IN THE NAME OF GOD

Pulpal and Periapical Disease

CHAPTER 3

Dr . Kheirandish Oral and maxillofacial pathology

Pulpitis

Periapical Granuloma

Periapical Cyst

Osteomyelitis

Osteomyelitis with Proliferative Periostitis

Alveolar Osteitis

PULPITIS

1. Mechanical damage

Traumatic accidents, iatrogenic damage, attrition, abrasion

2. Thermal injury

Large uninsulated metallic restorations, dental procedures

(cavity preparation, polishing)

3. Chemical irritation

Erosion , acidic dental materials

4. Bacterial effects

toxins or directly (caries)

I. Reversible pulpitis

I. Irreversible pulpitis

PULPITIS

Mimic pulpalgia : Myofascial pain

Trigeminal neuralgia

Atypical facial neuralgia

Migraine headaches

Cluster headaches

Nasal or sinus pathoses

Angina pectoris

Reversible pulpitis

Temperature extremes : short duration /mild-to-moderate

pain.

Cold,sweet or sour : pain

The pain does not occur without stimulation and subsides

within seconds after the stimulus is removed.

Electric pulp testing : lower levels

Mobility and sensitivity : absent.

Without treatment : Iirreversible

Irreversible pulpitis

Early stages :

o Sharp, severe pain on thermal stimulation

o Pain continues after the stimulus is removed

o Cold and heat

o Spontaneous or continuous pain

o Lies down

o Electric pulp testing : lower levels

o Early stages : localized pain / increasing discomfort : unable

to identify the offending tooth

Early stages

Later stages

Later stages :

o Increases pain

o Throbbing pressure

o Awake at night.

o Heat increases the pain

o Cold decrease pain

o Electric pulp testing : higher levels / -

o Mobility and sensitivity: absent

o Drainage (crown fracture, fistula formation) : symptoms resolve

CHRONIC HYPERPLASTIC PULPITIS

(pulp polyp)

Pulpal inflammation

Children and young adults

Large pulp exposures

Deciduous or succedaneous molars

Asymptomatic (masticatory function)

HISTOPATHOLOGIC FEATURES

Reversible pulpitis :

Hyperemia

Edema

Few inflammatory cells

Irreversible pulpitis :

Congestion of the venules

Chronic hyperplastic pulpitis :

Inflamed granulation tissue

Histopathologically resembles a pyogenic granuloma

TREATMENT AND PROGNOSIS

Reversible pulpitis

Removal the local irritant

Irreversible and chronic hyperplastic puIpitis

Root canal therapy

Extraction

PERIAPICAL GRANULOMA

(CHRONIC APICAL PERIODONTITIS)

Chronically inflamed granulation tissue

Apex of a nonvital tooth

Not true granulomatous inflammation microscopically

Apical periodontitis

Bacterial ( Yeasts / Cytomegalovirus / Epstein-Barr virus )

75% of apical inflammatory lesions

Early stages

Acute apical periodontitis

Constant dull / Throbbing pain

Vitality test : - / delayed positive

Pain : biting or percussion

Radiographic : -

Neutrophils

Prostaglandins ( activate osteoclasts )

Late stages

Asymptomatic

Radiographic : +

Response to thermal or electric pulp tests : -

Mobility or significant sensitivity to percussion

Chronic inflammatory cells (lymphocytes)

Reduce osteoclastic activity

Fibroblastic activity

Periapical cyst formation

Routine radiographic examination

Radiographic features are not diagnostic

Variable radiolucencies

Loss of apical lamina dura

Circumscribed or ill-defined

Root resorption

RG

Phoenix abscess : Secondary acute inflammatory changes

within a periapical granuloma

Unable to distinguish periapical granulomas from

periapical cysts

Greater than 200 mm2 : periapical cysts

Periapical inflammatory disease is not static and

granulomas can transform into cysts or abscesses

HISTOPATHOLOGIC FEATURES

Inflamed granulation tissue

Surrounded by a fibrous connective tissue wall

Lymphocytes ( neutrophils. plasma cells. Histiocytes )

Plasma cells :

Eosinophilic globules of gamma globulin (Russell

bodies)

Basophilic particles (Pyronine bodies)

Not specific

Rests of Malassez

Giant cells

Red blood cell extravasation

Hemosiderin pigmentation

Cholesterol clefts

Source of the cholesterol clefts is unclear (dying

inflammatory Cells / disintegrating red blood cells /

degenerating cystic epithelium)

TREATMENT AND PROGNOSIS

Root canal therapy

Goal of endodontics : reduce the microbial load

Extraction and curettage

Fail to heal :

Cyst formation

Persistent pulpal infection

Accumulation of endogenous debris

Associated periodontal disease

Penetration of the adjacent maxillary sinus

Fibrous scar formation

Periapical surgery:

larger than 2 cm

Endodontic therapy : -

All soft tissue removed during periapical surgical procedures

should be submitted for histopathologic examination.

Periapical fibrous scars :

facial and lingual cortical plates have been lost and lesions fill with

dense collagenous tissue rather than normal bone( Surgery - )

PERIAPICAL CYST

(RADICULAR CYST;

APICAL PERIODONTAL CYST)

Prevalence : 15%

Epithelium at the apex of a nonvital tooth presumably

can be stimulated by inflammation to form a true

epithelium-lined cyst ( periapical cyst ).

