DISEASES OF PULP

PROF. SHAZIA AKBAR,

HOD
DEPARTMENT OF ORAL PATHOLOGY,
DDC, DUHS
COURSE OUTLINE-BOOK PHILIPS

PULPITIS
 Reversible Pulpitis
 Irreversible Pulpitis
 Pulpal Necrosis
Common Diagnostic Techniques
 History and Nature of Pain
 Reaction to Thermal Changes
 Reaction to Electrical Stimulation
 Reaction to Tooth Percussion
 Radiographic Examination
 Visual Clinical Examination
 Palpation of Surrounding Area
COURSE OUTLINE-BOOK PHILIPS

Histopathology of Pulpal Disease

 Acute Pulpitis
 Chronic Pulpitis
 Chronic Hyperplastic Pulpitis

PERIAPICAL LESIONS
 Chronic Apical Periodontitis
 Periapical Granuloma
 Periapical Cyst

ACUTE PERIAPICAL CONDITION

 Periapical Abscess

OSTEOMYELITIS
 Acute Osteomyelitis
 Chronic Osteomyelitis
 Cellulitis
 Ludwig angina
 PULPITIS

Definition:
Inflammation of the pulpal tissue, categorized as acute or
chronic, symptomatic or asymptomatic, and reversible or
irreversible.
Types:
• Acute Pulpitis: Sudden onset, often caused by bacterial
invasion or trauma.
• Chronic Pulpitis: Long-standing inflammation, may result
from untreated acute pulpitis or low-grade irritation.
Symptoms:
• Acute: Severe, spontaneous pain, sensitivity to temperature
changes.
• Chronic: Dull, intermittent pain, sensitivity to chewing or
pressure.
PULPITIS
Treatment Options:
Reversible Pulpitis:
Dental fillings: Conservative restoration to repair
defective tooth structure and preserve pulp vitality.
Irreversible Pulpitis:
Root Canal Treatment (RCT): Removal of diseased pulpal
tissue to alleviate pain and infection while preserving the
tooth.
Advanced Irreversible Pulpitis:
Extraction: Removal of the entire tooth when RCT is not
feasible or if the tooth cannot be saved
 PATHOGENESIS PULPITIS:

1. Inflammation of Pulp Tissue:

 Inflammation occurs regardless of the presence of infectious agents.
 Pulp tissue is confined space with limited blood supply through apical foramen and
lacks collateral support.
2. Beneficial Inflammatory Process:
 Inflammation, usually beneficial in healing, becomes destructive in this confined
location.
 Inflammation is an expansile process involving:

1. Dilation of blood vessels.

2. Leakage of fluids into surrounding connective tissue.
3. Migration of cells into the area.
3. Intense Inflammation:
 Inflammatory process in pulpal chamber is intense.
 Produces sharp and prolonged pain due to internal pressure and strangulation of blood
supply.
4. Progression to Pulpal Necrosis:

ETIOLOGY OF PULPITIS
REVERSIBLE VS IRREVERSIBLE PULPITIS

To differentiate between reversible and

irreversible pulpitis, the following must be
assessed:
1. Whether the pain is spontaneous or brought
on by thermal changes
2. The duration of each episode of pain
3. The nature of the pain as described by the
patient
 Dental caries
replaced by dental
filling

REVERSIBLE PULPITIS
 Diagnosis: pulp is capable of a full
recovery if the irritating factors
subside or are removed.
 Symptoms reflect: An irritated
pulp tissue that reacts with the
mildest and earliest forms of the
inflammatory response consisting
of: Inflammatory
1. Vasodilation cells

2. some transudation
3. a slight infiltrate of lymphocytes
4. disruption of the odontoblastic
layer Vasodilatio
n
REVERSIBLE PULPITIS

 Pain: sharp and intense.

