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Periodontal Case History
The document explains the critical importance of taking a comprehensive case history in dental practice, which aids in accurate diagnosis and treatment planning. It details various factors such as patient demographics, medical and dental history, and occupational hazards that affect oral health. The document also outlines the systematic examination process and classifications for periodontal diseases, along with prognosis and treatment planning.
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Periodontal Case History
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- 2. IMPORTANCE OF CASE HISTORY First& most important step Correct diagnosis leads to correct treatment plan Proper clinical and radiographical examination is must 2
- 3. 3 NAME Helps to developbond with the patient Communication Records AGE Aggressive periodontitis – common in young; chronic periodontitis – common in old Wasting diseases like attrition and abrasion – common in elderly
- 4. 4 GENDER Localised aggressive periodontitiswith circumpubertal onset – common in females Osteoporosis – postmenopausal women – decreased bone density due to decreased estrogen levels SOCIAL STATUS Economically sound and socially well-placed – less dental problems Not well-placed – poor oral hygiene due to ignorance and fewer visits to the dentist
- 5. 5 OCCUPATION Occupational stress –attrition, dental and periodontal problems People working in chemical factories – erosion + dentinal sensitivity Healthcare workers- transmissible diseases (HIV, Hepatitis) ADDRESS Comunication Records Geographical distribution of diseases – ex. Dental fluorosis
- 6. CHIEF COMPLAINT Patient’s own words Chronologicalorder As descriptive as possible 6
- 7. HISTORY OF PRESENTILLNESS Onset – When did it start? Location – Endo – sharp and easy to locate pain; perio – dull and gnawing and cannot usually localise Duration – For how long? Character – Sharp pain – endo; dull pain - perio Aggravating factors – Factors which increase the pain Relieving factors – Factors which relieve the pain Timing & Severity –For how long does it last? Perio pain usually stays for a variable duration without any stimulus and dull in nature 7
- 8. 8 PAST DENTAL HISTORY Patient’sattitude towards past dental treatment Frequency of past dental visits Previous treatment Reasons for loss of teeth Untoward complications if any
- 9. 9 MEDICAL HISTORY Systemic conditionfor which the patient is under treatment and medications Major illness – h/o hospitalisation Injuries to the orofacial region ex. Injury to the chin – temporomandibular joint problem, trauma to the teeth – devitalization Medications – drug interactions, drug induced gingival enlargement (anticonvulsants, calcium channel blockers and immunosuppresants) Allergy Immunization and blood transfusions – high risk of transmission of diseases
- 10. Family history Systemic diseaseslike diabetes have genetic factors involved So, inquiry into presence of disease states in the family is essential
- 11. “ 11 Personal history Dietary habits& adverse habits Oral hygiene measures – which toothbrush, toothbrushing technique, toothpaste, interdental aids, tongue cleaning, how frequently toothbrush is replaced?
- 12. HARD TISSUE EXAMINATION Numberof teeth present Carious/decayed – examine with explorer and mention class Missing Filled – mention type of restoration Stains and deposits 12
- 13. 13 WASTING DISEASES Grippo 2004: Attrition– The loss of tooth structure due to tooth to tooth contact during normal or parafunctional masticatory activity Abrasion – The pathological wear of tooth substance due to biomechanical frictional processes ex. Toothbrushing
- 14. 14 Erosion - Theloss of tooth substance due to dissolution by acids of intrinsic or extrinsic origin ex. Gastric acid or dietary acids
- 15. 15 Abfraction – Thepathological loss of tooth substance caused by biomechanical loading forces due to tooth flexure leading to fatigue of enamel and dentin at a location away from point of loading. Types – hairline cracks, striations, saucer shaped, semilunar shaped and cusp tip invagination
- 16. 16 OCCLUSION Angle’s classification ofmalocclusion Food lodgement – passive accmulation of food Food impaction – forceful wedging of food into the periodontium. 2 types: vertical food impaction – due to open contacts and irregular marginal ridges & horizontal (lateral) food impaction – gingival inflammation causes enlarged gingival embrasures and lateral pressure from lips, cheeks and tongue causes food impaction
- 17. 17 Plunger cusps –cusps that tend to forcibly wedge food into the periodontium
- 18. PROXIMAL TOOTH CONTACTS Normalproximal contacts do not allow any food impaction in between the teeth Open contact areas are usually associated with food impaction and gingival inflammation Open contact areas can be found commonly in malaligned teeth or in proximal caries where contact has been lost due to tooth decay 18
