5.35). FIG. 5.34 (A–B) CT scans reveal severe cervical root resorption of maxillary central incisors and periapical abscess. (C) Crowns fractured because of resorption. (D) Biopsy of soft tissue from resorption. 382
FIG. 5.35 (A) Posttreatment clinical image of same patient depicted in Fig. 5.34 with implant-supported crowns and veneers on laterals. (B–C) CT scans of bone grafts and implants replacing central incisors lost as the result of severe cervical root resorption. Mucogingival Deformities and Conditions Around the Teeth Mucogingival deformity is a generic term used to describe the mucogingival junction and its relationship to the gingiva (Fig. 5.36), the alveolar mucosa, and frenula muscle attachments. A mucogingival deformity is a significant departure from the normal shape of the gingiva and the alveolar mucosa, and it may involve the underlying alveolar bone. Mucogingival surgery and periodontal plastic and aesthetic surgery correct defects in the morphology, position, or amount of gingiva. This subject is described in detail in Chapter 65. The surgical correction of mucogingival deformities may be performed for aesthetic reasons, to enhance function, or to facilitate oral hygiene.37 383
FIG. 5.36 (A) Mucogingival defect depicted by recession. (B) Defects extend into alveolar mucosa and lack keratinized gingiva. Mucogingival Deformities and Conditions of the Edentulous Ridges Mucogingival deformities, such as a lack of stable keratinized gingiva between the vestibular fornices and the floor of the mouth (Fig. 5.37A), may require soft-tissue grafting and vestibular deepening before prosthodontic reconstruction (Fig. 5.37B–D). Alveolar bone defects in edentulous ridges (Fig. 5.38A–B) usually require corrective surgery (Fig. 5.38C–D) to restore form and function before the placement of implants and prostheses to replace missing teeth (Fig. 5.39).37 384
FIG. 5.37 (A) Mucogingival ridge defect from floor of mouth to vestibular fornix. (B) Partial thickness flap with vestibular deepening. (C) Placement of free gingival graft. (D) Reestablishment of vestibular depth and keratinized attached gingiva. 385
FIG. 5.38 (A) Clinical image of edentulous ridge defect. (B) Pretreatment CT image of defect. (C) Reconstructed ridge using ramus block graft. (D) CT scan of grafted site. FIG. 5.39 (A) Clinical image of ridge 6 months after grafting. (B) Placement of implants in area of teeth #23 and #25. (C) Porcelain fused to metal (PFM) crowns for maxillary incisors and implant-supported bridge from teeth #23 to #25. 386
Occlusal Trauma The causes of trauma from occlusion and the effect of this trauma on the periodontium14 are discussed in detail in Chapters 26 and 55. Case Scenario 5.1 Patient: 63 year-old male, former smoker (20 pack-years) Chief Complaint: Presents for scheduled quarterly maintenance visit. Background Information The patient was treated with repeated sessions of scaling and root planing as well as periodontal flap surgery several years ago. He has since been very compliant with a 3-month maintenance schedule. Clinical Findings: Intraoral evaluation reveals 2 to 7 mm of clinical attachment loss throughout his dentition with probing depth measurements ranging from 1 to 3 mm. The plaque control record was 20%, and localized bleeding on probing was noted on the distal of #7 and lingual of #30. The diagnosis was determined to be localized gingivitis on a reduced periodontium. 387
CASE-BASED QUESTION SOLUTION AND EXPLANATION 1. If the patient's compliance becomes erratic and periodontitis relapses, how would you classify the patient's condition? A. Gingivitis B. Mild periodontitis C. Moderate periodontitis D. Severe periodontitis Answer: D Explanation: In the case of reduced periodontium, it is critical to consider the extent of preexisting attachment loss. This attachment loss is definitive, and further progression can negatively affect teeth prognosis. Case Scenario 5.2 Patient: 55-year-old male, nonsmoker Chief Complaint: “My gum has receded and it's bleeding.” Background Information The patient presents with aesthetic complaints associated with gingival recession and associated root exposure on the upper central incisors. The patient also reports occasional sensitivity and bleeding from the area. The patient was treated with repeated sessions of scaling and root planing as well as periodontal flap surgery several years ago. He has since been very compliant with a 3-month maintenance schedule. Current Findings: White striations on the gingiva facial of #9 and #10 were noted. During clinical examination, gentle finger rubbing of the mucosa coronal to #9 led to exfoliation of the epithelium. 388
CASE-BASED QUESTION SOLUTION AND EXPLANATION 1. Do you expect scaling and root planing to treat this condition? A. Yes B. No Answer: B Explanation: This mucocutaneous lesion was biopsied and the diagnosis of lichen planus was confirmed following clinical assessment and positive Nikolsky's sign. Appropriate corticosteroid treatment led to remission. Case Scenario 5.3 Patient: 62-year-old postmenopausal female Chief Complaint: “I have noticed that I have halitosis, and my gums bleed.” Background Information The patient says that she cannot brush her teeth because her gums have been painful for 6 months. Current Findings: Gingiva sloughs following the application of a cotton swab. 389
CASE-BASED QUESTION SOLUTION AND EXPLANATION 1. What is the most likely diagnosis? A. Acute necrotizing gingivitis B. Toothbrush abrasion C. Mucous membrane pemphigoid D. Sarcoidosis Answer: C Explanation: Immunofluorescence-labelled antibodies are used to mark an antigen/antibody complex in the basement membrane where autoimmune reaction causes degeneration of basal lamina, hemidesmosomes, and anchoring fibrils, thereby resulting in sloughing of epithelium. 390
Case Scenario 5.4 Patient: 28-year-old male Chief Complaint: “My lower front teeth are mobile.” Background Information Progressive recession through dentition over the past 2 years. Painful rampant recession in the anterior mandible recently. Current Findings: Cratered papillae, ulcerative gingiva with exposed interproximal bone. CASE-BASED QUESTION SOLUTION AND EXPLANATION 1. When you consult with the patient's physician, what is the most likely medical diagnosis? A. Osteoporosis B. Diabetes mellitus C. AIDS D. Medication- related osteonecrosis of the jaw Answer: C Explanation: Necrotizing ulcerative periodontitis may be observed among HIV+ patients with very low CD4 counts (AIDS) and be manifested as local ulceration and necrosis of gingival tissue with exposed bone. 391
Case Scenario 5.5 Patient: 59-year-old postmenopausal female Chief Complaint: “My lower jaw is sore and aches.” Background Information Lower first molar extracted ~ 4 months. Current Findings: Medication-related osteonecrosis of the jaw (MRONJ) with exposed alveolar bone. Radiographic Findings: Within normal limits. 392
CASE-BASED QUESTION SOLUTION AND EXPLANATION 1. What is the most likely medical diagnosis associated to MRONJ? A. Osteopenia B. Osteoporosis C. Malignant myeloma D. Localized osteomyelitis Answer: C Explanation: Bisphosphonates (BPs) inhibit osteoclast-mediated bone resorption. BPs are used to manage osteolytic bone disorders such as osteoporosis, Paget disease, metastatic bone cancers, and multiple myeloma. Case Scenario 5.6 Patient: 6-year-old male 393
Chief Complaint: “My classmates tease me and call me ‘gummy.’ I have difficulty chewing my food and talking.” Background Information Patient has had a kidney transplant. Current Findings: Severe gingival overgrowth. Radiographic Findings: Within normal limits. CASE-BASED QUESTION SOLUTION AND EXPLANATION 1. All of the following drug categories have been associated with gingival overgrowth EXCEPT which one? A. Antiarrhythmic, digoxin B. Anticonvulsant, phenytoin C. Calcium channel blocker, nifedipine D. Immunosuppressant, cyclosporine Answer: A Explanation: Phenytoin, nifedipine, and cyclosporine have all been associated with gingival overgrowth, while digoxin has not been associated with overgrowth. 394
Case Scenario 5.7 Patient: 27-year-old female Chief Complaint: “There is a bump on my gums that bleeds when I brush and floss.” Background Information Lesion developed over past ~ 2 months. Current Findings: Biopsy depicted in lower image. Radiographic Findings: Within normal limits. 395
CASE-BASED QUESTION SOLUTION AND EXPLANATION 1. What is the most likely diagnosis? A. Fibroma B. Lateral periodontal abscess C. Epulis fissuratum D. Pyogenic granuloma Answer: D Explanation: Biopsy depicts inflammatory cell infiltrate within the connective tissue and numerous capillaries engorged with erythrocytes. References 1. Albandar JM, Khattab R, Monem F, et al. The subgingival microbiota of Papillon-Lefèvre syndrome. J Periodontol. 2012;83:902–908. 2. Aldred MJ, Bartold PM. Genetic disorders of the gingivae and periodontium. Periodontol 2000. 1998;18:7. 3. American Academy of Periodontology Task Force Report on the update to the 1999 classification of periodontal diseases and conditions. J Periodontol. 2015;86:835–838. 4. American Association of Oral and Maxillofacial. Surgeons position paper on bisphosphonate-related osteonecrosis of the jaws. J Oral Maxillofac Surg. 2007;65:369–376. 5. Armitage GC. Development of a classification system for periodontal diseases and conditions. Ann Periodontol. 1999;4:1. 6. Attstrom R, Vander Velden U. Summary of session 1. Lang N, Karring T. Proceedings of the 1st European Workshop in Periodontology. Quintessence: Berlin; 1993. 7. Blieden TM. Tooth-related issues. Ann Periodontol. 1999;4:91. 8. Caton J. Periodontal diagnosis and diagnostic aids: consensus report. Proceedings of the Wold Workshop in Clinical. American Academy of Periodontology: Chicago; 1989. 9. Dalgic B, Bukulmez A, Sari S. Pyogenic liver abscess and peritonitis due to Rhizopus oryzae in a child with Papillon– Lefevre syndrome. Eur J Pediatr. 2011;170:803–805. 396

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1, Klasifikasi Newman and Carranza's Clinical Periodontology E-Book.pdf

  • 1.
    SECTION II Classification and Epidemiologyof Periodontal Diseases OUTLINE Chapter 5 Classification of Diseases and Conditions Affecting the Periodontium Chapter 6 Fundamentals in the Methods of Periodontal Disease Epidemiology 325
  • 2.