 Responds to: A sudden change in temperature.
 Time: The pain generally remains for 5 to 10 minutes
and rarely lasts longer than 20 minutes.
 The tooth remains without symptoms until it is
stimulated again.
 Changes in the position of the body, such as lying down,
do not generally affect the nature or the duration of the
pain.
 pain easily localized

Treatment:
1. protecting the pulp from further thermal stimulation.
2. placing sedative dressings in the base of the carious
IRREVERSIBLE PULPITIS

 The diagnosis determined that the pulp

will most likely not recover, regardless
of the attempts to treat it.
 The pulpal tissue will exhibit a wide
spectrum of acute and chronic
inflammatory changes
 Treatment:

1. Extraction
2. RCT
IRREVERSIBLE PULPITIS
 The pain usually less intense than that of reversible
pulpitis.
 The main feature of irreversible pulpitis:
1. pain is spontaneously initiated
2. not the result of a sudden temperature changes
3. it lasts for a prolonged period, usually longer than
20 minutes.
4. The pain may be initiated or accentuated when the
patient reclines (lying down)
5. Referrer pain another nearby location, such as the
lateral aspect of the face or to other teeth in the
arch.
 Definition: Pulp tissue that is no longer living.
Causes:
• Sudden traumatic events, such as a blow to the
tooth.
• Untreated irreversible pulpitis due to dental
caries.
Symptoms:
• Initially asymptomatic.
• Loss of acute and chronic symptoms due to
nerve degeneration.
PULPAL • Asymptomatic state is usually temporary.
NECROSIS Consequences:
• Pulpal tissue undergoes autolysis.
• Source of irritation to adjacent periodontal
membrane tissue.
• Infected pulpal necrosis can lead to pain.
Clinical Implications:
• Infection can extend into apical areas and
surrounding bone.
• Prompt diagnosis and treatment are essential
to prevent complications.
 Definition: Pulpal necrosis occurring without bacterial
infection.
Causes:
• Typically follows a traumatic incident.
• Symptoms may not manifest for months.
Signs and Symptoms:
• Initial sign: Change in tooth coloration.
• Altered translucency of the tooth.
• Loss of tooth hydration, leading to brittleness
NONINFEC and susceptibility to fractures.

TED • Accumulation of edema and exudate in bone

marrow spaces.
(ASEPTIC) • Exudate pressure may cause tooth extrusion and
PULPAL premature contact with opposing teeth.
• Sensitivity to pressure, especially during
NECROSIS chewing.
Pathogenesis:
• Decomposing tissue debris and breakdown
products of red blood cells enter dentinal
tubules, affecting dentin translucency.
Clinical Implications:
• Diagnosis based on color change and symptoms.
• Risk of tooth fractures and premature tooth loss.
• Management involves timely intervention to
 Dental abscess

change in the
coloration of
the tooth

Percussion A diagnostic tool used to determine if a tooth has

test: undergone pulpal necrosis consists of gently tapping
on several teeth in the area with a blunt instrument
COMMON DIAGNOSTIC TECHNIQUES

The diagnostic procedures that are commonly used to assess

the status of a symptomatic tooth and pulp are as follows:
1. History and nature of pain
2. Reaction to thermal changes
3. Reaction to mild electric stimulation
4. Reaction to tooth percussion
5. Radiographic examination
6. Visual clinical examination
7. Palpation of surrounding area.
.
HISTORY AND NATURE OF PAIN

The history and nature of the pain relate to the

circumstances of its occurrences:
1. Duration
2. Type of sensation experienced by the patient.
3. The pain of reversible pulpitis is sharp and intense.
4. The pain of irreversible pulpitis is dull, nagging, and not
localized.
REACTION TO THERMAL CHANGES
Procedure:
• Conducted in the dental office.
• Place a cold or very warm object on the tooth being assessed.
Results:
• Reversible Pulpitis:
• Immediate, sharp pain upon application.
• Pain lasts up to 20 minutes.
• Irreversible Pulpitis:
• Pain may be less sharp or dull.
• Pain persists for a longer duration compared to reversible pulpitis.