- 19. 19 PATHOLOGICAL TOOTH MIGRATION Toothdisplacement that results when the balance among factors that maintain physiologic tooth position is disturbed by periodontal disease Presents as facial flaring, extrusion, rotation, diastema, drifting of affected teeth Most common – facial flaring and diastema
- 20. 20 Posterior bite collapse– one of the reasons for pathological tooth migration Increased occlusal load and reduced periodontal support in case of secondary trauma from occlusion – forces from tongue, lips and cheeks put forces on teeth – sufficient to cause pathologic tooth migration
- 21. 21 FREMITUS TEST Abnormal forcesfrom opposing teeth may lead to slight discomfort to severe pain Occlusal disharmony is due to traumatic occlusion/ trauma from occlusion Fremitus test is used to detect trauma from occlusion Vibratory pattern of teeth is observed when they are brought into contact A dampened index finger is placed over the buccal and labial surface of the maxillary teeth. Patient is asked to tap teeth together in maximum intercuspal position and grind systematically in lateral, protrusive contacting positions
- 22. 22 Class I Mild vibrations or movementsare detected Class II Easily palpable vibrations but no visible movements Class III Movements visible with naked eye
- 23. SOFT TISSUE EXAMINATION Examinethe labial and buccal mucosa, tongue, soft and hard palate, floor of the mouth, vestibular depth and frenum attachment Examination of gingiva: Colour – coral or pale pink. Pigmentation may be present Chronic periodontitis – reddish pink / bluish in colour Acute periodontitis – bright red in colour 23
- 24. 24 Contour – healthy– scalloped with knife edged gingival margins that adapt closely around the tooth Papilla is pointed and pyramidal, fills interproximal areas In case of space between two teeth – saddle or flat- shaped Pre of inflammation – rounded gingival margins due to edematous and fibrotic changes; papilla is bulbous, flattened and blunted
- 25. Consistency – healthygingiva is firm and resilient. Can be checked by palpating with side of a blunt instrument Gingival inflammation – soft edematous (spongy) gingiva dents readily when gently pressed Chronic inflammation due to fibrotic changes (gingiva is pink and stippled but bleeding on probing present) – firm and hard Marginal gingiva easily displaced from the tooth surface with a light air blast – indicates destruction of gingival fibres that support gingival margin 25
- 26. 26 Surface texture –stippled appearance “orange peel appearance” Microscopic elevations and depressions due to connective tissue projections within the tissue Dry the gingiva with cotton and view it under broad daylight (light from all directions required to see it clearly) Stippling is absent in infancy, appears in about 5 years of age, increases until adulthood and frequently begins to disappear in old
- 27. Size– check fornormal size; enlarged in case of gingival enlargement or reduced in gingival recession Position – Normally present at CEJ Apical migration from CEJ is termed as gingival recession; coronal position – gingival enlargement Gingival exudate – discharge from gingival sulcus indicates disease activity Put slight pressure on the lateral surface of the gingiva – white purulent material oozing from gingival sulcus indicates presence of exudate 27
- 28. 28 Bleeding on probing– spontaneous, immediate or delayed indicator of tissue inflammatory response to bacteria First sign of gingivitis Chronic inflammation – gingiva may appear fibrotic but inflammation may be actively present in the gingival sulcus and junctional epithelium Smokers – reduced BOP due to effects of nicotine Acute – bleeding may occur even after slight provocation like short burst of compressed air
- 29. Embrasures – presentcervical to the interproximal contact area NORDLAND & TARNOW CLASSIFICATION OF INTERDENTAL PAPILLARY HEIGHT (1998) 29 Normal The interdental papilla occupies the entire embrasure space apical to the interdental contact point Class I Tip of interdental papilla is located between the interdental contact point and the level of CEJ on the proximal surface of the tooth Class II Tip of interdental papilla is located at or apical to the level of CEJ on the proximal surface of the tooth but coronal to the level of CEJ mid-buccally Class III Tip of interdental papilla is located at or apical to the level of CEJ mid-buccally
- 30. 30 Based on threeanatomic landmarks : Interdental contact point Coronal extent of proximal CEJ Apical extent of facial CEJ
- 31. McCall’s festoons –life preserver-shaped rolled margins of the gingiva where the gingiva shows fibrotic properties Stillman’s clefts – First sign of recession – formation of small groove in the gingiva; this term for the cleft like recession 31