    CHAPTER 5 Classification of Diseasesand Conditions Affecting the Periodontium James E. Hinrichs, Georgios A. Kotsakis CHAPTER OUTLINE Gingival Diseases Periodontitis Medication-Related Osteonecrosis of the Jaw Necrotizing Periodontal Diseases Abscesses of the Periodontium Periodontitis Associated With Endodontic Lesions Developmental or Acquired Deformities and Conditions Our understanding of the causes and pathogenesis of oral diseases 326
  • 3.
    and conditions changescontinually with increased scientific knowledge. In light of this fact, a classification can be most consistently defined by the differences in the clinical manifestations of diseases and conditions: they are clinically consistent and require little (if any) clarification by laboratory testing. The current classification of periodontal diseases is based on their extent (generalized versus localized), severity (slight, moderate, or severe), rate of progression (aggressive versus chronic), and localization (i.e., contained within the gingiva, as in gingivitis, or further involving periodontal bone loss, as in periodontitis). The existing definitions encompass the best available way to universally define a spectrum of diseases affecting the periodontal tissues and to guide therapeutic approaches. Nonetheless, the disease state is dynamic, and the appropriate diagnosis for an individual can change over time. For instance, a patient diagnosed with existing periodontitis who undergoes successful periodontal therapy may be classified as having a healthy but reduced periodontium (with slight, moderate, or severe attachment loss) at the reevaluation. Subsequently, if the same individual presents with gingival inflammation without signs of further attachment loss at a future appointment, the appropriate diagnosis would be “gingivitis on a reduced periodontium.” Depending on their future compliance with home care and maintenance visits, patients may progress to periodontitis or maintain a healthy but reduced periodontium. The case example highlights the importance of conceptualizing the dynamic nature of inflammatory diseases that affect the periodontium, while appreciating the importance of commonly accepted definitions for periodontal diseases. If a case of gingivitis on a reduced periodontium relapses into periodontitis, the prognosis of the affected teeth will depend on the preexisting attachment loss. The classification presented in this chapter is based on the most recent internationally accepted consensus on the diseases and conditions that affect the tissues of the periodontium. Box 5.1 presents the overall classification system that was proposed at the 1999 International Workshop for a Classification of Periodontal Diseases and Conditions. More recent views on the Classification of Periodontal Diseases and Conditions are also discussed. Each disease or condition is explored where clarification is needed. In 327
  • 4.
    each case, thereader is referred to pertinent reviews on the subject and specific chapters within this book that discuss the topics in more detail. Box 5.1 Classification of Periodontal Diseases and Conditions Gingival Diseases Plaque-induced gingival diseasesa Non–plaque-induced gingival lesions Chronic Periodontitisb Localized Generalized Aggressive Periodontitis Localized Generalized Periodontitis as a Manifestation of Systemic Diseases Necrotizing Periodontal Diseases Necrotizing ulcerative gingivitis (NUG) Necrotizing ulcerative periodontitis (NUP) Abscesses of the Periodontium Gingival abscess Periodontal abscess Pericoronal abscess 328
  • 5.
    Periodontitis Associated WithEndodontic Lesions Endodontic–periodontal lesion Periodontal–endodontic lesion Combined lesion Developmental or Acquired Deformities and Conditions Localized tooth-related factors that predispose to plaque- induced gingival diseases or periodontitis Mucogingival deformities and conditions around teeth Mucogingival deformities and conditions on edentulous ridges Occlusal trauma a These diseases may occur on a periodontium with no attachment loss or on a periodontium with attachment loss that is stable and not progressing. b Chronic periodontitis can be further classified based on extent and severity. As a general guide, extent can be characterized as localized (<30% of teeth involved) or generalized (>30% of teeth involved). Severity can be characterized based on the amount of clinical attachment loss (CAL) as follows: slight = 1 or 2 mm CAL, moderate = 3 or 4 mm CAL, and severe ≥5 mm CAL. Data from Armitage GC: Development of a classification system for periodontal diseases and conditions. Ann Periodontol 4:1, 1999. An updated classification system, which is currently being developed jointly by the American Academy of Periodontology (AAP) and the European Federation of Periodontology (EFP), is scheduled to publish around the time of the release of this book. The goal of this effort is to address some of the shortcomings that exist with the current classification system (discussed in this chapter), including diagnostic inaccuracy and significant overlap of disease entities. Several working groups were created to focus on specific disease entities using the currently available scientific evidence, resulting in the most substantial update to the classification system since 1999. To view the updated AAP/EFP 2018 classification system, visit 329
  • 6.
    the companion websitewww.expertconsult.com. Gingival Diseases Dental Plaque–Induced Gingival Diseases Gingivitis that is associated with retained dental plaque is the most common form of gingival disease (Fig. 5.1). Box 5.2 outlines the classifications of gingival diseases. These diseases may occur on a periodontium with no attachment loss or on a periodontium with attachment loss that is stable and not progressing (i.e., reduced periodontium). The epidemiology of periodontal diseases is reviewed in Chapter 6, and its causes are detailed in Chapters 7 through 15 in this textbook.15,23,26,39,40 What separates gingivitis from periodontitis is the containment of the inflammatory lesion within the gingiva in the former. As such, gingivitis is not associated with progressive attachment loss. This is not to say that gingivitis is solely associated with teeth showing no attachment loss (Fig. 5.2). Gingivitis can also be diagnosed in the gingiva of periodontitis- affected teeth that have previously lost attachment but that have been successfully treated with periodontal therapy to prevent any further attachment loss. In these treated cases, where gingival inflammation recurs around teeth with existing attachment loss due to a history of treated periodontitis, the appropriate diagnosis would be gingivitis on a reduced periodontium. This implies that gingivitis may be the diagnosis for inflamed gingival tissues associated with a tooth with no previous attachment loss or with a tooth that has previously undergone attachment and bone loss (i.e., with reduced periodontal support) and is not currently losing attachment or bone, even though gingival inflammation is present. Clinical attachment levels and radiographic records are needed to establish this diagnosis. 330
  • 7.
    FIG. 5.1 (A)Plaque-related gingivitis depicts marginal and papillary inflammation, with 1- to 4-mm probing depths and generalized zero clinical attachment loss, except recession in tooth #28. (B) Radiographic images of the patient. Box 5.2 Gingival Diseases Dental Plaque–Induced Gingival Diseases These diseases may occur on a periodontium with no attachment loss or with attachment loss that is stable and not progressing. I. Gingivitis associated with dental plaque only A. Without local contributing factors B. With local contributing factors (see Box 5.4) II. Gingival diseases modified by systemic factors A. Associated with endocrine system 331
  • 8.
    1. Puberty-associated gingivitis 2.Menstrual cycle–associated gingivitis 3. Pregnancy associated a. Gingivitis b. Pyogenic granuloma 4. Diabetes mellitus–associated gingivitis B. Associated with blood dyscrasias 1. Leukemia-associated gingivitis 2. Other III. Gingival diseases modified by medications A. Drug-influenced gingival diseases 1. Drug-influenced gingival enlargements 2. Drug-influenced gingivitis a. Oral contraceptive–associated gingivitis b. Other IV. Gingival diseases modified by malnutrition A. Ascorbic acid deficiency gingivitis B. Other Non–Plaque-Induced Gingival Lesions I. Gingival diseases of specific bacterial origin A. Neisseria gonorrhoeae B. Treponema pallidum C. Streptococcus species D. Other II. Gingival diseases of viral origin A. Herpesvirus infections 1. Primary herpetic gingivostomatitis 2. Recurrent oral herpes 3. Varicella zoster B. Other III. Gingival diseases of fungal origin A. Candida species infections: generalized gingival candidiasis B. Linear gingival erythema 332
  • 9.
    C. Histoplasmosis D. Other IV.Gingival lesions of genetic origin A. Hereditary gingival fibromatosis B. Other V. Gingival manifestations of systemic conditions A. Mucocutaneous lesions 1. Lichen planus 2. Pemphigoid 3. Pemphigus vulgaris 4. Erythema multiforme 5. Lupus erythematosus 6. Drug induced 7. Other B. Allergic reactions 1. Dental restorative materials a. Mercury b. Nickel c. Acrylic d. Other 2. Reactions attributable to the following: a. Toothpastes or dentifrices b. Mouth rinses or mouthwashes c. Chewing gum additives d. Foods and additives 3. Other VI. Traumatic lesions (factitious, iatrogenic, or accidental) A. Chemical injury B. Physical injury C. Thermal injury VII. Foreign body reactions VIII. Not otherwise specified Data from Holmstrup P: Non–plaque-induced gingival lesions. Ann Periodontol 4:20, 1999; and Mariotti A: Dental plaque-induced gingival diseases. Ann Periodontol 4:7, 1999. 333
  • 10.
    FIG. 5.2 Maxillarysecond molar exhibits mild inflammation at mesial-palatal surface. However, the clinical attachment loss has been stable for 15 years after apical positioned flap and periodontal maintenance, which is consistent with remission. The appropriate diagnosis is gingivitis on a reduced periodontium. Key Fact Gingivitis may be the diagnosis for inflamed gingival tissues associated with a tooth without previous attachment loss or with a tooth that has previously undergone attachment and bone loss (i.e., with reduced periodontal support) but is not currently losing attachment, even though gingival inflammation is present. In the latter case the appropriate definition would be “gingivitis on a reduced periodontium.” Gingivitis Associated With Dental Plaque Only Plaque-induced gingival disease is the result of an interaction between the microorganisms found in the dental plaque biofilm and the inflammatory host response. A cause-and-effect relationship between microbial plaque and gingivitis has been elegantly demonstrated by a classic experiment demonstrating that the cessation of oral hygiene consistently leads to the manifestation of gingivitis within 2 to 3 weeks in healthy adults.25 Clinical 334
  • 11.
    gingivitis is histologicallycharacterized by a dense infiltrate of lymphocytes and other mononuclear cells, fibroblast alterations, increased vascular permeability, and continuing loss of collagen in response to the microbial challenge. However, the alveolar bone is not affected. Microbial plaque is thus considered to be the primary etiologic factor for gingivitis. The severity and duration of the inflammatory response interaction can be altered by the modifying local (see Chapter 13) or systemic modifying factors (see Chapters 14 and 15). Gingivitis is fully reversible in otherwise healthy persons within weeks following the removal of local factors and reduction of the microbial load around the teeth. As noted earlier, gingivitis is rapidly established in cases of generalized or localized inefficient plaque removal. Therefore it is crucial that patients are instructed in oral hygiene to maintain long-term gingival health. Gingival Diseases Modified by Systemic Factors Systemic factors that contribute to gingivitis—such as the endocrine changes associated with puberty (Fig. 5.3), the menstrual cycle, pregnancy (Fig. 5.4A), and diabetes—may exacerbate the gingival inflammatory response to plaque.23,39 This altered response appears to result from the effects of systemic conditions on the host's cellular and immunologic functions, but the primary etiologic factor is still considered to be microbial plaque. One example of altered host response due to systemic factors is apparent during pregnancy when the incidence and severity of gingival inflammation may increase even in the presence of low levels of plaque. 335
  • 12.