Clinical Significance:
• Helps differentiate between reversible and irreversible pulpitis.
• Sharp, short-lived pain indicates reversible pulpitis.
• Dull or prolonged pain suggests irreversible pulpitis
  A positive reaction to percussion
indicates that inflammation exists in
the apical periodontal tissue of a
particular tooth.
 Large portion of pulp tissue is
REACTION nonvital.
TO TOOTH  Indicate irreversible pulpitisis.
PERCUSSIO
N
REACTION TO ELECTRICAL STIMULATION

Procedure:
•Conducted using low-voltage direct current.
•Electrical stimulus applied to the tooth being assessed.
Purpose:
•Evaluates the excitability of nerves in the pulp.
Results:
Reversible Pulpitis:
•Nerves easily excited.
•Responds at a lower-than-normal voltage level.
Irreversible Pulpitis:
•Nerve tissue more severely damaged.
•Higher voltage required for patient response.
Pulp Necrosis/Abscess/Non-vital Tooth:
•No reaction even at the highest voltage level.
Clinical Significance:
•Helps distinguish reversible from irreversible pulpitis.
•Lower voltage response indicates reversible pulpitis.
•Lack of response at any voltage level suggests pulp necrosis or non-vital tooth.
VISUAL CLINICAL EXAMINATION

• Cortical Plate Expansion:

• Expansion of alveolar bone cortical
plates may be observed.
• Indicates periapical inflammation
extending into surrounding bone.
• Clinical Significance:
• Helpful in identifying periapical
inflammation attempting to drain to the
surface.
• Parulis (Dental Fistula):
• Small, raised, reddish papule or nodule.
• Occurs over the apex of the tooth.
• Represents the stoma (opening) of a
draining sinus tract of a periapical
 RADIOGRAPHIC EXAMINATION:

Help determining
An increase in
The presence of the cause of
the width of the
radiolucency at vague pain in a
apical
the apex of a quadrant of the
periodontal
tooth mandible or
space.
maxilla.

Grossly
Carious tooth

1. Periapical
radiolucency
2. Increase in the
apical
periodontal
space
PALPATION OF SURROUNDING AREA

Clinical Assessment:
• Palpation of periapical area elicits pain in
the patient.
• Indicates inflammation has reached tissue
surrounding tooth apex.
Significance:
• Indicates pulp necrosis.
• Urges filling of pulpal chambers to prevent
inflammation spread to surrounding bone
 ACUTE PULPITIS
 Histopathologic Features of Acute Pulpitis
• Similarity to Abscesses:
• Histopathologic features akin to abscesses in other body parts.
• Types:
• Focal Acute Pulpitis:
• Confined to one horn of the coronal pulp.
• Total Acute Pulpitis:
• Involves the entire pulp.
• Characteristics:
• Rapid bacterial invasion.
• Common in children and adolescents.
• Large-diameter (nonsclerosed) dentinal tubules susceptible.
 ACUTE PULPITIS
Pathogenesis of Acute Pulpitis
• Exudate Accumulation:
• Exudate confined within the enclosed pulp chamber.
• Builds pressure rapidly, extending to all parts of the healthy
pulp.
• Sudden Overheating:
• Pulp overheats, leading to rupture of blood vessels.
• Results in focal areas of hemorrhage, triggering acute pulpitis.
Causes of Acute Pulpitis:
• Iatrogenic Causes:
• During dental procedures like crown preparation.
• Inadequate cooling during high-speed tooth structure removal.
• Dental Caries:
PULPAL ABSCESS
Characteristics of Pulpal Abscess:
• Composition: Purulent exudate consisting of:
• Polymorphonuclear leukocytes.
• Fibrin.
• Necrotic tissue debris.
• Extravasated red blood cells.
• Surrounding Tissue: Zone of granulation tissue:
• Newly formed capillary blood vessels.
• Plump fibroblasts.
• Plasma cells.
• Lymphocytes.
• Rapid Process:
• Pulpal tissue involvement is small.
• Process progresses swiftly.
• Absence of Fibrous Capsule:
• No outer fibrous connective capsule present.
• Spread of Toxins:
• Autolytic enzymes and exotoxins spread rapidly to healthy pulp and adjacent periodontal
membrane.
• Complications:
• Irritant virulent bacteria and lack of drainage can lead to:
• Penetration of purulent exudate into surrounding cortical bone.
• Invasion of medullary bone, causing focal acute suppurative osteomyelitis.
CHRONIC PULPITIS
Etiology:
• Chronic pulpitis commonly found in older teeth.
• Teeth with previous restorations are predisposed.
• Often associated with slow progressive dental caries.
Pathogenesis:
• Slow progressive caries leads to dentinal tubules
narrowing (sclerosis).
• Deposition of tertiary (reparative) dentin.
• Sclerosed dentinal tubules act as a barrier against
bacterial progression.
• Pulp develops its own immune response.
CHRONIC PULPITIS
Histopathology:
• Loose, delicate connective tissue with dense collagen
bundles.
• Reduction in size and number of vascular structures and
nerves.
• Diffuse infiltrate of lymphocytes and plasma cells.
• Stage referred to as pulpal fibrosis.
• Pulp may develop calcifications:
• Pulp stones (spherical calcifications).
• Dystrophic calcifications (linear calcifications).
• Calcifications present in coronal and root pulpal tissues.
Progression:
 Spheric
calcificatio
ns:
Pulp stone

