National Board Dental Examination / Integrated National Board Dental Examination (INBDE) General and Oral Pathology Syllabus

Differentiate a thrombus from a postmortem clot and from an embolus.

A thrombus is an attached intravascular mass formed in life with lines of Zahn; a postmortem clot is gelatinous/'chicken fat,' not attached. An embolus is a detached intravascular mass carried to a distant site.

Distinguish transudate from exudate in terms of protein content, specific gravity, and cause.

Transudate: low protein, specific gravity <1.012, due to hydrostatic/oncotic imbalance (e.g., heart failure). Exudate: high protein, specific gravity >1.020, due to increased vascular permeability (inflammation).

Define infarction and contrast a red (hemorrhagic) versus white (pale) infarct.

Infarction is ischemic necrosis from vascular occlusion. Red infarcts occur in loose/dual-blood-supply tissues (lung, intestine) or with reperfusion; white infarcts occur in solid end-arterial organs (heart, kidney, spleen).

Differentiate innate from adaptive immunity by speed, specificity, and memory.

Innate: immediate, non-specific (PAMP recognition), no memory (neutrophils, macrophages, NK cells, complement). Adaptive: slower, antigen-specific, has memory (T and B lymphocytes).

Match each immunoglobulin class to its primary function: IgG, IgM, IgA, IgE, IgD.

IgG: most abundant, secondary response, crosses placenta. IgM: first/primary response, pentamer, best complement activator. IgA: mucosal/secretory (saliva). IgE: allergy/parasites (mast cells). IgD: B-cell receptor, surface marker.

Contrast MHC class I and class II in cell distribution and the T cells they activate.

MHC I: on all nucleated cells, presents endogenous antigen to CD8+ cytotoxic T cells. MHC II: on antigen-presenting cells (dendritic, macrophages, B cells), presents exogenous antigen to CD4+ helper T cells.

Name the three pathways of complement activation and the central convergence component.

Classical (antigen-antibody complexes), alternative (microbial surfaces), and lectin (mannose-binding lectin) pathways — all converge on C3, leading to the C5–C9 membrane attack complex.

Classify the four types of hypersensitivity (Gell and Coombs) by mechanism.

Type I: IgE-mediated immediate (anaphylactic). Type II: antibody-mediated cytotoxic (IgG/IgM vs cell antigens). Type III: immune complex deposition. Type IV: delayed, T-cell mediated.

Give a classic clinical example for each hypersensitivity type I-IV.

Type I: anaphylaxis/asthma/hay fever. Type II: hemolytic disease of newborn, Goodpasture, pemphigus. Type III: SLE, serum sickness, post-strep glomerulonephritis. Type IV: TB skin test, contact dermatitis, transplant rejection.

What is the timeframe and key mediator distinguishing type I from type IV hypersensitivity reactions?

Type I is immediate (minutes), mediated by preformed IgE/histamine from mast cells. Type IV is delayed (48–72 hours), mediated by sensitized T cells and cytokines, no antibody involved.

Which autoimmune disease is characterized by anti-dsDNA and anti-Smith antibodies, and what oral finding may occur?

Systemic lupus erythematosus (SLE); oral findings include painful oral ulcers and lichenoid/lupus mucosal lesions, often on the palate.

What is Sjögren syndrome, its classic triad, and the associated autoantibodies?

An autoimmune exocrinopathy with the triad of xerostomia, keratoconjunctivitis sicca (dry eyes), and arthritis/connective tissue disease. Associated with anti-SS-A (Ro) and anti-SS-B (La); increases risk of MALT lymphoma.

Distinguish DiGeorge syndrome from Bruton agammaglobulinemia as immunodeficiencies.

DiGeorge: thymic aplasia (22q11 deletion) causing T-cell deficiency, hypocalcemia, cardiac defects. Bruton (X-linked): BTK mutation, no mature B cells, low all immunoglobulins, recurrent bacterial infections after 6 months.

What are the four interacting factors required for dental caries (the modified Keyes diagram)?

A susceptible tooth/host surface, cariogenic bacteria (plaque biofilm), fermentable carbohydrate (substrate), and time.

Which bacteria are most associated with caries initiation versus progression, and what is the critical pH for enamel demineralization?

Streptococcus mutans is key for initiation; Lactobacilli are associated with progression of deep lesions. Critical pH for enamel demineralization is approximately 5.5.

Describe the histologic zones of an enamel caries (incipient white spot) lesion from deep to surface.

From the advancing front outward: translucent zone, dark zone, body of the lesion (largest, most demineralization), and the relatively intact surface zone.