    FIG. 5.3 A13-year-old female with hormone- exaggerated marginal and papillary inflammation, with 1- to 4-mm probing depths yet minimal clinical attachment loss. (A) Facial view. (B) Lingual view. FIG. 5.4 (A) Clinical image of pyogenic granuloma in a 27-year-old pregnant female. (B) Histologic image depicts dense inflammatory infiltrate and prominent vessels. 336
  • 13.
    Clinical Correlation Increased estrogenand progesterone levels in pregnant women during their third trimester have been associated with increased severity of gingivitis via substituting nutrient needs for certain oral bacteria and stimulating their proliferation. One species that has been specifically associated with gingivitis during pregnancy is Prevotella intermedia. In blood dyscrasias (e.g., leukemia), the reduced number of immunocompetent lymphocytes in the periodontal tissues is associated with increased edema, erythema, and bleeding of the gingiva as well as gingival enlargement that may be associated with the swollen, spongy gingival tissues caused by the excessive infiltration of malignant blood cells (Fig. 5.5). FIG. 5.5 A 12-year-old female with a primary medical diagnosis of leukemia that exhibits swollen/spongy gingiva. Gingival Diseases Modified by Medications Gingival diseases that are modified by medications include gingival overgrowth due to anticonvulsant drugs such as phenytoin, immunosuppressive drugs such as cyclosporine (Fig. 5.6), and 337
  • 14.
    calcium channel blockerssuch as nifedipine (Fig. 5.7), verapamil, diltiazem, and sodium valproate.15,26,39 The development and severity of gingival enlargement in response to medications is patient specific and may be influenced by uncontrolled plaque accumulation as well as by elevated hormonal levels. The increased use of oral contraceptives by premenopausal women has also been previously associated with a higher incidence of gingival inflammation and gingival enlargement. Although this fact stood true for earlier contraceptive formulations, existing contraceptives that include more modest doses of active ingredients are not commonly associated with gingival inflammation. FIG. 5.6 Clinical images of a 9-year-old male with severe gingival overgrowth secondary to heart transplant and cyclosporine therapy. 338
  • 15.
    FIG. 5.7 Clinicalimages of gingival overgrowth following use a of calcium channel blocker to control hypertension. Gingival Diseases Modified by Malnutrition Gingival diseases modified by malnutrition have received attention because of clinical descriptions of bright red, swollen, and bleeding gingiva associated with severe ascorbic acid (vitamin C) deficiency or scurvy.26 Various nutrients, such as long chain omega-3 fatty acids, have been found to have immunomodulatory properties, whereas others act to ameliorate the destructive effects of reactive oxygen species (ROS) functioning as ROS scavengers. Nonetheless, the available evidence to support a clinically impactful role for mild nutritional deficiencies in the development or severity of gingival inflammation in humans is limited. Data have shed light on the implication of increased dietary carbohydrate intake on gingivitis, in addition to its known causal role on the occurrence of dental caries.19 Non–Plaque-Induced Gingival Lesions Oral manifestations of systemic conditions that produce lesions in the tissues of the periodontium are less common than plaque- induced gingivitis. This category mainly encompasses lesions of autoimmune or idiopathic etiology that can manifest in the gingiva. Benign mucous membrane pemphigoid is an example of a non– plaque-induced lesion associated with sloughing gingival tissues, which leave painful ulcerations of the gingiva (Fig. 5.8). In pemphigoid, autoimmune antibodies are targeted at the basement membrane, and histologically the destruction resembles a 339
  • 16.
    subepithelial blister (Fig.5.8C–D). Case Scenario 5.2 depicts gingival recession accompanied by a mucosal lesion located on the gingiva manifesting with a white lacy pattern with characteristic striations. FIG. 5.8 A 62-year-old female with benign mucous membrane pemphigoid. (A–B) Clinical image with sloughing epithelial surface. (C) Hematoxylin and eosin (H&E) stain depicting separation of epithelium from connective tissue. (D) Immunofluorescent-labeled antibodies to basement membrane. Gingival Diseases of Specific Bacterial Origin Gingival diseases of this category are attributed to specific bacteria that cause characteristic lesions in the gingiva. Neisseria gonorrhoeae and Treponema pallidum that can be transferred as a result of sexually transmitted diseases such as gonorrhea and syphilis, respectively, cause characteristic lesions in the gingiva.41,46 Refer to the online references for further description. Streptococcal gingivitis or gingivostomatitis is a rare entity that may present as an acute condition with fever, malaise, and pain associated with acutely inflamed, diffuse, red, and swollen gingiva with increased bleeding and occasional gingival abscess formation. The gingival infections 340
  • 17.
    are usually precededby tonsillitis. Gingival Diseases of Viral Origin Gingival diseases of viral origin may be caused by a variety of deoxyribonucleic acid and ribonucleic acid viruses, with the most common being the herpesviruses. A case example of herpetic stomatitis is demonstrated in Fig. 5.9A–B. Herpetic lesions are not uncommon and develop as intraoral blisters, usually grouped together, that quickly burst, leaving minuscule ulcerations. Lesions are frequently related to the reactivation of latent viruses, especially as a result of reduced immune function. The oral manifestations of viral infection have been comprehensively reviewed.20,45 Viral gingival diseases are treated with topical or systemic antiviral drugs (Fig. 5.9C–D). FIG. 5.9 (A–B) A 29-year-old male with primary herpetic infection and severe gingival inflammation. (C–D) Six weeks post systemic acyclovir. 341
  • 18.
    Clinical Correlation Unlike otherherpetic recurrences, varicella zoster virus (VZV) usually manifests with a prodrome of tingling, itching, burning, or a unilateral numbness at the affected dermatome. These symptoms are followed by moderate to severe pain shortly after initiation and are very important for differential diagnosis. Gingival Diseases of Fungal Origin Gingival diseases of fungal origin are relatively uncommon in immunocompetent individuals, but they occur more frequently in immunocompromised individuals and in those with disturbed microbiota by the long-term use of broad-spectrum antibiotics.20,46,47 The most common oral fungal infection is candidiasis (Candida albicans is often implicated). Candidiasis can also be seen under prosthetic devices, in individuals using topical steroids, and in individuals with decreased salivary flow, increased salivary glucose, or decreased salivary pH. A generalized candidal infection may manifest as white patches on the gingiva, tongue, or oral mucous membrane that can potentially be removed with gauze and leave a red, bleeding surface. In human immunodeficiency virus (HIV) seropositive persons, candidal infection may present as continuous erythematous stripe of the attached gingiva; this has been referred to as linear gingival erythema or HIV-associated gingivitis (see Chapter 30). The diagnosis of candidal infection can be made by culture, smear, or biopsy. Less common fungal infections have also been described.46,47 Gingival Diseases of Genetic Origin Gingival diseases of genetic origin may involve the tissues of the periodontium and have been described in detail.2 One of the most clinically evident conditions is hereditary gingival fibromatosis, which exhibits autosomal-dominant or (rarely) autosomal-recessive modes of inheritance. The gingival enlargement may completely cover the teeth, delay eruption, and present as an isolated finding; alternatively, it may be associated with several more generalized syndromes. 342
  • 19.
    Gingival Manifestations ofSystemic Conditions Gingival manifestations of systemic conditions may appear as desquamative lesions, ulcerations of the gingiva, or both.20,38,46 Allergic reactions that manifest with gingival changes are uncommon but have been observed in association with several restorative materials (Fig. 5.10A), toothpastes, mouthwashes, chewing gums (Fig. 5.11), and foods (see Box 5.2). The diagnosis of these conditions may prove difficult and may require an extensive history and the selective elimination of potential causes. Conjoint assessment with an allergologist is indicated, and percutaneous tests are often recommended. Histologic traits of biopsies from gingival allergic reactions include a dense infiltrate of eosinophilic cells (Fig. 5.10B–C). FIG. 5.10 (A) Localized pronounced gingival inflammation secondary to nickel allergy. (B–C) Biopsy 343
  • 20.
    depicts dense infiltrateof plasma cells. FIG. 5.11 Generalized severe allergic response of gingiva as a result of additive in chewing gum. Traumatic Lesions Traumatic lesions may be self-inflicted and factitious in origin, which means that they are intentionally or unintentionally produced by artificial means (Fig. 5.12). Other examples of traumatic lesions include toothbrush trauma that results in gingival ulceration, recession, or both. FIG. 5.12 Self-inflicted gingival dehiscence induced via 344
  • 21.
    patient's fingernail. Clinical Correlation Individualswho perform aggressive horizontal brushing are often found to have gingival recession or cervical abrasion on the teeth quadrants contralateral to their dominant hand. Iatrogenic trauma (i.e., induced by the dentist or health professional) to the gingiva may also lead to a gingival lesion. Such trauma may be caused directly (i.e., via use of dental instruments) or by the induction of cement or preventive or restorative materials (Fig. 5.13A). Peripheral ossifying fibroma may develop in response to the embedment of a foreign body (Fig. 5.13B–C). Self-inflicted accidental damage to the gingiva may also occur as a result of minor burns from hot foods and drinks.20 FIG. 5.13 (A) Proliferative gingival overgrowth secondary to impaction of foreign body. (B) Histology of peripheral ossifying fibroma. (C) Higher magnification of image in part B. (D) Four weeks post 345
  • 22.