Linear
dystrophic
calcification
Periapical Granuloma:
Associated with chronic pulpitis.
Typically indolent and asymptomatic.
Composed of a circumscribed nodule of
fibrous tissue.
Contains a mild infiltrate of lymphocytes
and plasma cells.
CHRONIC HYPERPLASTIC PULPITIS
• Common Site: Primarily found in the molars of children.
• Pathogenesis:
• Result of rampant acute caries in young teeth.
• Rapid progression of caries leads to pulp exposure
before complete necrosis.
• Disintegration of crown exposes the well-nourished
pulp to infection, resulting in open pulpitis.
• Young children have wide open apical foramen,
allowing for good blood supply to the injured pulp.
• Combination of open chronic pulpitis, generous blood
supply, and increased regenerative capacity
stimulates pulpal tissue proliferation or granulation
tissue formation.
CHRONIC HYPERPLASTIC PULPITIS-PULP
POLYP:

Histopathology:
 Hyperplastic nodule will have a surface layer of stratified
squamous epithelium.
 Pulpal tissue may undergo excessive overgrowth
(hyperplasia) and project out of the crown of the tooth.
 The exposed tissue and the pulp remaining within the tooth
eventually become fibrotic and produce a firm nodule.
 Lesion clinically projects from the pulpal chamber, it is
commonly referred to as a pulp polyp.

Hyperplasia: Increase Hypertrophy: Increase

in the no. of cells in the size of cells
CHRONIC HYPERPLASTIC PULPITIS-
PULP POLYP:

Clinically:
 Ulcerative pulp polyp: It is not covered
with epithelium or becomes ulcerated, it
will appear reddish
 Normally: The same color as the rest of the
oral tissue.
 Normally: Lesions produce no symptoms
because they are said to be deficient in
nerve fibers.
Treatment: Extraction.
 STRATIFIED
SQUAMOUS
EPITHELIUM
FIBROTIC PULP
POLYP
 PERIAPICAL LESIONS
 Nature and Behavior of Lesions at Tooth Apex
 Factors Influencing Lesion Formation:

1. Presence of Pulpitis:
Open or closed chronic pulpitis.
2. Virulence of Microorganisms:
Determines severity of infection.
3. Extent of Dentinal Tubule Sclerosis:
Influences bacterial penetration.
4. Host Immune Response:
Competency affects lesion progression.
 Mild and Chronic Changes at Apex:

1. Pulpitis: Open chronic pulpitis.

2. Microorganisms: Low virulence.
3. Dentinal Tubules: Sclerotic in older tooth.
CHRONIC APICAL PERIODONTITIS

Extension of Inflammation to Periodontal Membrane

 Process: Inflammatory process spreads from pulp to periodontal
membrane via apical foramen.
 Clinical Signs:

1. Vitality Test: Faint response to electrical stimulation.

2. Percussion Test: Positive reaction.
 Histopathologic Findings:

1. Variability: Reflects pulp inflammation type.

2. Influence: Dictated by extent of pulp infection.
 Appearance of Periodontal Membrane:

1. Widened: Indicative of inflammation extension.

PERIAPICAL GRANULOMA

 Most common lesion that occurs after pulpal necrosis.