- 32. 32 Examination of theperiodontium: Done in a systematic way, examining all the surfaces of every tooth and record the findings in the periodontal chart Pocket depth – The distance between the gingival margin and the base of the pocket Clinical attachment level – The distance between the CEJ and base of the pocket CLINICAL ATTACHMENT LEVEL POCKET DEPTH CE J GINGIVAL MARGIN
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- 34. 34 TOOTH MOBILITY The movementof tooth in the socket resulting from an applied force Physiologic tooth mobility present normally Apply firm pressure with either one metal instrument and a gloved finger or two metal instruments
- 35. 35 Norm al Physiologic tooth mobility Class I Mobilityless than 1mm in horizontal direction Class II Mobility more than 1mm in horizontal direction Class III Mobility more than 1mm in horizontal & vertical direction TOOTH MOBILITY CLASSIFICATION (MILLER 1985)
- 36. 36 Grad e I Slightly morethan normal Grad e II Moderately more than normal Grad e III Severe tooth mobility faciolingually or mesiodistally with vertical displacement TOOTH MOBILITY GRADING (GLICKMAN 1972)
- 37. FURCATION INVOLVEMENT The extensionof inflammatory periodontal disease into the interradicular area of the multirooted teeth is known as furcation involvement. Diagnosis is based on clinical and radiographic findings. Clinical detection – Nabers probe Mandibular molar furcation easy to detect since 2 roots Maxillary molar furcation – mesial furcation– go for palatal direction (mesial furcation is located palatal to the midpoint on mesial surface); distal furcation – 37
- 38. 38 GLICKMAN’S CLASSIFICATION (1953)– FOR HORIZONTAL COMPONENT Grade I Incipient or early stage of furcation involvement. Suprabony pocket and primarily affects soft tissues. No radiographic changes Grade II Cul-de-sac with a definite horizontal component. Radiographs may or may not depict furcation involvement. Grade III Bone is not attached to the dome of the furcation. Difficulty in passing the probe through the furcation because of the interference with the bifurcational ridges or facial/lingual bony margins. Radiographically, radiolucent area in the crotch of the tooth. Grade IV Interdental bone is destroyed and the soft tissues have receded apically so that the furcation opening is clinically
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- 40. 40 TARNOW & FLETCHER’SCLASSIFICATION (1984) – FOR VERTICAL COMPONENT (Depending on the distance from the base of the defect to the roof of the furcation) Subgroup A Vertical destruction of bone upto 1/3rd of the inter-radicular height (1-3mm) Subgroup B Vertical destruction of bone upto 2/3rd of the inter-radicular height (4-6mm) Subgroup C Vertical destruction beyond the apical third(7mm or more)
- 41. 41 GINGIVAL RECESSION The apicalmigration of the gingival margin from the normal position at the CEJ is known as gingival recession SULLIVAN & ATKIN’S CLASSIFICATION (1968) Shallow- narrow Shallow-wide Deep-narrow Deep-wide
- 42. 42 MILLER’S CLASSIFICATION OFGINGIVAL RECESSION (1985) Class I Marginal tissue recession not extending to the mucogingival junction. No loss of interdental bone or soft tissue Class II Marginal tissue recession extends to or beyond mucogingival junction. No loss of interdental bone or soft tissue. Class III Marginal tissue recession extends to or beyond the mucogingival junction. Loss of interdental bone or soft tissue or teeth malpositioning. Class IV Marginal tissue recession extends beyond mucogingival junction. Loss of interdental bone and soft tissue loss interdentally and/or severe tooth malpositioning
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- 44. WIDTH OF ATTACHED GINGIVA Identify2 landmarks – sulcus/pocket depth and mucogingival junction For mucogingival junction identification – TENSION TEST – Stretch the lip/cheek outwards. Identify the junction of immovable attached gingiva and movable alveolar mucosa ROLL TEST – Roll the alveolar mucosa over the attached gingiva with a blunt instrument. Here, the movable alveolar mucosa accumulates ahead of the instrument till the mucogingival junction when pushed coronally 44
- 45. Measurement approach –Measure the sulcus/pocket depth. Measure the distance from the gingival margin to the mucogingival junction. Subtract the two measurements = width of attached gingiva 45
- 46. Histochemical method –Schiller’s potassium or Lugol’s iodine is painted on the gingiva and oral mucosa. Due to glycogen content of alveolar mucosa – brown colour. Attached gingiva – glycogen free – unstained. Now, measure the total width of unstained gingiva and subtract the sulcus/pocket depth = width of attached gingiva Greatest in the incisor region (3.5-4.5mm in maxilla, 3.3-3.9mm in mandible) and less in the first premolar areas (1.9mm in maxilla and 1.8mm in mandible) 46
- 47. 47 DEPTH OF VESTIBULE Relatedto the width of attached gingiva If the width is normal. The vestibular depth is adequate If the width of attached gingiva is minimal – shallow vestibule – vestibular depth inadequate