    excisional biopsy. Foreign-Body Reactions Foreign-bodyreactions lead to localized inflammatory conditions of the gingiva and are caused by the introduction of foreign material into the gingival connective tissues through breaks in the epithelium.20 Common examples are the introduction of amalgam into the gingiva during the placement of a restoration, the extraction of a tooth, or an endodontic apicoectomy with retrofill leaving an amalgam tattoo (Fig. 5.14A), with resultant metal fragments observed during biopsies (Fig. 5.14B); abrasives may also be introduced during polishing procedures. FIG. 5.14 (A) Gingival pigmentation associated with previous apicoectomy and amalgam retro-fill. (B) Biopsy depicts metal fragments. Periodontitis Periodontitis is defined as “an inflammatory disease of the supporting tissues of the teeth caused by specific microorganisms or groups of specific microorganisms, resulting in progressive destruction of the periodontal ligament and alveolar bone with increased probing depth formation, recession, or both.”51 The clinical feature that distinguishes periodontitis from gingivitis is the presence of clinically detectable attachment loss as a result of 346
  • 23.
    inflammatory destruction ofthe periodontal ligament and alveolar bone. This loss is often accompanied by periodontal pocket formation and changes in the density and height of the subjacent alveolar bone. In some cases, recession of the marginal gingiva may accompany attachment loss, thereby masking ongoing disease progression if only probing depth measurements are taken without measurements of clinical attachment levels. Key Fact Probing depth measurement alone is inadequate for an assessment of periodontitis. Clinical attachment loss is usually assessed by adding the extent of gingival recession to the probing depth measurement to estimate the total extent of tissue loss from the cementoenamel junction (CEJ) of the tooth. However, when recession is not visible, it is essential that height of the marginal gingiva coronal to the CEJ be determined and that measurement subtracted from the probing depth to establish the extent of clinical attachment loss. The measurement of clinical attachment around a tooth provides insights on the history and extent of periodontal destruction around the tooth. One common pitfall of clinical periodontal examination is the direct translation of probing depths as clinical attachment levels when the gingival margin lies above the cementoenamel junction, leading to an overestimation of attachment levels. Clinical signs of inflammation—such as changes in color, contour, and consistency as well as bleeding with probing—may not always be positive indicators of ongoing attachment loss. However, the presence of continued bleeding with probing during sequential visits has proved to be a reliable indicator of the presence of inflammation and an increased risk for subsequent attachment loss at the bleeding site. The attachment loss associated with periodontitis may occur in a cyclic fashion, with attachment loss progressing either continuously or in episodic bursts of disease activity. However, the available clinical instruments for detecting disease are not sensitive enough to capture the cycles of attachment loss and repair that occur during disease activity and remission, 347
  • 24.
    respectively (i.e., theperiodontal probe is graded in 1-mm increments). Key Fact In the AAP/EFP 2018 classification of periodontal diseases, a multidimensional staging and grading system will be introduced to subclassify periodontitis disease entities. The severity of periodontal disease at the time of presentation and the complexity of disease management will dictate the staging, while grading offers additional information, including the rate of past progression of the disease and the risk for future progression. Although many classifications of the different clinical manifestations of periodontitis have been presented since the late 1990s, consensus workshops in North America in 19898 and in Europe in 19936 identified that periodontitis may present in early- onset, adult-onset, and necrotizing forms (Table 5.1). In addition, the AAP consensus concluded that periodontitis may be associated with systemic conditions (e.g., diabetes, HIV) and that some forms of periodontitis may be refractory to conventional therapy. Early- onset disease was distinguished from adult-onset disease by the age of onset (< 35 years of age was set as an arbitrary separation of diseases), the rate of disease progression, and the presence of alterations in host defenses. The early-onset diseases were more aggressive, occurred in individuals younger than 35 years old, and were associated with defects in host defenses. Adult forms of disease were slowly progressive, became clinically more evident during the fourth decade of life, and were not associated with defects in host defenses. In addition, early-onset periodontitis was subclassified into prepubertal, juvenile, and rapidly progressive forms with localized or generalized disease distributions. TABLE 5.1 Classification of the Various Forms of Periodontitis Classification Forms of Periodontitis Disease Characteristics AAP World Workshop in Adult periodontitis Age of onset >35 years 348
  • 25.
    Clinical Periodontics, 19895 Slowrate of disease progression No defects in host defenses Early-onset periodontitis (may be prepubertal, juvenile, or rapidly progressive) Age of onset <35 years Rapid rate of disease progression Defects in host defenses Associated with specific microflora Periodontitis associated with systemic disease Systemic diseases that predispose to rapid rates of periodontitis Diseases: diabetes, Down syndrome, HIV infection, Papillon–Lefèvre syndrome Necrotizing ulcerative periodontitis Similar to acute necrotizing ulcerative gingivitis but with associated clinical attachment loss Refractory periodontitis Recurrent periodontitis that does not respond to treatment European Workshop in Periodontology, 19933 Adult periodontitis Age of onset: fourth decade of life Slow rate of disease progression No defects in host response Early-onset periodontitis Age of onset: before fourth decade of life Rapid rate of disease progression Defects in host defense Necrotizing periodontitis Tissue necrosis with attachment and bone loss AAP International Workshop for Classification of Periodontal Diseases, 19992 Chronic periodontitis Aggressive periodontitis Periodontitis as a manifestation of systemic diseases See Box 5.3 AAP, American Academy of Periodontology; HIV, human immunodeficiency virus. Extensive clinical and basic scientific research involving these disease entities has been performed in many countries, and emerging information has provided support for the unification of many of the preexisting disease categories.13,23,49 In particular, supporting evidence was lacking for the distinct classifications of adult periodontitis, refractory periodontitis, and the various different forms of early-onset periodontitis as outlined by the AAP Workshop for the International Classification of Periodontal Diseases in 19995 (see Table 5.1). It has been observed that chronic periodontal destruction caused by the accumulation of local factors (e.g., plaque, calculus) can occur before the age of 35 years and that the aggressive disease seen in young patients may be independent of age and instead have a familial (genetic) association. With 349
  • 26.
    respect to refractoryperiodontitis, little evidence supports the theory that this condition is indeed a distinct clinical entity. The causes of continued loss of clinical attachment and alveolar bone after periodontal therapy are currently poorly defined and apply to many disease entities. In addition, clinical data from the medical community emerged to support the belief that forms of periodontitis that were collectively referred to as prepubertal periodontitis were in fact representing periodontitis as a manifestation of distinct systemic diseases, such as in leukocyte adhesion deficiency syndromes. As a result, the AAP held an International Workshop for the Classification of Periodontal Diseases in 1999 to further refine the classification system with the use of current clinical and scientific data.5 The resulting classification of the different forms of periodontitis was simplified to describe three general disease forms: chronic periodontitis, aggressive periodontitis, and periodontitis as a manifestation of systemic disease (Table 5.1 and Box 5.3). Box 5.3 Periodontitis The disease periodontitis can be subclassified into the following three major types based on clinical, radiographic, historical, and laboratory characteristics. Chronic Periodontitis The following characteristics are common to patients with chronic periodontitis: • Prevalent in adults but can occur in children • Amount of destruction consistent with local factors • Associated with a variable microbial pattern • Subgingival calculus frequently found • Slow-to-moderate rate of progression with possible periods of rapid progression • Possibly modified by or associated with the following: 350
  • 27.
    • Systemic diseasessuch as diabetes mellitus and human immunodeficiency virus (HIV) infection • Local factors predisposing to periodontitis • Environmental factors such as cigarette smoking and emotional stress Chronic periodontitis may be further subclassified into localized and generalized forms and characterized as mild, moderate, or severe based on the common features described previously and the following specific features: • Localized form: <30% of teeth involved • Generalized form: >30% of teeth involved • Mild: 1 to 2 mm clinical attachment loss (CAL) • Moderate: 3 to 4 mm CAL • Severe: ≥5 mm CAL Aggressive Periodontitis The following characteristics are common to patients with aggressive periodontitis: • Otherwise clinically healthy patient (note the distinction with periodontitis as a manifestation of systemic disease) • Rapid attachment loss and bone destruction • Familial aggregation of diseased individuals The following characteristics are common but not universal: • Amount of microbial deposits inconsistent with disease severity • Increased levels of Actinobacillus actinomycetemcomitans • Abnormalities in phagocyte function • Hyper-responsive macrophages, producing increased prostaglandin E2 (PGE2) and interleukin-1β (IL-1β) • In some cases, self-arresting disease progression 351
  • 28.
    Aggressive periodontitis maybe further classified into localized and generalized forms based on the common features described here and the following specific features. Localized Form • Circumpubertal onset of disease • Localized first molar or incisor disease with proximal attachment loss on at least two permanent teeth, one of which is a first molar • Robust serum antibody response to infecting agents Generalized Form • Usually affecting persons under 30 years of age (however, may be older) • Generalized proximal attachment loss affecting at least three teeth other than first molars and incisors • Pronounced episodic nature of periodontal destruction • Poor serum antibody response to infecting agents Periodontitis as a Manifestation of Systemic Diseases Periodontitis may be observed as a manifestation of the following systemic diseases: 1. Hematologic disorders a. Acquired neutropenia b. Leukemias c. Other 2. Genetic disorders a. Familial and cyclic neutropenia b. Down syndrome c. Leukocyte adhesion deficiency syndromes d. Papillon–Lefèvre syndrome e. Chédiak–Higashi syndrome f. Histiocytosis syndromes g. Glycogen storage disease 352
  • 29.