Keratinocyte growth factor (increased proliferation of

normally quiescent Epithelium)

Source of the epithelium :

Rest of Malassez

Crevicular epithelium

Sinus lining

Epithelial lining of fistulous tracts

Periapical pocket cysts

incomplete epithelial lining

Periapical true cysts

complete epithelium lined

(baglike structure)

PERIAPICAL CYST

Lateral radicular cyst

Along the lateral aspect

Rests of Malassez

Pulpal necrosis

Radiographically : mimic developmental lateral

periodontal cysts

Residual periapical cyst

Dystrophic calcification /radiopacity

Grow slowly

Nonvital

No symptoms

large size (swelling and mild sensitivity)

Mobility of adjacent teeth

Radiographic : resemble periapical granuloma

Greater size than periapical granulomas

Loss of lamina dura

Root resorption is common

Significant growth

Stratified squamous epithelium

Exocytosis

Spongiosis

Hyperplasia

Mucous cells

Ciliated pseudostratified columnar epithelium

HISTOPATHOLOGIC FEATURES

Rushton bodies (Arch-shaped calcifications)

Dystrophic calcification

Cholesterol clefts

Multinucleated giant cells

Red blood cells

Hemosiderin

Inflammatory infiltration (lymphocytes,neutrophils,plasma

cells,histiocytes,mast cells and eosinophils)

Hyaline bodies (pulse granuloma,giant-cell hyaline

angiopathy)

Chronic intraosseous inflammation

TREATMENT AND PROGNOSIS

Nonsurgical

Surgical

Extraction

Biopsy is indicated

OSTEOMYELITIS

Osteomyelitis is an acute or chronic inflammatory process

in the medullary spaces or cortical surfaces of bone that

extends away from the initial site of involvement.

Bacterial infections

Lytic destruction of the involved bone

All ages

Male

Mandible

Osteoradionecrosis (hypoxia,hypocellularity and

hypovascularity)

Uncommon in developed countries

Developd countries : Odontogenic infections or

traumatic fracture

Africa : acute necrotizing ulcerative gingivitis (ANUG)

or NOMA.

Predispose people to osteomyelitis:

o Chronic systemic diseases

o Immunocompromised status

o Disorders associated with decreased vascularity

o Tobacco

o Alcohol

o IV drug abuse

o Diabetes mellitus

o Malaria

o Sickle cell anemia

o Malnutrition

o Malignancy

o AIDS

o Radiation

o Diseases (e.g., osteopetrosis, late Paget's disease,

end-stage cementoosseous dysplasia)

Acute suppurative osteomyelitis

Young patients

Signs and symptoms

Acute inflammatory process

1 month in duration

Swelling: may be present

Fever

Leukocytosis

Lymphadenopathy

Significant sensitivity

Radiographs : unremarkable / ill-defined radiolucency

Paresthesia of the lower lip

Necrotic bone

Sequestrum

Fragment of necrotic bone

Spontaneous exfoliation

Involucrum

Necrotic bone surrounded by new vital bone

Chronic suppurative osteomyelitis

If acute osteomyelitis is not resolved or primarily without a

previous acute episode.

Granulation tissue

Dense scar tissue

Swelling

Pain

Sequestrum formation

Tooth loss

Pathologic fracture

Radiographs : patchy, ragged. and ill-defined radiolucency

(central radiopaque)

HISTOPATHOLOGIC FEATURES

ACUTE SUPPURATIVE OSTEOMYELITIS

Biopsy not common (lack of a soft tissue component)

Necrotic bone

Loss of the osteocytes

Peripheral resorption

Bacterial colonization

Acute inflammatory cells

CHRONIC SUPPURATIVE OSTEOMYELITIS

Significant soft tissue component Chronically inflamed fibrous connective

Scattered sequestra

Abscess formation

TREATMENT AND PROGNOSIS

ACUTE SUPPURATIVE OSTEOMYELITIS

Antibiotic therapy

CHRONIC SUPPURATIVE OSTEOMYELITIS

Surgical Intervention

Antibiotic therapy

OSTEOMYELITIS WITH PROLIFERATIVE

PERIOSTITIS (PERIOSTITIS OSSIFICANS)

Garre sosteomyelitis

Periosteal reaction to the presence of inflammation

Periosteum : Several rows of reactive vital bone that

parallel each other

Children and young adults (13 y/o)

premolar and molar (mandible)

Radiopaque laminations of bone (NO=1 to 12 )

Dental caries

( periapical inflammatory disease, Periodontal infections,

fractures, buccal bifurcation cysts, and nonodontogenic

infections)

Causes of periosteal new bone formation :

Osteomyelitis

Trauma

Cysts

Fluorosis

Avitaminosis C

Congenital syphilis

Neoplasms (Ewing sarcoma, Langerhans cell histiocytosis, and

osteogenic sarcoma)

o CT scanning

o Panoramic

o Lateral oblique

o Occlusal

o posteroanterior

ALVEOLAR OSTEITIS

(DRY SOCKET; FIBRINOLYTIC ALVEOLITIS)

• Destruction of the initial clot ( plasminogen to plasmin)

• Mandible (posterior areas) :Impacted mandibular third molars

• 20 - 40 y/o

o Poor oral hygiene o Inexperienced surgeons o Traumatic extractions o Oral contraceptive o Presurgical infections o Tobacco

• Dirty gray clot

• Bare bony socket

• Sensitive bone

• Severe pain

• Foul odor

• 3 to 4 days

• 10 to 40 days

High risk patients :

Oral contraceptives

Smoke

Pericoronitis

Traumatic extractions

History of alveolar osteitis

TREATMENT AND PROGNOSIS

Curettage of the socket is not recommended,

Eugenol (every 24 hours for the first 3 days)