 Painless.
 Progresses slowly.

Pathogenesis:
1. An open pulpal chamber may become blocked with food
or a wooden toothpick, inhibiting drainage.
2. When drainage of the exudate(pus) is inhibited
3. A periapical granuloma can be transformed into an
acute periapical abscess.
Transforamtion: long-standing periapical granuloma 
into a periapical cyst.
PERIAPICAL GRANULOMA

• Appearance: Oval or rounded radiolucency.

• Outline: Well-demarcated, often at tooth
apex.
• Associated Findings:
1.Hypercementosis: Excessive cementum
at root apex.
2.Root Resorption: Blunting of root tip due
to resorption.
Well demarcated radiolucency at the
apex of 2nd maxillary premolar
PERIAPICAL GRANULOMA

HISTOPATHOLOGY:
• Composition:
• Outer Capsule: Dense fibrous tissue.
• Central Zone: Granulation tissue.
• Cellular Components:
• Macrophages: Often with foamy cytoplasm from
phagocytized cholesterol.
• Cholesterol Crystals: Surrounded by multinucleated
giant cells.
• Lymphocytes and Plasma Cells: Present in diffuse
infiltrate.
• Epithelial Islands: Irregular islands and strands, remnants
of Hertwig root sheath.
 Cortical
bone
Fibrous
capsule
Granulati
on tissue

Root
apex
PERIAPICAL GRANULOMA
TREATMENT:
1. Apicoectomy:
 If the root canal cannot be filled and the granuloma is
accessible for surgery.
 Procedure involves the removal of the granuloma from
the apex of the tooth.
2. Extraction with Curettage:
 Extraction of the tooth followed by curettage of the
periapical granuloma through the tooth socket.
3. Prevention of Periapical Cyst:
 Failure to resolve or remove the granuloma may lead
to the development of a periapical cyst.
 PERIAPICAL CYST
 Longstanding Periapical Granuloma:
• Origin: Arises from the rests of Malassez, which are
epithelial remnants persisting after root formation.
• Pathogenesis:
1. Stimulation of the rests of Malassez by the low-grade
inflammation of the preceding periapical granuloma.
2. Proliferation of the stimulated rests leads to the
formation of a cystic lesion.
• Prevalence: Most common type of cysts found in the jaws.
 This cystic lesion typically develops as a consequence of
untreated and longstanding periapical granuloma.
PERIAPICAL CYST

RADIOGRAPHIC FEATURES:

• Appearance:
• Well-circumscribed, often with a
distinct thin line of cortication
around it.
• Rounded and unilocular in shape.
• Associated Findings:
• Resorption of the apices of the
affected teeth.
• Displacement of the roots or
adjacent structures.
• Size:
• Can vary greatly and may become
very large.
• Large cysts can lead to erosion of
the inferior border of the mandible
or maxilla.
• Bulging of the buccal and lingual
cortical plates may also be
observed.
 A well
circumscribed
unilocular
radiolucency at
the apex of the
nonvital tooth
Revision of histology
 Stratified
squamous
epithelium

Keratin cell
layer

Prickle cell
and granular
cell layer

Basal cell
layer

C.T
parakeratiniza orthokeratiniza
tion tion
Retension of No nucleus in
pyknotic the keratin cell
nucleus in the layer
keratin cell
layer