    h. Infantile geneticagranulocytosis i. Cohen syndrome j. Ehlers-Danlos syndrome (types IV and VIII autosomal dominant [AD]) k. Hypophosphatasia l. Other 3. Not otherwise specified Data from Flemmig TF: Periodontitis. Ann Periodontol 4:32, 1999; Kinane DF: Periodontitis modified by systemic factors. Ann Periodontol 4:54, 1999; and Tonetti MS, Mombelli A: Early-onset periodontitis. Ann Periodontol 4:39, 1999. Since the establishment of the currently accepted 1999 classification, a taskforce commissioned by the AAP proposed an update to the existing classification scheme in 2015.3 The update focused on suggestions to address the challenges in clinical documentation of attachment level changes and the distinction between chronic and aggressive periodontitis. In particular, the AAP task force recommended the consideration of probing depth levels, in addition to attachment levels, in determining the severity of periodontitis to avoid overestimation. The classification of diseases and conditions of the periodontium discussed in this chapter will focus on the currently accepted 1999 classification with references to the AAP update when appropriate. Chronic Periodontitis Chronic periodontitis is the most common form of periodontitis13 ; Box 5.3 includes the characteristics of this form of periodontitis. Chronic periodontitis is most prevalent in adults, but it can also be observed in children. Different classification schemes have confirmed or discarded the age range of more than 35 years to separate chronic versus aggressive periodontitis. According to the existing definition, persons younger than 35 years may exhibit a rate of progression of disease consistent with the definition of chronic periodontitis. Nonetheless, epidemiologic evidence supports the suggestion that persons younger than 25 years at disease onset are likely to exhibit aggressive periodontitis. Intraoral radiographs along with periodontal charting records are of 353
  • 30.
    paramount importance tothe documentation of disease onset and rate of progression. Chronic periodontitis is associated with the accumulation of plaque and calculus. It generally has a slow to moderate rate of disease progression, but periods of more rapid destruction may also be observed. Increases in the rate of disease progression may be caused by the impact of local, systemic, or environmental factors that may influence the normal host–bacteria interaction. Local factors may influence plaque accumulation (Box 5.4), whereas systemic diseases (e.g., diabetes mellitus, HIV) may influence the host's defenses, and environmental factors (e.g., cigarette smoking, stress) may influence the response of the host to plaque accumulation. Chronic periodontitis may occur as a localized disease in which less than 30% of evaluated teeth demonstrate attachment and bone loss, or it may occur as generalized when more than 30% of teeth are affected. Box 5.4 Developmental or Acquired Deformities and Conditions Localized Tooth-Related Factors That Modify or Predispose to Plaque-Induced Gingival Diseases or Periodontitis 1. Tooth anatomic factors 2. Dental restorations or appliances 3. Root fractures 4. Cervical root resorption and cemental tears Mucogingival Deformities and Conditions Around Teeth 1. Gingival or soft tissue recession a. Facial or lingual surfaces b. Interproximal (papillary) 2. Lack of keratinized gingiva 354
  • 31.
    3. Decreased vestibulardepth 4. Aberrant frenum or muscle position 5. Gingival excess a. Pseudopocket b. Inconsistent gingival margin c. Excessive gingival display d. Gingival enlargement (see Box 5.2) e. Abnormal color Mucogingival Deformities and Conditions on Edentulous Edges 1. Vertical and/or horizontal ridge deficiency 2. Lack of gingiva or keratinized tissue 3. Gingival or soft tissue enlargements 4. Aberrant frenum or muscle position 5. Decreased vestibular depth 6. Abnormal color Occlusal Trauma 1. Primary occlusal trauma 2. Secondary occlusal trauma Data from Blieden TM: Tooth-related issues. Ann Periodontol 4:91, 1999; Halmon WW: Occlusal trauma: effect and impact on the periodontium. Ann Periodontol 4:102, 1999; and Pini Prato GP: Mucogingival deformities. Ann Periodontol 4:98, 1999. Key Fact Chronic periodontitis is classified by extent and severity of disease, such as generalized (extent), moderate (severity) chronic periodontitis. Chronic periodontitis can be further classified on the basis of its extent and severity. The severity of disease has been traditionally determined as either slight/mild (1 to 2 mm of loss; Fig. 5.15), moderate (3 to 4 mm of loss; Fig. 5.16), or severe (≥5 mm of loss; Fig. 355
  • 32.
    5.17) on thebasis of the amount of clinical attachment loss (see Box 5.3). Clinical attachment levels provide important benefits over probing depth alone to monitor disease progression using the CEJ as a fixed reference point. In fact, probing depth levels only have poor to moderate sensitivity for predicting attachment level changes overtime. Nonetheless, clinical experience has revealed that oftentimes measurement of clinical attachment levels in practice may prove to be erroneous. The most common error occurs in the case of sites without gingival recession, whereby the location of the gingival margin is coronal to the CEJ. If the clinician in such a case only records the probing depth without charting the location of the CEJ (often charted as “positive recession” in electronic periodontal charts), the resulting attachment levels will be erroneously recorded as being equal to the probing depth. To prevent such an overestimate of disease, it has been suggested that clinicians consider that mild periodontitis be associated with probing depths of <4 mm, moderate periodontitis with probing depths of 5 to 6 mm, and severe periodontitis with probing depths of ≥7 mm. However, probing depths alone should not be used to classify periodontitis without simultaneous consideration of clinical attachment levels and radiographic bone loss. 356
  • 33.
    FIG. 5.15 (A)Clinical image of plaque-related slight/early chronic periodontitis with 1- to 2-mm clinical attachment loss in 40-year-old female. (B) Radiographic images of the patient. 357
  • 34.
    FIG. 5.16 (A)Clinical image of plaque-related moderate chronic periodontitis with 3- to 4-mm clinical attachment loss in a 53-year-old male smoker. (B) Radiographic images of the patient. FIG. 5.17 (A) Clinical image of plaque-related severe/advanced chronic periodontitis with >5 mm clinical attachment loss in a 47-year-old female. (B) Radiographic images of the patient. Key Fact In the AAP/EFP 2018 classification of periodontal diseases, one of the major changes that will be implemented is avoidance of a separate category of “aggressive periodontitis.” Both chronic and aggressive periodontitis disease entities will be grouped together and will be simply called periodontitis. Aggressive Periodontitis 358
  • 35.
    Aggressive periodontitis differsfrom the chronic form primarily by the rapid rate of disease progression seen in an otherwise healthy individual (Figs. 5.18 and 5.19). The absence of large accumulations of plaque and calculus, with a positive family history of aggressive disease, is suggestive of a genetic trait34,49 (see Box 5.3). This form of periodontitis was previously classified as early-onset periodontitis (see Table 5.1) and therefore still includes many of the characteristics previously identified with the localized and generalized forms of early-onset periodontitis. Although the clinical presentation of aggressive disease appears to be universal, the causative factors involved are not always consistent. Box 5.3 outlines additional clinical, microbiologic, and immunologic characteristics of aggressive disease that may be present. As was previously described for early-onset disease, aggressive forms of periodontitis usually affect young individuals during or shortly after puberty and may be observed during the second and third decades of life (i.e., 10 to 30 years of age). The disease may be localized, as previously described for localized juvenile periodontitis, or generalized, as previously described for generalized juvenile periodontitis and rapidly progressive periodontitis (see Table 5.1). Box 5.3 describes the common features of the localized and generalized forms of aggressive periodontitis. 359
  • 36.
    FIG. 5.18 (A)Clinical image of plaque-related aggressive moderate periodontitis with 1- to 7-mm PD and 3- to 4-mm clinical attachment loss in a 31-year- old male. (B) Radiographic images of the patient. 360
  • 37.
    FIG. 5.19 (A)Clinical image of plaque-related aggressive severe periodontitis with 3- to 13-mm PD and 7- to 15-mm clinical attachment loss in a 32-year- old male. (B) Radiographic images of the patient. Flash Back Recall that chronic periodontitis is also categorized by the extent of localized or generalized disease according to the percentage of teeth involved with 30% of teeth being the cutoff between the two categories. Importantly, there is a distinct difference in the use of these definitions in the context of aggressive periodontitis. For aggressive periodontitis, the localized form is recognized to have a specific clinical phenotype, which is typically limited to incisor and first molar teeth. Periodontitis as a Manifestation of Systemic Disease Several hematologic and genetic disorders have been associated 361
  • 38.
    with the developmentof periodontitis in affected individuals22,23 (see Box 5.3). The majority of existing publications are case reports, whereas only a few research studies have been performed to investigate the exact nature of the effect of the specific condition on the tissues of the periodontium primarily because of the rare occurrence of many of these diseases. It is speculated that the major effect of these disorders is through alterations in immune response, such as in the case of interleukin-17 overexpression in leukocyte adhesion deficiency30 or due to tissue metabolic disorders such as in some forms of Ehlers–Danlos syndrome.2 The clinical manifestation of many of these disorders appears at an early age and may be confused with aggressive forms of periodontitis depicting rapid attachment loss and the potential for early tooth loss. This was one of the drivers for the transition from the term early-onset periodontitis, which characterized a heterogeneous group of diseases, to the definitions of aggressive periodontitis and periodontitis as a manifestation of systemic diseases. With the introduction of this form of periodontitis (see Table 5.1), the potential exists for overlap and confusion between periodontitis as a manifestation of systemic disease in both the aggressive and the chronic forms of disease when a systemic component is suspected. At present, periodontitis as a manifestation of systemic disease is the diagnosis to be used when the systemic condition is the major predisposing factor and when local factors (e.g., large quantities of plaque and calculus) are not clearly evident or their presence alone does not justify the severity or progression of disease. This definition is reserved for a specific group of diseases and syndromes that have been documented to have a profound destructive effect on the periodontium. The removal of local factors as part of conventional periodontal therapy in such cases is often inadequate to arrest the periodontal destruction due to the systemic effect. When periodontal destruction is clearly the result of local factors but has been exacerbated by the onset of conditions such as diabetes mellitus (Figs. 5.20 and 5.21) or HIV infection, the diagnosis should be chronic periodontitis modified by the systemic condition. 362
  • 39.
    FIG. 5.20 (A)Clinical image of plaque-related severe aggressive periodontitis in a 53-year-old male, smoker with diabetes and hemoglobin A1c (HbA1c) = 10.7. (B) Radiographic images of the patient. 363
  • 40.
