Pulp and Periapical Diseases Quiz

Diseases of the Pulp and Periapical Tissues

• Presented by Dr./ Eman Allam, Lecturer of Oral Pathology, Sphinx University.

Significance of Pulp Anatomy in Inflammation

• Pulp is enclosed within hard dentin, preventing edema.
• Nerves, arteries, and veins enter through a small apical foramen.
• Pulp lacks collateral circulation.
• Teeth respond to sudden temperature changes (20°C to 45°C).
• Pulp lacks regeneration capacity.
• Nerve supply does not allow precise localization of offending tooth.

Etiology of Pulp Diseases

• Living Irritants (Bacteria):

  • Dental caries is the most common cause.
  • Trauma (e.g., tooth fracture).
  • Pulp exposure during cavity preparation (odonto-iatrogenic).
  • Extension of adjacent periapical infection.
  • Hematogenous infection (anachoretic pulpitis).
  • Spread from adjacent infected teeth.

• Non-living Irritants:

  • Physical: Mechanical, thermal, electrical, aeronautical, irradiation.
  • Chemical: Acids, alkalis, poisons (Odonto-iatrogenic pulpitis).

Focal Reversible Pulpitis (Pulp Hyperemia)

• Definition: Earliest form of pulpitis, focal reversible pulp inflammation.
• Etiology and Clinical Features: Deep caries, deep metallic restoration without base, or a defective marginal restoration. Sensitivity to thermal changes, particularly cold. Sharp shooting pain that subsides within seconds after removal of irritant. Pulp tester response at a lower level than normal tooth.
• Histologic Features: Vasodilation, inflammatory fluid exudate, intact odontoblastic layer, localized area usually the pulp horn.
• Treatment: Remove the cause, use a temporary zinc oxide and eugenol filling. Reversible on removal of the irritant.

Acute Pulpitis

• Definition: Acute pulp inflammation.
• Etiology: High virulence bacteria, low body resistance, living or non living irritants (mechanical, thermal, electrical).
• Clinical Features: Severe, continuous, sharp lancinating or throbbing pain. Pain worsens when lying down and with cold temperatures. Pain persists after the irritant is removed. In later stages, pain might increase with heat ('hot tooth') but ease with cold. Pain can be spontaneous and wake the patient. The extreme pain due to pressure of fluid exudate on nerve endings as the pulp is enclosed in hard dentin chamber that doesn't allow edema, inflammation products like histamine and serotonin acting on nerve endings. Pulp tester response at a far lower threshold than normal.
• Histologic Features: Destruction of odontoblastic layer, vasodilation, fluid exudate, acute inflammatory cells (PMNs), pus formation (minute pulp abscess) predominantly in the pulp horn. Pus is composed of dead and live bacteria, dead and live PMNs, and liquefied necrotic cells; numerous abscesses coalesce for total pulp liquefaction (Total suppurative pulpitis).
• Treatment: Endodontic treatment or tooth extraction.

Chronic Pulpitis

• A. Chronic Closed Pulpitis:

  • Definition: Chronic closed pulp inflammation.
  • Etiology: May follow acute pulpitis, low virulence bacteria, good body resistance, chronic caries with incomplete removal of caries, pulp capping following traumatic exposure, hematogenous (anachoretic pulpitis).
  • Clinically: Intermittent dull achy pain, less sensitive to hot and cold, pulp tester responds at a higher level than normal (chronic irritations degenerate nerve endings).
  • Histopathology: Reparative dentin (mild irritant), granulation tissue (proliferating fibroblasts, blood vessels, newly formed collagen fibrils), chronic inflammatory cells (lymphocytes & plasma cells).

• B. Chronic Open Pulpitis:

  • Types: Chronic hyperplastic pulpitis (pulp polyp), chronic ulcerative pulpitis. Characterized by a large carious cavity, wide pulp exposure.
  • Chronic hyperplastic pulpitis: Common in young adults, good resistance. The pulp is vital, painless red mass filling carious cavity. Lesion is less sensitive because of nerve degeneration. Differentiate from gingival polyp, which is attached to gingiva and sensitive to manipulation.
  • Chronic ulcerativePulpitis: Large carious cavity, wide pulp exposure; the pulp tissue is typically replaced by granulation tissue; the pulp tissue is filled with inflammatory cells (lymphocytes & plasma cells). Non or slight dull pain increase with thermal changes as fluid exudate escapes from the pulp exposure.

Pulp Necrosis and Gangrene

• Untreated pulpitis leads to pulp death.
• Inflammatory exudates, compressed within hard dentin, compress blood vessels, leading to infection and necrosis.
• Term "pulp gangrene" applied to this condition. Clinical presentations: Symptom-less tooth, or dark in color tooth. Microscopic view shows empty pulp chambers, or necrotic areas.

Pathology of the Periapical Area

• Changes due to different levels of irritation:
  • Very mild and long-standing irritation: Production of new bone (sclerosis).
  • Mild irritation: Dental granulomas.
  • Moderate irritation: Cysts.
  • Severe irritation: Periapical abscess.

Dental Granuloma

• Definition: Localized mass of chronic inflammatory granulation tissue.
• Types: Periapical, lateral, inter-radicular, odonto-iatrogenic.
• Etiology: Low-grade pulpitis, infection through gingival crevice, trauma, hematogenous infection, and odonto-iatrogenic (deep restorations, unsterilized instruments, antiseptics application).
• Clinical Features: Associated with nonvital tooth, slight sensitivity to percussion due to apical periodontal ligament inflammation, mild pain during chewing.

Periapical Abscess

• Definition: Localized suppurative process of the dental periapical region.
• Etiology: Pulp necrosis and infection, trauma, acute exacerbation of periapical granuloma, hematogenous infection, odonto-iatrogenic factors.
• Clinical features: Systemic manifestations from fever and swelling to lymphadenitis. Local manifestations: severe pain upon percussion, feelings of tooth extrusion or displacement within socket, abscess "pointing."
• Histology: Filled with pus surrounded by neutrophils

Spread of Dental Infection

• Direct spread through pulp chamber or gingival crevice.
• Lymphatic spread causing lymphadenitis (inflamed lymph nodes) and affecting structures such as maxilla or maxillary sinuses.
• Vascular spread affecting cavernous sinus thrombosis, including other potential complications such as embolism and impacting other areas of the body - including brain and lung.