Dental Pathology and Pulpitis Quiz

Routine Histotechnique and Staining

• Histology is the microscopic study of normal tissues.
• Histopathology studies structural changes due to diseases.
• Histotechnology prepares tissues for study.
• Fixation preserves tissues in a lifelike state.
• Grossing isolates the tissue area.
• Tissue processing replaces the aqueous environment with a hydrophobic one, allowing infiltration with paraffin wax.
• Embedding secures the specimen in a wax block for section cutting.
• Sectioning on a microtome cuts very fine sections.
• Staining techniques demonstrate tissue components, such as carbohydrates.

Classification of Stains

• Periodic Acid Schiff (PAS) stain: Oxidizes substances with vicinal glycol groups. Used to show glycogen and neutral mucoprotein. Can aid in diagnoses for conditions such as poorly differentiated adenocarcinoma, hepatocellular carcinoma.
• Lipid stains: Oil red O and Sudan Black B stain lipids. Oil red O stains lipids red, while nuclei stain blue.
• Nucleic acid stains: Feulgen stain, Methyl green pyronin stain
• Connective tissue stains: Reticulin, Masson's Trichrome, Van Gieson stains.
• Stains for pigments and minerals: Perl's stain.
• Stains for microorganisms: Ziehl-Neelsen stain, Gomori methenamine silver stain.
• Enzyme digestion technique,
• Stains for amyloid,
• Congo red stain,
• Crystal/Methyl violet stain.

Developmental Disturbances of Oral and Para Oral Structures

• Developmental anomalies refer to defects from growth and development disturbances.
• Malformation: An abnormal shape or structure, interfering with function (e.g., cleft palate).
• Deformation: An alteration in shape of previously normally formed structures (e.g., torticollis).
• Anomaly: Any deviation from normal, without functional interference (e.g., peg-shaped lateral).
• Anomalad: A developmental malformation and structural changes (e.g., Robin anomalad).

Developmental Disturbances of Soft Tissue

• Lip pits: Congenital pits, usually at lip corners.
• Frenal tag: Autosomal dominant, extra labial frenum.
• Fordyce granules: Bilateral sebaceous glands on buccal mucosa.

Developmental Disturbances of Hard Tissues

• Microdontia: Teeth smaller than normal.
• Macrodontia: Teeth larger than normal.
• Rhizomicri: Smaller than normal tooth roots.
• Rhizomegaly: Larger than normal tooth roots.
• Anodontia: Absence of teeth.
• Supernumerary teeth: Extra teeth.
• Gemination: Incomplete division of a tooth germ, creating a single root, multiple crowns.
• Fusion: Union of two adjacent tooth germs, resulting in a single crown and root.
• Concrescence: Union of roots of adjacent teeth by cementum.
• Dilaceration: Abnormal bend/curve in root or crown.
• Talon's cusp: Anomalous projection on the lingual side of incisor.
• Dens invaginatus: Deep surface invagination of a dental crown or root, lined by enamel.
• Dens evaginatus: A small, globe-shaped projection on a tooth crown.
• Taurodontism: Enlargement of pulp chamber and body of a tooth.
• Ectopia: Tooth in an abnormal location.
• Rotation: Tooth turned.
• Transposition: Teeth switch positions.
• Inversion/Transmigration teeth occur in a different direction from normal.

Tooth Eruption & Structure

• Premature eruption
• Delayed eruption
• Embedded tooth
• Submerged tooth
• Eruption sequestrum
• Enamel, dentin, enamel+dentin, and cementum (structures) affected

Microdontia/Macrodontia

• Generalized micro/macrodontia: Uniformly small/large teeth. Associated syndromes include pituitary dwarfism/gigantism, Down's syndrome.
• Focal micro/macrodontia: Irregular small/large teeth. Associated syndromes include facial hemihypertrophy.
• Total anodontia: Absence of all teeth.

Anomalies Numbers of Teeth

• Hypodontia: Absence of one or more teeth (<6).
• Oligodontia: Absence of more than 6 teeth.

Types of Developmental Anomalies

• Enamel hypoplasia: Defective enamel formation
• Amelogenesis imperfecta: Hereditary enamel dysplasia.
• Dentinogenesis imperfecta: Hereditary dentin dysplasia.
• Dentin dysplasia - Rootless
• Regional odontodysplasia.

