1. IN THE NAME OF GOD

2. Pulpal and Periapical Disease
CHAPTER 3
Dr . Kheirandish
Oral and maxillofacial pathology

3. Pulpitis
Periapical Granuloma
Periapical Cyst
Osteomyelitis
Osteomyelitis with Proliferative Periostitis
Alveolar Osteitis

4. PULPITIS 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)

5. Irreversible pulpitis PULPITIS
Mimic pulpalgia :
Myofascial pain
Trigeminal neuralgia
Atypical facial neuralgia
Migraine headaches
Cluster headaches
Nasal or sinus pathoses
Angina pectoris

6. 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

7. Irreversible pulpitis
Early stages
Later stages
Early stages :
Sharp, severe pain on thermal stimulation
Pain continues after the stimulus is removed
Cold and heat
Spontaneous or continuous pain
Lies down
Electric pulp testing : lower levels
Early stages : localized pain / increasing discomfort : unable to identify the offending tooth

8. Later stages : Increases pain Throbbing pressure Awake at night.
Heat increases the pain
Cold decrease pain
Electric pulp testing : higher levels / -
Mobility and sensitivity: absent
Drainage (crown fracture, fistula formation) : symptoms resolve

9. CHRONIC HYPERPLASTIC PULPITIS (pulp polyp)
Pulpal inflammation
Children and young adults
Large pulp exposures
Deciduous or succedaneous molars
Asymptomatic (masticatory function)

11. 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

12. TREATMENT AND PROGNOSIS
Reversible pulpitis
Removal the local irritant
Irreversible and chronic hyperplastic puIpitis
Root canal therapy
Extraction

13. 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

14. Early stages Acute apical periodontitis Constant dull / Throbbing pain
Vitality test : - / delayed positive
Pain : biting or percussion
Radiographic : -
Neutrophils
Prostaglandins ( activate osteoclasts )

15. 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

16. RG Routine radiographic examination
Radiographic features are not diagnostic
Variable radiolucencies
Loss of apical lamina dura
Circumscribed or ill-defined
Root resorption RG

19. 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
Phoenix abscess : Secondary acute inflammatory changes within a periapical granuloma

20. 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

21. 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)

23. TREATMENT AND PROGNOSIS
Root canal therapy
Goal of endodontics : reduce the microbial load
Extraction and curettage

24. Fail to heal : Cyst formation Persistent pulpal infection
Accumulation of endogenous debris
Associated periodontal disease
Penetration of the adjacent maxillary sinus
Fibrous scar formation

25. 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 - )

26. APICAL PERIODONTAL CYST)
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)

27. 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

28. Residual 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

32. 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

35. HISTOPATHOLOGIC FEATURES
Stratified squamous epithelium
Exocytosis
Spongiosis
Hyperplasia
Mucous cells
Ciliated pseudostratified columnar epithelium

37. 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

39. TREATMENT AND PROGNOSIS
Nonsurgical
Surgical
Extraction
Biopsy is indicated

40. 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

41. Osteoradionecrosis (hypoxia,hypocellularity and hypovascularity)
Uncommon in developed countries
Developd countries : Odontogenic infections or traumatic fracture
Africa : acute necrotizing ulcerative gingivitis (ANUG) or NOMA.

42. Predispose people to osteomyelitis:
Chronic systemic diseases
Immunocompromised status
Disorders associated with decreased vascularity
Tobacco
Alcohol
IV drug abuse
Diabetes mellitus
Malaria
Sickle cell anemia
Malnutrition
Malignancy
AIDS
Radiation
Diseases (e.g., osteopetrosis, late Paget's disease, end-stage cementoosseous dysplasia)

43. Acute suppurative osteomyelitis
Young patients
Signs and symptoms
Acute inflammatory process
1 month in duration
Swelling: may be present
Fever
Leukocytosis
Lymphadenopathy
Significant sensitivity

44. 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

46. Chronic suppurative osteomyelitis
If acute osteomyelitis is not resolved or primarily without a previous acute episode.
Granulation tissue
Dense scar tissue
Swelling

47. Pain
Sequestrum formation
Tooth loss
Pathologic fracture
Radiographs : patchy, ragged. and ill-defined radiolucency (central radiopaque)

49. 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

51. TREATMENT AND PROGNOSIS
ACUTE SUPPURATIVE OSTEOMYELITIS
Antibiotic therapy
CHRONIC SUPPURATIVE OSTEOMYELITIS
Surgical Intervention

52. 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 )

54. 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)

55. CT scanning
Panoramic
Lateral oblique
Occlusal
posteroanterior

56. (DRY SOCKET; FIBRINOLYTIC ALVEOLITIS)
ALVEOLAR OSTEITIS
(DRY SOCKET; FIBRINOLYTIC ALVEOLITIS)
Destruction of the initial clot ( plasminogen to plasmin)
Mandible (posterior areas) :Impacted mandibular third molars
y/o
Poor oral hygiene
Inexperienced surgeons
Traumatic extractions
Oral contraceptive
Presurgical infections
Tobacco

57. Dirty gray clot
Bare bony socket
Sensitive bone
Severe pain
Foul odor
3 to 4 days
10 to 40 days

58. High risk patients : Oral contraceptives Smoke Pericoronitis
Traumatic extractions
History of alveolar osteitis

59. TREATMENT AND PROGNOSIS
Curettage of the socket is not recommended,
Eugenol (every 24 hours for the first 3 days)