    FIG. 5.21 Selectiveprobing depths of the same 53- year-old diabetic patient shown in Fig. 5.20 with severe aggressive periodontitis. Papillon–Lefèvre syndrome (PLS) is one example of a condition that causes severe periodontitis as one of its manifestations. PLS is an autosomal-recessive disorder caused by mutations in the cathepsin C gene located on chromosome 11q14.17 The clinical manifestations of the syndrome include severe aggressive periodontitis and diffuse keratoderma on the palms, the soles, the knees, or all three16 (Figs. 5.22 and 5.23). The consanguinity of the parents is a common finding in approximately one-third of the cases.31 FIG. 5.22 Panoramic radiograph and clinical photos of a 13-year-old female with Papillon–Lefèvre syndrome (PLS). PLS is an autosomal recessive disorder caused by mutations in the cathepsin C gene located on chromosome 11q14. The clinical manifestations of the syndrome are severe aggressive periodontitis as well as diffuse keratoderma on the palms, soles, or knees. 364
  • 41.
    In PLS patientsby the age of 4 to 5 years, the primary teeth have typically exfoliated or been extracted due to severe periodontal destruction. Subsequently, an edentulous phase occurs during which a reduction in the oral microbial load is noted and gingival health is restored. Following eruption of the permanent dentition, a similar cycle of severe periodontal inflammation is repeated that generally does not respond to conventional periodontal therapy. An increase in tooth mobility and periodontal abscesses is frequently observed shortly after the eruption of permanent teeth. (Courtesy Dr. Georgios Kotsakis, Seattle, Washington.) FIG. 5.23 Patient with Papillon-Lefèvre (PLS) syndrome exhibiting hyperkeratosis on palms of the hand and soles of the feet. PLS clinically affects both the primary and permanent dentition. Signs of palmoplantar keratoderma usually appear simultaneously with the eruption of the first primary teeth (5–6 months), but may appear as early as 1 month of age. (Courtesy Dr. Georgios Kotsakis, Seattle, Washington.) 365
  • 42.
    Clinical Correlation When monogenicdiseases are encountered, consanguinity can be a common finding particularly in certain ethnic cultures where it is socially acceptable. Appropriate genetic counseling is advisable. In addition, when the diagnosis for the proband (the first offspring for whom disease is noted) is established, it is crucial that the siblings are carefully examined for prompt diagnosis of additional cases. Impaired neutrophil function is considered to be the primary cause of PLS and to eventually result in the deregulation of the polymorphonuclear leukocyte response to microbial infection.11 Although the subgingival microbiota associated with PLS is diverse, opportunistic periodontal pathogens such as Aggregatibacter actinomycetemcomitans (Aa), Porphyromonas gingivalis, Tannerella forsythia, Fusobacterium nucleatum, and Prevotella intermedia are frequently identified among plaque samples from PLS patients.1,50 Serum immunoglobulin G titers against Aa are typically elevated in individuals with PLS, thereby implicating Aa as a significant causative factor.50 Individuals with PLS are often initially screened by a dermatologist or a pediatrician, and the phenotype of the syndrome may be mistaken for atopic dermatitis (eczema) or palmoplantar keratoderma.35 The case presented in Figs. 5.22 and 5.23 was treated for several years by a dermatologist as atopic dermatitis with occasional cauterization of misdiagnosed “plantar warts.” The diagnosis of PLS was established in a periodontal office. A multidisciplinary treatment approach for these patients including referral to a periodontist cannot be overemphasized. After a diagnosis of PLS has been established, it is important to collect a complete family history and to construct a pedigree to help identify undiagnosed or misdiagnosed siblings (Fig. 5.24). In 1979 Haneke proposed palmoplantar hyperkeratosis, the loss of primary and permanent teeth, and an autosomal- recessive pattern of inheritance as being essential criteria to verify a diagnosis of PLS.16 Secondary manifestations of PLS may include ectopic intracranial calcifications and increased susceptibility to infections, including pyogenic liver abscesses that can be fatal.9 366
  • 43.
    FIG. 5.24 Nohistory of consanguinity was reported in this case. However, approximately one-third of the diagnosed Papillon-Lefèvre (PLS) cases descend from same ancestor. Offsprings III1, III3, and III4 display a PLS phenotype. All siblings should be thoroughly examined by a periodontist once a case of PLS has been diagnosed. PLS clinically affects both the primary and permanent dentition. Signs of palmoplantar keratoderma usually appear simultaneously with the eruption of the first primary teeth (i.e., 5 to 6 months of age), but they may appear as early as the age of 1 month. By the age of 4 to 5 years, the primary teeth have typically exfoliated or been extracted as a result of severe periodontal destruction. Subsequently, an edentulous phase occurs during which a reduction in the oral microbial load is noted and gingival health is restored. After the eruption of the permanent dentition, a similar cycle of severe periodontal inflammation is repeated that generally does not respond to conventional periodontal therapy.11 An increase in tooth mobility and periodontal abscesses is frequently observed shortly after the eruption of the permanent teeth. The periodontal prognosis for patients with PLS has significantly improved in response to an increase in the prompt and accurate diagnosis of the syndrome, the better understanding of its pathogenesis, and more efficient professional supervision. There appears to be a consensus among clinicians that the successful treatment of periodontitis among individuals with PLS requires the 367
  • 44.
    eradication of Aa.10,12,43 Treatmentof the primary dentition includes frequent prophylaxis appointments to ensure that the patient maintains adequate masticatory function and nutrition during early childhood. To create a healthy environment for the permanent teeth to erupt into, it has been advocated that a course of antibiotics effective against Aa be systemically administered along with the extraction of all primary teeth 6 to 12 months before the eruption of the first permanent tooth. However, culture and sensitivity testing of the subgingival plaque may enhance the selection of the most effective antibiotic regimen. De Vree and colleagues described two patients with PLS.10 Aa was eradicated from one individual, who was able to retain most of his teeth over a 15-year period; the second individual's Aa was found to be resistant to the antibiotics combination, and he lost all of his teeth despite intensive treatment. The combination of trimethoprim and sulfamethoxazole (i.e., cotrimoxazole) has also been shown to be effective against Aa and to lead to a significant improvement in neutrophilic function against Aa.24 A stringent periodontal maintenance schedule is of utmost importance to efficaciously monitor the patient's oral hygiene and to be able to intercede promptly if signs of inflammation reoccur.32 Retinoids, which are synthetic analogues of vitamin A, a treatment modality against PLS skin manifestations, have also been considered as immunomodulatory adjuncts for the treatment of PLS-associated periodontitis.12,24 Sarcoidosis is a chronic disease that is expressed as a cell- mediated, delayed-type hypersensitivity that primarily affects the lungs, lymph nodes, skin, eyes, liver, spleen, and small bones of the hands and feet.36 Sarcoidosis rarely affects the oral cavity, with incidence of occurrence in descending order noted in the lymph nodes, lips, soft palate, buccal mucosa, gingiva, tongue, and bone.36 Fig. 5.25 depicts the pretreatment pattern of bone loss and recession associated with sarcoidosis, with pulmonary parenchymal fibrous infiltrate noted in the lungs as depicted by a white lacy pattern on a chest radiograph (Fig. 5.25C). Histologic features of sarcoidosis include the presence of an intense chronic inflammatory infiltrate with focal areas of noncaseating granulomas and a positive Kveim test (Fig. 5.26C). The remineralization of alveolar bone is noted on radiographs obtained 1 year after the systemic administration of 368
  • 45.
    steroids (e.g., prednisone)(Fig. 5.26A). FIG. 5.25 Sarcoidosis pretreatment. (A) Intraoral x- rays depict more extensive bone loss for anterior teeth than clinical attachment loss. (B) Extensive recession plus clinical attachment loss. (C) Pulmonary parenchymal fibrous infiltrate. 369
  • 46.
    FIG. 5.26 Sarcoidosisafter treatment with prednisone. (A) Intraoral x-rays depict remineralization of bone. (B) Reduction in gingival inflammation while extensive recession and clinical attachment loss persist. (C) Pretreatment biopsy. Medication-Related Osteonecrosis of the Jaw Medication-related osteonecrosis of the jaw (MRONJ) is an updated term that has replaced the phrase bisphosphonate-related osteonecrosis of the jaw (BRONJ). Bisphosphonates (BPs) are pyrophosphate analogues with a high affinity for hydroxyapatite crystals. They inhibit osteoclast-mediated bone resorption and play a key role in the management of osteolytic bone disorders, including osteoporosis, Paget disease, bone metastasis, and multiple myeloma.44 However, their prolonged use is associated with MRONJ.18 The American Association of Oral and Maxillofacial Surgeons defined MRONJ as “exposed bone in the maxillofacial area 370
  • 47.
    occurring in theabsence of head and neck irradiation and showing no evidence of healing for at least 8 weeks after identification in patients treated with BP therapy”4 (Figs. 5.27 and 5.28). To date, the true incidence of, causes of, and risk factors for the development of MRONJ are largely unknown. An overwhelming proportion (i.e., 97%) of the reported cases are related to the high-dose intravenous BP given to patients with cancer. However, a small fraction (i.e., 3%) has been reported in patients with osteoporosis and patients with Paget disease who are receiving oral BP.18 The estimated incidence of MRONJ in patients with osteoporosis who are receiving oral BP is around 0.7 per 100,000 persons/years of exposure.4 The incidence of MRONJ among patients with cancer who are receiving intravenous BP ranges from 0.72% to 7.4%.18 FIG. 5.27 Exposed bone on buccal lower premolar and molar in medication-related osteonecrosis of the jaw (MRONJ) patient following extraction of the first molar. (Courtesy Dr. Vivek Thumbigere Math, Minneapolis.) 371
  • 48.
    FIG. 5.28 Medication-relatedosteonecrosis of the jaw (MRONJ) patient with exposed bone on lingual aspect of lower premolar and molar following root canal treatment. (Courtesy Dr. Vivek Thumbigere Math, Minneapolis.) MRONJ lesions may be asymptomatic, or they may present with pain, purulent discharge, swelling, tooth mobility, and paresthesia, culminating in a reduced ability to eat and speak. MRONJ occurs most frequently in the mandible (65%), followed by the maxilla (26%) and both jaws (95%).52 The frequency of MRONJ is higher in the posterior region of the jaw. Among patients who develop MRONJ, approximately 60% of cases occur after an invasive dental procedure (e.g., tooth extraction), whereas 40% develop spontaneously.48 Radiographic evaluation is usually inconclusive for early lesions. In advanced cases, a poorly defined moth-eaten radiolucency is noted with radiopaque sequestra. Currently, there is no effective treatment for MRONJ. The discontinuance of BP is not helpful because BPs tend to reside in the bone for very long periods of time. Radical surgical intervention often exacerbates the condition, and the merit of hyperbaric oxygen treatment for the management of MRONJ is not conclusive. Patients are typically treated via minimally invasive conservative debridement, antibiotics, and chlorhexidine mouth rinses to limit the extent of the damage and to facilitate wound healing.48 The American Dental Association suggests that an oral health program that consists of sound hygiene practices and regular dental care is a valuable approach to lowering the risk of developing MRONJ.18 372
  • 49.