Pulp and Periapical Pathology

• Pulpitis: Inflammation of the dental pulp.
  • Reversible pulpitis: Mild, pulp to normal after stimulus removal. Signs include pulp hyperemia, edema, and inflammation.
  • Irreversible pulpitis: Severe, pulp cells die. Signs include edema, vascular dilation, inflammation, odontoblast destruction, pulp abscess
  • Chronic pulpitis: Inflammation for longer period.
  • Acute suppurative pulpitis: Pulp liquefaction & necrosis by abscess formation.
  • Chronic hyperplastic pulpitis (pulp polyp): Overgrowth in pulp chamber as a mass. Signs include granulation tissue, inflammatory cells, and sometimes an epithelial lining like oral mucosa.
• Pulpal Resorption:
  • Internal resorption: Odontoclastomas.
  • External resorption: Not in these notes
• Pulpstones:
  • True (rare) includes dentin with distinct tubules, lined by odontoblasts
  • False (common): Layers of mineralized tissue, arise from degenerating cells.
• Apical periodontitis: Inflammation of periodontium (around tooth root) due to trauma/irritation/infection.
• Periapical Abscess: Acute or chronic suppuration; often arises from a periapical granuloma.
  • Clinical:Painful, sometimes systemic. Microscopic: Neutrophils, cellular debris, bacteria, dilated PDL, bone tissue showing inflammation.
• Periapical granuloma: A chronic lesion resulting from inflammation, typically sterile.
  • Microscopic: Fibrous tissue, inflammation, possible macrophages, lymphocytes, plasma cells. Can be sterile, or secondary infection can occur.
• Osteomyelitis: Severe bone infection, a sequela of apical infection.
  • Necrotic bone, inflammatory exudates.
• Cellulitis: Diffuse inflammation of soft tissues.
  • Micro: Inflammatory cell infiltration, serous fluid, fibrin formation.

Bacterial Infections

• Scarlet Fever: Streptococcus infection. May involve the oral cavity with small red spots on the palate and uvula, 'strawberry tongue'. Microscopic: Neutrophils with spongiosis, parakeratosis, necrosis
• Tuberculosis: Mycobacterium tuberculosis. Oral cavity ulcerations, mainly on the tongue, palate, lips, gingiva, and buccal mucosa. Microscopic: Epithelioid cells and multinucleated giant cells (Langhan's giant cells).
• Diphtheria: Corynebacterium diphtheria. Characterized by a pseudomembrane from suppurative exudates; ulceration. Microscopic: fibrin, necrotic cells, and neutrophils
• Actinomycosis: (Lumpy jaw) Chronic granulomatous infection, with sulfur granules. Microscopic: Granulomatous, suppurative, colonies of organisms, radiating filaments
• Syphilis: Treponema pallidum.
  • Primary: Chancre, indurated nodule, ulceration. Microscopic: Acanthetic epithelium, lymphocytic response
  • Secondary: Mucous patches, generalized skin/mucosal lesions. Microscopic: Psoriasiform hyperplasia, neutrophils
  • Tertiary: Gummas (chronic granulomatous lesions). Microscopic: Necrotizing granulomatous inflammation.
• NOMA: (Cancrum oris, Gangrenous stomatitis). Destructive oral tissue necrosis. Microscopic: Extensive necrosis, destruction of soft tissues and bone.
• Acute Necrotizing Ulcerative Gingivitis (NUG): also known as Vincent's infection. Microscopic: Bacterial, including rods, fusiform, spirochetes. Necrotic zone
• Leprosy: Mycobacterium leprae. Macules, nodules(leproma) that ulcerate. Microscopic: Granulomatous inflammation, histiocytes, lymphocytes, giant cells.
• Botriomycosis: Localized granulomatous infection. Microscopic: Suppurative foci; "sulfur granules," radiating actinomycetes.
• Granuloma Inguinale: Chronic granulomatous infection. Microscopic: Granulation tissue, macrophages, and Donovan bodies (intracellular cysts, rod-shaped structures)
• Pyostomatitis vegetans: Large papillary projections, abscesses. Microscopic: Hyperplastic surface epithelium, densely infiltrated by inflammatory cells including plasma cells, lymphocytes, and neutrophils.