- 48. FRENUM ATTACHMENT TENSION TEST- Lip is moved outwards, upwards or downwards and sidewards – marginal or interdental papilla moves away from the tooth surface – positive tension test 48 PLACEK CLASSIFICATION (1974) Mucosal Frenal fibres are attached upto mucogingival junction Gingival Frenal fibres are attached within the attached gingiva Papillary Fibres extend into the interdental papilla Papilla penetrating The frenal fibres cross the alveolar process and extend upto palatine papilla
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- 50. ABSCESS Gingival abscess –localised painful swelling affecting marginal and interdental gingiva; impaction of foreign objects ex. Fish bone, popcorn kernel Periodontal abscess – localised purulent inflammation of periodontal tissues including deep pockets, furcation, vertical osseous defects (lateral or parietal abscess) Pericoronal abscess – localised purulent inflammation surrounding crown of a partially or fully erupted tooth Periapical abscess – localised purulent inflammation surrounding apex of the tooth 50
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- 52. 52 RADIOGRAPHIC FINDINGS Used toknow the extent of periodontal destruction in the form of bone loss Periapical radiographs or orthopantomogram Record the amount of bone remaining, bone density, continuity of lamina dura, radiolucent areas, pattern of bone loss
- 53. 53 PROVISIONAL DIAGNOSIS Initially determinedto be the diagnosis Followed by investigations which help in making the final diagnosis Generalised (>30% of sites involved) / Localised (<30% of sites involved) Marginal Marginal & Papillary Diffuse (Marginal, Papillary and Attached gingiva involvement) CHRONIC Mild (1-2mm) Moderate (3-4mm) Severe (>5mm) (*After recording mean CAL) 1 2 3 4 GINGIVITIS PERIODONTITIS
- 54. “ 54 HOW TO RECORD CAL? 4 2 NORMALSULCUS DEPTH = 2-3mm 1 4 2 0 MEAN CAL = 6 + 5 2 = 5.5 SEVERE
- 55. 55 CLASSIFICATION Gingival Diseases Plaque inducedgingival diseases Associated with dental plaque only Gingival diseases modified by systemic factors – diabetes mellitus, puberty, pregnancy associated Gingival diseases modified by medications – Drug induced gingival diseases Non-plaque induced gingival diseases Bacterial, viral, fungal, genetic origin Gingival manifestations of systemic conditions Allergic reactions, traumatic lesions, foreign body reactions
- 56. 56 Chronic Periodontitis Aggressive Periodontitis Periodontitisas a manifestation of systemic diseases Necrotising Periodontal Diseases Abscesses of the periodontium Periodontitis associated with Endodontic Lesions Developmental and Acquired Deformities and Conditions Mucogingival Deformities and conditions Occlusal trauma
- 57. 57 SPECIAL INVESTIGATIONS Routine bloodexamination – complete blood count, bleeding time, clotting time, haemoglobin levels Study casts Biopsy – in case of gingival overgrowth Microbiological analysis – culture for isolation and identification of bacteria
- 58. FINAL DIAGNOSIS Complete andaccurate diagnosis is important for an appropriate treatment plan Final diagnosis should involve all the periodontal conditions for which the patient requires treatment Ex. Generalised marginal chronic gingivitis with localised severe chronic periodontitis with periodontal abscess/ pericoronitis/ trauma from occlusion with respect to ____ 58
- 59. 59 PROGNOSIS Prediction of theprobable course, duration and outcome of the disease based on the general knowledge of the pathogenesis of the disease and the presence of risk factors for the disease Overall prognosis – patient’s age, systemic factors, severity of the disease, smoking, presence of plaque, calculus, patient compliance, prosthetic possibilities Individual prognosis –determined after overall prognosis and affected by it
- 60. 60 PROGNOSIS Good prognosis Controlof etiologic factors and adequate periodontal support Fair prognosis Approx 25% attachment loss and/or Class I furcation involvement Poor prognosis 50% attachment loss and Class II furcation involvement Questionable prognosis >50% attachment loss, poor crown-root ratio, poor root form, Class II or class III furcation involvement, >Grade II mobility, root proximity Hopeless prognosis Inadequate attachment to maintain health, comfort and function
- 61. 61 TREATMENT PLAN An accurateand complete diagnosis helps to formulate an appropriate treatment plan Divided into 4 phases: If the patient is in pain – elimination of pain or other emergency treatment After completion of phase I therapy – patient is placed on maintenance phase (phase IV) to preserve the results obtained and prevent any further deterioration and disease recurrence. Phase I / Etiotropic phase Phase II Phase III Phase IV Preliminary phase
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- 65. TAKE HOME MESSAGE Casehistory is the blueprint of the treatment plan Appropriate treatment plan may prevent unnecessary complications Case history provides detailed information regarding risk factors associated with disease progression
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