    Practitioners are encouragedto use atraumatic surgical techniques and to minimize the extent of dentoalveolar manipulation. Communication with the patient's physician and proper risk assessment are fundamental to the successful management of patients who are receiving BP therapy. The use of the term MRONJ was introduced to capture the rising number of osteonecrosis cases of the jaw that are associated with new types of medication, such as other antiresorptive (denosumab) and antiangiogenic therapies, by the American Association of Oral and Maxillofacial Surgeons (AAOMS) in their 2014 update. Readers are referred to the position paper by the AAOMS for additional information on MRONJ.4 Necrotizing Periodontal Diseases The clinical characteristics of necrotizing periodontal diseases may include (but are not limited to) ulcerated and necrotic papillary and marginal gingiva that is covered by a yellowish white or grayish slough or pseudomembrane, blunting and cratering of the papillae, bleeding on provocation or spontaneous bleeding, pain, and fetid breath. These diseases may be accompanied by fever, malaise, and lymphadenopathy, although these characteristics are not consistent. Two forms of necrotizing periodontal disease have been described: necrotizing ulcerative gingivitis (NUG) (Fig. 5.29) and necrotizing ulcerative periodontitis (NUP) (Fig. 5.30). NUG was previously classified as “gingival disease” or “gingivitis,” because clinical attachment loss is not a consistent feature. NUP has been classified as a form of “periodontitis,” because attachment loss is present. Nonetheless, NUP cases are almost exclusively reported in immunocompromised persons. Both NUG and NUP have been determined to constitute a separate group of diseases that have tissue necrosis as a primary clinical feature (see Box 5.1). 373
  • 50.
    FIG. 5.29 (A)Ulcerative gingivitis illustrating sloughing of marginal gingiva. (B) Phase-contrast microscopy reveals spirochetes in subgingival plaque sample. 374
  • 51.
    FIG. 5.30 (A)Necrotizing ulcerative periodontitis with severe clinical attachment loss in a 28-year-old male infected with human immunodeficiency virus (HIV). (B) Spirochetes noted on surface of sloughed epithelial cells. Necrotizing Ulcerative Gingivitis The clinical and causative characteristics of NUG42 are described in detail in Chapter 20. The defining characteristics of NUG are its bacterial cause, necrotic lesion, and predisposing factors, such as psychologic stress, smoking, and immunosuppression. In addition, malnutrition may be a contributing factor in developing countries. NUG is usually seen as an acute lesion that responds well to antimicrobial therapy in combination with professional plaque and calculus removal as well as improved oral hygiene. Necrotizing Ulcerative Periodontitis NUP differs from NUG in that the loss of clinical attachment and alveolar bone is a consistent feature originating from the proximal region.33 The characteristics of NUP are described in detail in Chapter 29. NUP may be observed among HIV seropositive individuals with low CD4 counts. Clinical manifestations include local ulceration and the necrosis of gingival tissue with the exposure and rapid destruction of underlying bone as well as spontaneous bleeding and severe pain. HIV+ persons with NUP are 20.8 times more likely to have CD4+ cell counts of less than 200 cells/mm3 of peripheral blood as compared with those without NUP, which suggests that immunosuppression is a major contributing factor. NUP has also been associated with severe malnutrition in developing countries. More aggressive cases of necrotizing stomatitis exhibit tissue necrosis beyond the confines of the periodontium to include other oral tissues, such as the hard palate. Key Fact 375
  • 52.
    Necrotizing stomatitis isa serious inflammatory condition that develops in systemically compromised individuals and is characterized by soft tissue necrosis that extends beyond the gingiva, with potential bony sequestrum formation. This disease entity is now included in the AAP/EFP 2018 classification of periodontal disease. Abscesses of the Periodontium A periodontal abscess is a localized purulent infection of periodontal tissues, and it is classified by its tissue of origin as gingival, periodontal, or pericoronal abscesses.28 The clinical, microbiologic, immunologic, and predisposing characteristics are discussed in Chapters 8, 9, and 13. Periodontitis Associated With Endodontic Lesions The classification of lesions that affect the periodontium and the pulp is based on the sequence of the disease process. Endodontic–Periodontal Lesions Pulpal necrosis precedes periodontal changes in endodontic– periodontal lesions. A periapical lesion that originates with pulpal infection and necrosis may drain to the oral cavity through the periodontal ligament, resulting in the destruction of the periodontal ligament and the adjacent alveolar bone. This may present clinically as a localized, deep, periodontal probing depth that extends to the apex of the tooth (Fig. 5.31A). If the endodontic infection is left untreated in such cases, an extensive alveolar ridge defect may occur (Fig. 5.31B−C), thereby necessitating reconstructive surgery (Fig. 5.31D) before the placement of implants and prostheses (Fig. 5.32) to reestablish a functional and aesthetic outcome. Pulpal infection may also drain through accessory canals, especially in the area of the furcation, which may lead to furcal involvement through the loss of clinical attachment and alveolar bone. 376
  • 53.
    FIG. 5.31 (Aand C) Clinical images of extensive loss of alveolar ridge secondary to periapical endodontic lesion. (B) CT scan depicts alveolar bone loss. (D) CT image of regenerated ridge via allogenic bone graft, tenting screw, and membrane. 377
  • 54.
    FIG. 5.32 Samepatient depicted in Fig. 5.31. (A–B) CT scans of regenerated ridge with implants placed in areas 7, 9, and 10. (C–D) Clinical images of implant- supported bridge. Clinical Correlation In early stages of primary endodontic lesions, root canal therapy may be the only treatment necessary to restore the periodontal apparatus. Periodontal–Endodontic Lesions It is more uncommon for periodontal disease to lead to endodontic disease than vice versa. In a periodontal–endodontic lesion, the bacterial infection from a periodontal pocket leads to loss of attachment, and root exposure then spreads to the pulp, resulting in pulpal necrosis. In the case of advanced periodontal disease, the infection may reach the pulp through the apical foramen. Nonetheless, existing studies have shown that although scaling and 378
  • 55.
    root planing removecementum and underlying dentin, they may lead to dentine hypersensitivity but not to irreversible pulpitis. Combined Lesions Combined lesions occur when pulpal necrosis and a periapical lesion occur on a tooth that is also periodontally involved. An intrabony defect that communicates with a periapical lesion of pulpal origin results in a combined periodontal–endodontic lesion. In all cases of periodontitis associated with endodontic lesions, the endodontic infection should be controlled before the definitive management of the periodontal lesion begins, especially when regenerative or bone-grafting techniques are planned.29 Tooth prognosis in combined lesions highly depends on the outcome of the periodontal treatment. Developmental or Acquired Deformities and Conditions Localized Tooth-Related Factors That Modify or Predispose Individuals to Plaque-Induced Gingival Diseases or Periodontitis In general, localized tooth-related factors contribute to the initiation and progression of periodontal disease through the enhancement of plaque accumulation or the prevention of effective plaque removal via normal oral hygiene measures.7 These factors fall into the four subgroups outlined in Box 5.4. Tooth Anatomic Factors Tooth anatomic factors are associated with malformations of tooth development or tooth location. Anatomic factors (e.g., cervical enamel projections, palatal grooves, enamel pearls) have been associated with clinical attachment loss, especially in furcation areas. Cervical enamel projections are found on 15% to 24% of 379
  • 56.
    mandibular molars andon 9% to 25% of maxillary molars, and strong associations have been observed with furcation involvement.27 Palatogingival grooves, which are found primarily on maxillary incisors, are observed in 8.5% of the population and are associated with increased plaque accumulation and clinical attachment as well as bone loss. Proximal root grooves on incisors and maxillary premolars also predispose individuals to plaque accumulation, inflammation, and the loss of clinical attachment and bone. Tooth location is considered important for the initiation and development of disease. Misaligned teeth predispose individuals to plaque accumulation with resultant inflammation in children, and they may predispose adults to clinical attachment loss, especially when they are associated with poor oral hygiene habits. Open interproximal contacts that contribute to food impaction have been associated with an increased loss of attachment.21 Dental Restorations and Appliances Dental restorations or appliances are frequently associated with the development of gingival inflammation. Restorations placed deep in the sulcus or within the junctional epithelium may impinge on the biologic width resulting in inflammation and the loss of clinical attachment and bone. Contour of a complete crown restoration can affect plaque retention with flat surfaces being more hygienic as compared to convex restorations exhibiting increased bulk of material at the cervical region. Root Fractures Root fractures may be associated with endodontic or restorative procedures as well as traumatic forces (Fig. 5.33A–C) and may lead to periodontal involvement through the apical migration of plaque along the fracture line (Fig. 5.33D). 380
  • 57.
    FIG. 5.33 (A–B)Clinical images of fistula tract. (C) Root fracture. (D) Resultant alveolar ridge defect. Flash Back Vertical root fractures involving both the pulp and PDL are true combined endodontic–periodontal lesions. Cervical Root Resorption and Cemental Tears Invasive cervical root resorption (ICR) (as noted on the cone beam computed tomography scans shown in Fig. 5.34A–B) and cemental tears may lead to periodontal destruction when the lesion communicates with the oral cavity and allows bacteria to migrate subgingivally. The atraumatic removal of teeth with progressed cervical resorption lesions and the reconstruction of resultant ridge defects with bone grafts, dental implants, and prostheses are viable solutions for such defects (Fig. 5.35). Avulsed teeth that are reimplanted frequently develop ankylosis and cervical root resorption many years after reimplantation. If the patient is still in the phase of skeletal growth, decoronation may be the treatment of choice for ridge preservation. In adults with completed skeletal growth, atraumatic removal of such ankylosed teeth, followed by ridge reconstruction and placement of implants and prosthesis, is a 381
  • 58.
    viable treatment optionin adults (see Fig. 5.35). FIG. 5.34 (A–B) CT scans reveal severe cervical root resorption of maxillary central incisors and periapical abscess. (C) Crowns fractured because of resorption. (D) Biopsy of soft tissue from resorption. 382
  • 59.