Fungal and Viral Infections

• Pseudomembranous candidiasis (thrush): White plaques on oral mucosa, adhere to surface and are removable. Microscopic: PAS-positive hyphae, hyperkeratosis, neutrophils, chronic inflammatory infiltrate

• Erythematous candidiasis: Red patches, depapillated/de-keratinized tongue. Microscopic: Hyperplastic epithelium; yeasts, hyphae, neutrophils

• Angular cheilitis: Erythema, fissuring, and scaling at corners of mouth. Microscopic: Superficial candidal infection, perioral skin involvement

• Denture stomatitis: Erythema, petechial hemorrhages in denture-bearing areas. Microscopic: Epithelial hyperplasia/atrophy, leucocytes.

• Central papillary atrophy: (median rhomboid glossitis). Erythematous area, mid-posterior dorsal tongue. Microscopic: Atrophic mucosa, loss of papillae

• Hyperplastic candidiasis (leukoplakia): Least common, superimposed candidiasis on a leukoplakic lesion. Microscopic: candidal infection.

• Histoplasmosis: Granulomatous fungal disease. Microscopic: Macrophage aggregates, granulomas, yeasts

• Blastomycosis: Microscopic: Large yeasts (Blastomyces dermatidis), acute/granulomatous inflammation.

• Cryptococcosis: Rare fungal disease, presenting with ulcers or erythematous plaques. Microscopic: Granulomatous response, yeasts, mucopolysaccharide capsule identified by staining

• Zygomycosis (Mucormycosis; Phycomycosis): Nasal obstruction, pain, swelling. Microscopic: Extensive necrosis, large, non-septate hyphae

• Aspergillosis: Microscopic: Septate hyphae; invasive form

• Toxoplasmosis: Intracellular protozoa. Microscopic, Lymph node changes include germinal centers. Accumulations of eosinophilic macrophages

• Herpetic Simplex Infection: HSV-1 or HSV-2. Vesicles, ulcerations. Microscopic: Acantholysis, ballooning degeneration, intranuclear inclusions (Lipschütz bodies)

• Varicella: Varicella-zoster virus (VZV). Vesicles, ulcerations. Microscopic: Acantholysis

• Herpes Zoster: Reactivation of VZV.

• Infectious Mononucleosis: Epstein-Barr virus (EBV), HHV-4. Transient petechiae. Microscopic details not found

• CMV (Cytomegalovirus) Infection: Microscopic features include swollen cells with inclusions.

• Other infections: Rubeola, Measles, Oral hairy leukoplakia

Allergic and Immunologic Diseases

• Transient lingual papillitis: Painful, recurrent crops of ulcers, affecting oral mucosa.
• Recurrent aphthous stomatitis (RAS): Recurrent oral ulcers, classified into minor, major, or herpetiform types.
• Minor: Most common, small, shallow ulcers with a yellow-white membrane.
• Major: Less common, larger, deeper ulcers.
• Herpetiform: Dozens of tiny ulcers.
• Behçet's syndrome: Chronic multi-system inflammatory disorder. Oral manifestations include aphthous ulcers, and other systemic symptoms. Microscopic findings are nonspecific, often resembling recurrent aphthous ulcers. May include vasculitis.
• Sarcoidosis: Multisystem granulomatous disorder, causing oral granulomas. Microscopic: Epithelioid histiocytes, lymphocytes, giant cells.
• Orofacial granulomatosis: Idiopathic immune disorder; clusters of noncaseating granulomas.
  • Melkersson-Rosenthal syndrome: Combination of oral lesions (cheilitis granulomatosa), facial nerve paralysis, and fissured tongue. Microscopic: Edema, lymphatics, lymphocytes, histiocytes present.
• Wegener's granulomatosis: Necrotizing granulomatous lesions and vasculitis. Microscopic: Mixed inflammation centered around blood vessels, neutrophilic infiltration, necrosis, 'nuclear dust' (leukocytoclastic vasculitis.
• Reiter's syndrome: Associated with urethritis, balanitis, conjunctivitis. Microscopic: Parakeratosis, acanthosis
• Angioedema: Swelling of skin and mucosa due to fluid accumulation.
• Drug allergy: Lesions including ulcers, necrosis, hyperplasia, pigmentation, altered saliva/taste. Microscopic: Subacute mucositis, lymphocytes, eosinophils, neutrophils