Proliferation of
epithelium
into the C.T

Rete
pegs
 PERIAPICAL CYST
HISTOPATHOLOGY:
• Outer Tissue Composition:
• Dense fibrous connective tissue capsule.
• Central Lumen Contents:
• Thick, proteinaceous fluid.
• Cellular debris.
• Lumen Lining:
• Nonkeratinized, stratified squamous epithelium.
• Rete pegs, often elongated and branched.
• Cellular Components:
• Collections of cholesterol-laden macrophages.
• Diffuse infiltration of plasma cells and lymphocytes.
• Characteristic Findings:
• Cholesterol crystals surrounded by foreign-body giant cells.
• Presence of eosinophilic refractile hyaline bodies, known as Rushton bodies.
 Cyst
lumen Stratified squamous
epithelium

Inflammatory
infiltrates Fibrous capsule
PERIAPICAL CYST

TREATMENT: Enucleating.
Residual cyst:
A periapical cyst that remains or forms after the offending tooth
has been extracted is referred to as a residual cyst.
ACUTE PERIAPICAL CONDITION
 Factors Contributing to Acute Apical Lesions
1. Young Tooth with Open Tubules:
Increased susceptibility to bacterial invasion.
2. Rampant Caries:
Rapid progression of carious lesions, leading to pulp
involvement.
3. Closed Acute Pulpitis:
Sudden inflammation of the pulp, often due to trauma
or bacterial invasion.
4. Presence of Highly Virulent Microorganisms:
Bacteria capable of rapid tissue destruction and
infection.
5. Weakened Host Defense System:
Reduced ability to combat bacterial invasion and
inflammation.
 Consequences of Acute Apical Lesions:
1. Rapid and intense inflammatory response.
2. Severe pain and discomfort.
3. Spread of infection to adjacent structures and systemic
 PERIAPICAL ABSCESS
Pathogenesis of Acute Apical Abscess

Progression from Acute Pulpitis:

• Originates from inflammation of the dental pulp.
• Exudate containing bacteria and toxins extends into adjacent tissues.

Presence of Virulent Bacterial Organisms:

• Exudate often harbors highly aggressive bacterial strains.
• These bacteria produce potent exotoxins and lytic enzymes.

Tissue Breakdown and Extrusion:

• Exotoxins and enzymes rapidly degrade tissue barriers.
• Internal pressure builds up within the closed tooth.

Extrusion and Extension of Exudate:

• Pressure forces the tooth to extrude from the socket.
• Exudate rapidly extends into the surrounding medullary bone.

Consequences:

Severe tissue destruction and inflammation.

Extrusion of the affected tooth.

Rapid spread of infection to surrounding structures.

PERIAPICAL ABSCESS
Clinical Features:
• Patients experience intense, throbbing pain in the
affected tooth.
Severe Pain: • Pain worsens with occlusal contact and may be
aggravated by hot or cold stimuli.
Systemic • Elevated body temperature (fever).
Symptoms: • Generalized malaise and fatigue.

• The affected tooth may extrude from the socket due

Extrusion and to internal pressure.
Occlusal • Occlusal interference causes increased pain upon
Interference: contact with opposing teeth.

Local Swelling and • Inflammation leads to swelling and redness of the

Redness: surrounding soft tissues.