    FIG. 5.35 (A)Posttreatment clinical image of same patient depicted in Fig. 5.34 with implant-supported crowns and veneers on laterals. (B–C) CT scans of bone grafts and implants replacing central incisors lost as the result of severe cervical root resorption. Mucogingival Deformities and Conditions Around the Teeth Mucogingival deformity is a generic term used to describe the mucogingival junction and its relationship to the gingiva (Fig. 5.36), the alveolar mucosa, and frenula muscle attachments. A mucogingival deformity is a significant departure from the normal shape of the gingiva and the alveolar mucosa, and it may involve the underlying alveolar bone. Mucogingival surgery and periodontal plastic and aesthetic surgery correct defects in the morphology, position, or amount of gingiva. This subject is described in detail in Chapter 65. The surgical correction of mucogingival deformities may be performed for aesthetic reasons, to enhance function, or to facilitate oral hygiene.37 383
  • 60.
    FIG. 5.36 (A)Mucogingival defect depicted by recession. (B) Defects extend into alveolar mucosa and lack keratinized gingiva. Mucogingival Deformities and Conditions of the Edentulous Ridges Mucogingival deformities, such as a lack of stable keratinized gingiva between the vestibular fornices and the floor of the mouth (Fig. 5.37A), may require soft-tissue grafting and vestibular deepening before prosthodontic reconstruction (Fig. 5.37B–D). Alveolar bone defects in edentulous ridges (Fig. 5.38A–B) usually require corrective surgery (Fig. 5.38C–D) to restore form and function before the placement of implants and prostheses to replace missing teeth (Fig. 5.39).37 384
  • 61.
    FIG. 5.37 (A)Mucogingival ridge defect from floor of mouth to vestibular fornix. (B) Partial thickness flap with vestibular deepening. (C) Placement of free gingival graft. (D) Reestablishment of vestibular depth and keratinized attached gingiva. 385
  • 62.
    FIG. 5.38 (A)Clinical image of edentulous ridge defect. (B) Pretreatment CT image of defect. (C) Reconstructed ridge using ramus block graft. (D) CT scan of grafted site. FIG. 5.39 (A) Clinical image of ridge 6 months after grafting. (B) Placement of implants in area of teeth #23 and #25. (C) Porcelain fused to metal (PFM) crowns for maxillary incisors and implant-supported bridge from teeth #23 to #25. 386
  • 63.
    Occlusal Trauma The causesof trauma from occlusion and the effect of this trauma on the periodontium14 are discussed in detail in Chapters 26 and 55. Case Scenario 5.1 Patient: 63 year-old male, former smoker (20 pack-years) Chief Complaint: Presents for scheduled quarterly maintenance visit. Background Information The patient was treated with repeated sessions of scaling and root planing as well as periodontal flap surgery several years ago. He has since been very compliant with a 3-month maintenance schedule. Clinical Findings: Intraoral evaluation reveals 2 to 7 mm of clinical attachment loss throughout his dentition with probing depth measurements ranging from 1 to 3 mm. The plaque control record was 20%, and localized bleeding on probing was noted on the distal of #7 and lingual of #30. The diagnosis was determined to be localized gingivitis on a reduced periodontium. 387
  • 64.
    CASE-BASED QUESTION SOLUTIONAND EXPLANATION 1. If the patient's compliance becomes erratic and periodontitis relapses, how would you classify the patient's condition? A. Gingivitis B. Mild periodontitis C. Moderate periodontitis D. Severe periodontitis Answer: D Explanation: In the case of reduced periodontium, it is critical to consider the extent of preexisting attachment loss. This attachment loss is definitive, and further progression can negatively affect teeth prognosis. Case Scenario 5.2 Patient: 55-year-old male, nonsmoker Chief Complaint: “My gum has receded and it's bleeding.” Background Information The patient presents with aesthetic complaints associated with gingival recession and associated root exposure on the upper central incisors. The patient also reports occasional sensitivity and bleeding from the area. The patient was treated with repeated sessions of scaling and root planing as well as periodontal flap surgery several years ago. He has since been very compliant with a 3-month maintenance schedule. Current Findings: White striations on the gingiva facial of #9 and #10 were noted. During clinical examination, gentle finger rubbing of the mucosa coronal to #9 led to exfoliation of the epithelium. 388
  • 65.
    CASE-BASED QUESTION SOLUTION AND EXPLANATION 1.Do you expect scaling and root planing to treat this condition? A. Yes B. No Answer: B Explanation: This mucocutaneous lesion was biopsied and the diagnosis of lichen planus was confirmed following clinical assessment and positive Nikolsky's sign. Appropriate corticosteroid treatment led to remission. Case Scenario 5.3 Patient: 62-year-old postmenopausal female Chief Complaint: “I have noticed that I have halitosis, and my gums bleed.” Background Information The patient says that she cannot brush her teeth because her gums have been painful for 6 months. Current Findings: Gingiva sloughs following the application of a cotton swab. 389
  • 66.
    CASE-BASED QUESTION SOLUTION AND EXPLANATION 1.What is the most likely diagnosis? A. Acute necrotizing gingivitis B. Toothbrush abrasion C. Mucous membrane pemphigoid D. Sarcoidosis Answer: C Explanation: Immunofluorescence-labelled antibodies are used to mark an antigen/antibody complex in the basement membrane where autoimmune reaction causes degeneration of basal lamina, hemidesmosomes, and anchoring fibrils, thereby resulting in sloughing of epithelium. 390
  • 67.
    Case Scenario 5.4 Patient: 28-year-oldmale Chief Complaint: “My lower front teeth are mobile.” Background Information Progressive recession through dentition over the past 2 years. Painful rampant recession in the anterior mandible recently. Current Findings: Cratered papillae, ulcerative gingiva with exposed interproximal bone. CASE-BASED QUESTION SOLUTION AND EXPLANATION 1. When you consult with the patient's physician, what is the most likely medical diagnosis? A. Osteoporosis B. Diabetes mellitus C. AIDS D. Medication- related osteonecrosis of the jaw Answer: C Explanation: Necrotizing ulcerative periodontitis may be observed among HIV+ patients with very low CD4 counts (AIDS) and be manifested as local ulceration and necrosis of gingival tissue with exposed bone. 391
  • 68.
    Case Scenario 5.5 Patient: 59-year-oldpostmenopausal female Chief Complaint: “My lower jaw is sore and aches.” Background Information Lower first molar extracted ~ 4 months. Current Findings: Medication-related osteonecrosis of the jaw (MRONJ) with exposed alveolar bone. Radiographic Findings: Within normal limits. 392
  • 69.
    CASE-BASED QUESTION SOLUTION AND EXPLANATION 1.What is the most likely medical diagnosis associated to MRONJ? A. Osteopenia B. Osteoporosis C. Malignant myeloma D. Localized osteomyelitis Answer: C Explanation: Bisphosphonates (BPs) inhibit osteoclast-mediated bone resorption. BPs are used to manage osteolytic bone disorders such as osteoporosis, Paget disease, metastatic bone cancers, and multiple myeloma. Case Scenario 5.6 Patient: 6-year-old male 393
  • 70.
    Chief Complaint: “My classmatestease me and call me ‘gummy.’ I have difficulty chewing my food and talking.” Background Information Patient has had a kidney transplant. Current Findings: Severe gingival overgrowth. Radiographic Findings: Within normal limits. CASE-BASED QUESTION SOLUTION AND EXPLANATION 1. All of the following drug categories have been associated with gingival overgrowth EXCEPT which one? A. Antiarrhythmic, digoxin B. Anticonvulsant, phenytoin C. Calcium channel blocker, nifedipine D. Immunosuppressant, cyclosporine Answer: A Explanation: Phenytoin, nifedipine, and cyclosporine have all been associated with gingival overgrowth, while digoxin has not been associated with overgrowth. 394
  • 71.
    Case Scenario 5.7 Patient: 27-year-oldfemale Chief Complaint: “There is a bump on my gums that bleeds when I brush and floss.” Background Information Lesion developed over past ~ 2 months. Current Findings: Biopsy depicted in lower image. Radiographic Findings: Within normal limits. 395
  • 72.
    CASE-BASED QUESTION SOLUTION AND EXPLANATION 1.What is the most likely diagnosis? A. Fibroma B. Lateral periodontal abscess C. Epulis fissuratum D. Pyogenic granuloma Answer: D Explanation: Biopsy depicts inflammatory cell infiltrate within the connective tissue and numerous capillaries engorged with erythrocytes. References 1. Albandar JM, Khattab R, Monem F, et al. The subgingival microbiota of Papillon-Lefèvre syndrome. J Periodontol. 2012;83:902–908. 2. Aldred MJ, Bartold PM. Genetic disorders of the gingivae and periodontium. Periodontol 2000. 1998;18:7. 3. American Academy of Periodontology Task Force Report on the update to the 1999 classification of periodontal diseases and conditions. J Periodontol. 2015;86:835–838. 4. American Association of Oral and Maxillofacial. Surgeons position paper on bisphosphonate-related osteonecrosis of the jaws. J Oral Maxillofac Surg. 2007;65:369–376. 5. Armitage GC. Development of a classification system for periodontal diseases and conditions. Ann Periodontol. 1999;4:1. 6. Attstrom R, Vander Velden U. Summary of session 1. Lang N, Karring T. Proceedings of the 1st European Workshop in Periodontology. Quintessence: Berlin; 1993. 7. Blieden TM. Tooth-related issues. Ann Periodontol. 1999;4:91. 8. Caton J. Periodontal diagnosis and diagnostic aids: consensus report. Proceedings of the Wold Workshop in Clinical. American Academy of Periodontology: Chicago; 1989. 9. Dalgic B, Bukulmez A, Sari S. Pyogenic liver abscess and peritonitis due to Rhizopus oryzae in a child with Papillon– Lefevre syndrome. Eur J Pediatr. 2011;170:803–805. 396