Premalignant Lesions and Conditions

• Leukoplakia: White patch/plaque, often from tobacco.
  • Homogenous: Well-defined white patch, low malignant potential.
  • Non-homogenous (nodular): Mixed red & white regions, high malignant transformation potential
  • Verrucous: Rough surface, papillary projections, high malignant potential - Proliferative verrucous leukoplakia specifically has thicker white lesions with raised projections.
• Leukoedema: White/gray patch on oral mucosa, intracellular edema. Microscopic: Increased thickness, abnormal rete pegs
• Erythroplakia: Red patch, high-risk for malignancy. Microscopic: Mild changes in cellular arrangement & size
• Carcinoma in situ: Precancerous condition, where cells display malignant changes. Microscopic: Intraepithelial dysplasia, sometimes keratin production issues present.
• Actinic cheilitis: Precancerous lesion from sun exposure. Microscopic: Atrophy/hyperplasia, inflammation, dysplasia, elastosis
• Stomatitis nicotina: Palate lesions from tobacco. Microscopic: hyperorthokeratosis
• Snuff dipper lesion: Lesion in reverse smokers/smokers who don't use direct flame sources. Microscopic: parakeratin, hyperplasia
• Oral submucous fibrosis: Abnormal rigidity of mucosa; fibrotic transformation. Microscopic: hyalinization, atrophy, collagen bundles
• Lichen planus: Chronic inflammatory disease, presents with six Ps. Microscopic: epidermal damage, hyperkeratosis, atrophy, lymphocytes.
  • Lichenoid reaction: Similar to LP but drug-induced
• Discoid lupus erythematosus: Skin and mucous membrane disorder. Microscopic: hyperkeratosis, sub-epithelial hydropic change

Histopathology of Dental Caries

• Morphology based on Chronology:
  • Incipient caries, mild discoloration
• Morphology based on location of enamel:
  • Pit & fissure caries, found in pits and fissures
  • Smooth surface caries
  • Cervical caries, located near the neck of the tooth, crescent shaped cavity.
  • Root caries, initiated at dentin root, occurs in older age
• Morphology based on severity:
  • Rampant caries (rapid destruction).
  • Arrested caries (growth stops)
  • Recurrent caries(regrowth beneath fillings)
• Initial stages of caries: Enamel caries. Microscopic/physical changes include loss of inter-rod substance, mucopolysaccharides
• Dentin caries: Demineralization of dentin, bacterial invasion, changes such as fatty degeneration of Tomes' fibers, dentinal sclerosis occur in response to bacterial colonization, may lead to liquefaction of dentin.
• Different zones of dentin caries:
• Zones of fatty degeneration of Tomes' fibers; Dentinal sclerosis;
• Demineralization and a zone of bacterial invasion;
• Zone of decomposed and dead dentin.
• Salivary factors: Saliva's role in preventing caries; composition and buffering capacity of saliva and factors like lysozymes, lactoperoxidase, and lactoferrin

Histopathology of Periodontal Diseases

• Incipient gingivitis: Mild polymorphonuclear leukocyte infiltration.
• Chronic gingivitis: Increased lymphocytes, plasma cells, monocytes.
• Necrotizing ulcerative gingivitis (NUG): Ulceration, intense polymorphonuclear leukocyte infiltration, bacteria.
• Plasma cell gingivitis: Intense plasma cell infiltrate.
• Granulomatous gingivitis: Granulomas with histiocytes, lymphocytes, and giant cells.
• Drug-induced gingival enlargement: Not hyperplasia/hypertrophy.
• Hormonal/nutritional/systemic-induced gingival enlargement: Increased vascularity, fibroblasts, leukocytes with edema
• Gingival fibromatosis: Dense, hypocellular, hypovascular fibrous tissue.
• Gingival Abscess: Localized polymorphonuclear leukocyte exudate with secondary changes in epithelium (Possible cell swelling, ulcerations.
• Pericoronitis: Inflammation around impacted or partially erupted teeth. Microscopic: Hyperplasia, edema, lymphocytes

Test your knowledge on dental pathology with this quiz that covers topics such as fordyce granules, pulpitis, and dental anomalies. Understand the characteristics and consequences of various oral conditions. Ideal for dental students and professionals looking to reinforce their understanding.