Positive Percussion • Tapping on the affected tooth elicits intense pain due
Test: to inflammation of the periapical tissues.
• The tooth may be relatively insensitive to hot, cold,
Reduced and electrical stimulation.
Sensitivity to • However, gentle tapping on it produces significant
Stimulation: pain.
PERIAPICAL ABSCESS
RADIOGRAPHIC FEATURE:
1. Widening of Apical Periodontal Space:
Initially, a slight widening of the apical periodontal space
may be observed.
2. Loss of Lamina Dura:
Gradual loss of the adjacent alveolar bone, including the
lamina dura, becomes apparent.
3. Increased Radiolucency:
 As the purulent exudate extends into the surrounding
medullary bone, there is a progressive increase in
radiolucency.
 This reflects the bone loss and destruction caused by
the spreading infection.
 PERIAPICAL ABSCESS
HISTOPATHOLOGY:
1. Fibrous Capsule:
The abscess is encapsulated by a thin layer of fibrous tissue.
2. Inflammatory Infiltrate:
The fibrous capsule is infiltrated with lymphocytes and plasma cells,
indicating an inflammatory response.
3. Granulation Tissue:
 Surrounding the capsule is a wide zone of granulation tissue.
 This tissue contains a mixture of neutrophils, lymphocytes, plasma cells,
and macrophages, reflecting the body's attempt to combat the infection.
4. Central Core:
 At the center of the abscess is a core of tissue that has undergone
disintegration and liquefaction.
 This central core is composed of purulent exudate, containing bacterial
colonies
PERIAPICAL ABSCESS
OSTEOMYELITIS:
ACUTE OSTEOMYELITIS:
• Definition: Osteomyelitis refers to a destructive inflammatory
process affecting the trabecular bone and bone marrow.
• Origin: Typically arises from an acute inflammatory source.
• Pathogen: Primarily caused by virulent strains of bacteria.
• Progression: Rapid in cases of highly virulent bacteria or
compromised host immunity.
• Causes:
1. Direct extension of untreated periapical abscess is a
common cause.
2. Minor traumatic incidents can also lead to osteomyelitis.
3. Osteoradionecrosis: High doses of radiation in head and
neck malignancy treatment can compromise mandibular
blood supply, predisposing to osteoradionecrosis.
ACUTE OSTEOMYELITIS
• Intense Pain: Patients often experience severe and
persistent pain.
• Physical Illness: Patients may feel generally unwell,
experiencing symptoms such as malaise.
• Exudate Build-Up: Pus accumulation occurs in soft tissue
spaces surrounding the affected tooth, leading to erosion of
cortical bone and infiltration into the medullary space.
• Drainage: Adequate drainage aids in symptom resolution,
while inadequate drainage results in worsening pain and
systemic symptoms like fever.
• Mandibular Involvement: In the mandible, exudate may
affect the inferior alveolar canal, causing altered sensation
(paresthesia) in the lower lip.
ACUTE OSTEOMYELITIS
RADIOGRAPHIC FINDINGS:
• Initial Appearance: Initially, the affected area may
have faint visibility on radiographs.
• Progression: Over time, the affected area becomes
diffusely blotchy or mottled, with unclear margins.
• Islands of Intact Bone: Islands of apparently
intact bone may be visible within the affected area.
However, these are actually dead, non-resorbed
bone fragments surrounded by purulent exudate.
• Sequestra: Dead bone fragments, known as
sequestra, may be present. These sequestra can be
externalized by the body and may appear as loose
pieces of bone on the mucosal surface.
ACUTE OSTEOMYELITIS

Histopathological Features of Osteomyelitis:

• Granulation Tissue: Microscopic examination
reveals granulation tissue intermixed with
neutrophils, fibrin, and tissue debris.
• Necrotic Bone Spicules: Within the affected bone,
spicules of bone are observed where the osteocytes
have undergone necrosis.
• Peripheral Tissue: Near the junction with
unaffected bone, the soft tissue consists of loose,
delicate connective tissue with an infiltrate of
lymphocytes and plasma cells.
 ACUTE OSTEOMYELITIS
 Treatment of Acute Osteomyelitis:
1. Surgical Intervention:
 Establish drainage of purulent exudate.
 Removal of necrotic tissue.
 Alleviation of pressure.
2. Antibiotic Therapy:
 Administer high doses based on culture and sensitivity
testing.
 Target specific microorganisms causing the infection.
3. Supportive Care:
 Manage pain.
 Provide intravenous fluids.
 Offer nutritional support.
 Definition: Not inflammation of cells.

Acute soft tissue condition.

Pathogenesis Purulent exudate with virulent bacteria.

:
Involves facial planes.
Often extends from periapical abscess.
Etiology: Extension from periapical infection.

CELLULITIS: Erosion through mandibular/maxillary cortical plate.

A
Clinical Parulis: Sinus tract opening on gingiva.
Features:

MISNOMER
Oroantral fistula: Oral cavity to maxillary space.

Complication Infection spread.

s:
Abscess formation.
Systemic involvement risk.
Treatment: Antibiotics targeting bacteria.
Surgical drainage intervention.
Symptom management.
Prevention: Prompt dental infection treatment.
Oral hygiene maintenance.
Regular dental check-ups.
CELLULITIS

Soft Tissue Complications of

Periapical Abscess
• Pathogenesis:
• Purulent exudate penetrates
alveolar bone.
• Lytic enzymes and
inflammation affect fascia.
 CELLULITIS
• Clinical Features:
1. Facial swelling and discomfort.
2. Systemic signs:
• Elevated temperature.
• Malaise.
• Lethargy.
• Lymphadenopathy.
3. Maxillary involvement:
• Periocular swelling.
• Temporary loss of sight.
4. Mandibular involvement:
• Puffy, pendulous swelling.
• Resembles mumps.
CELLULITIS
Complications:
• Spread of infection.
• Abscess formation.
• Systemic infection risk.
Treatment:
• Antibiotics.
• Surgical drainage if indicated.
• Symptom management.
Prevention:
• Timely dental care.
• Oral hygiene maintenance.
CELLULITIS
Complications of Cellulitis
1. Ludwig’s Angina:
1. Swelling around epiglottis.
2. Life-threatening due to airway obstruction.
3. Medical emergency requiring immediate intervention.
2. Thrombophlebitis:
1. Extension into maxillary cavernous sinus.
2. Risk of:
 Fatal brain abscess.
 Acute meningitis.
3. Rapid intervention essential to prevent severe outcomes.
 Management:
• Urgent medical attention.
1. Airway management in Ludwig’s angina.
2. Antibiotic therapy.
3. Surgical drainage if necessary.
CHRONIC OSTEOMYELITIS

• Characteristics:
• Differs from acute types.
• Induces bone formation and densification.
• Results from low-grade inflammatory process.
• Pathogenesis:
• Irritant stimulates osteocytes.
• Trabecular bone densifies.
• Additional bone laid down, reducing marrow spaces.
• Clinical Presentation:
• Often asymptomatic or minimal pain.
• Radiographically: Mottled, radiopaque areas.
• Histologically: Osteosclerosis observed.
 Types:
• Focal Chronic
Sclerosing
Osteomyelitis:
CHRONIC Confined to specific
OSTEOMYELITI tooth root areas.
S • Diffuse Chronic
Sclerosing
Osteomyelitis:
Involves larger bone
areas or edentulous
regions.
Radioopaque
 Fibrous
connective tissue

Trabecular bone

Inflammatory
infiltrates
THANK YOU
LOGBOOK WORK UP
DR. UMER BIN IRFAN
DR. RIDA FATIMA
LOGBOOK PICTURES
 LOGBOOK WORKUP?
1. DEFINE REVERSIBLE AND
IRREVERSIBLE PULPITIS?
2. DIFFERENTAITE BETWEEN
REVERSIBLE AND IRREVERSIBLE
PULPITIS?
3. WHAT IS THE PATHOGENESIS OF
PULPITIS?
4. PULPITIS?
5. ETIOLOGY OF PULPITIS?
 LOGBOOK WORKUP:
1. DEFINE PULPAL NECROSIS?
2. TYPES OF PULPAL
NECROSIS?
3. PATHOGENESIS OF
NECROSIS?
 LOGBOOK WORKUP:
• WHAT IS PULPITIS? TYPES OF PULPITIS?
• TYPE OF ACUTE PULPITIS?
• ETIOLOGY/CAUSE ?
• PATHOGENESIS?
 LOGBOOK WORKUP:
• What are pulp stones?
• What are the two types of calcifications?
 LOGBOOK WORKUP?
1. OTHER NAME OF PULP POLYP?
2. LABELLED THE HISTOPATHOLOGICAL DIAGRAM?
3. WHICH ARE THE MOST COMMONLY TEETH THAT HAS
DEVELOP PULP POLYP?
 What is cellulitis?
Define characteristic features of
Ludwig angina?