Name and describe three developmental anomalies of tooth shape: dens invaginatus, dens evaginatus, and taurodontism.

Dens invaginatus (dens in dente): infolding of enamel into the tooth (often lateral incisor). Dens evaginatus: tubercle projecting from occlusal surface. Taurodontism: enlarged pulp chamber with apically displaced furcation ('bull-like' tooth).

Differentiate amelogenesis imperfecta from dentinogenesis imperfecta.

Amelogenesis imperfecta: defective enamel (hypoplastic/hypocalcified), normal dentin. Dentinogenesis imperfecta: defective dentin, opalescent blue-gray/brown teeth, obliterated pulp chambers, enamel chips off; associated with osteogenesis imperfecta.

Distinguish fusion, gemination, and concrescence of teeth.

Fusion: union of two tooth germs producing fewer teeth in the arch. Gemination: single germ partially splits, normal tooth count when counted as one. Concrescence: two adjacent teeth joined only by cementum after formation.

Compare reversible and irreversible pulpitis clinically.

Reversible pulpitis: short, sharp pain to stimuli (cold/sweet) that stops when stimulus is removed. Irreversible pulpitis: lingering, spontaneous, often throbbing pain that persists after stimulus removal; may be worse with heat.

Differentiate a periapical (radicular) granuloma, periapical abscess, and periapical (radicular) cyst.

All follow pulp necrosis. Granuloma: chronic granulation tissue with inflammatory cells, no epithelium-lined cavity. Abscess: acute purulent collection, painful. Radicular cyst: epithelial-lined (rests of Malassez) fluid cavity, the most common odontogenic cyst.

Define attrition, abrasion, erosion, and abfraction (the four types of tooth wear).

Attrition: wear from tooth-to-tooth contact (bruxism). Abrasion: wear from external mechanical agent (hard toothbrushing — cervical notch). Erosion: chemical/acid dissolution (GERD, citrus, bulimia). Abfraction: cervical wedge lesions from occlusal flexural stress.

What history or location helps distinguish erosion from abrasion as a cause of tooth wear?

Erosion: smooth, cupped, broad concavities, often lingual (acid reflux/vomiting) or facial (dietary acid), no plaque retention. Abrasion: notched/V-shaped cervical lesions on facial surfaces aligned with horizontal toothbrushing.

Differentiate an odontogenic keratocyst (OKC) from a dentigerous cyst.

OKC: arises from dental lamina rests, aggressive, parakeratinized corrugated epithelium, high recurrence, associated with Gorlin syndrome. Dentigerous cyst: surrounds the crown of an unerupted tooth attached at the CEJ, less aggressive.

What is the most common odontogenic cyst, and what is its origin?

The radicular (periapical) cyst — an inflammatory cyst arising from epithelial rests of Malassez at the apex of a non-vital tooth following pulpal necrosis.

Name two non-odontogenic (developmental, fissural) cysts and their typical locations.

Nasopalatine duct (incisive canal) cyst — heart-shaped radiolucency in anterior maxilla midline; and nasolabial cyst — soft tissue cyst in the nasolabial fold/upper lip.

What is the most common odontogenic tumor, and describe its key features.

Ameloblastoma — benign but locally aggressive epithelial odontogenic tumor, commonly posterior mandible, classically a multilocular 'soap-bubble/honeycomb' radiolucency with high recurrence if not excised with margins.

Distinguish odontoma, ameloblastic fibroma, and adenomatoid odontogenic tumor (AOT).

Odontoma: most common odontogenic tumor (hamartoma) — compound (tooth-like denticles) or complex (disorganized mass). Ameloblastic fibroma: epithelium + mesenchyme in young patients. AOT: '2/3 tumor' — anterior maxilla, young females, around unerupted canine, snowflake calcifications.

Compare fibrous dysplasia and ossifying fibroma as fibro-osseous lesions.

Fibrous dysplasia: GNAS mutation, 'ground-glass' radiopacity, blends into bone (poorly defined), maxilla, monostotic/polyostotic (McCune-Albright). Ossifying fibroma: well-demarcated/encapsulated, mandible, can be enucleated.

What is the difference between leukoplakia and erythroplakia in terms of definition and malignant potential?

Leukoplakia: white patch that cannot be rubbed off or diagnosed as another disease — variable, lower malignant transformation. Erythroplakia: red velvety patch — much higher malignant potential, often already severe dysplasia or carcinoma in situ.

Name the major risk factors and most common intraoral site for oral squamous cell carcinoma.

Risk factors: tobacco (smoked/smokeless), alcohol (synergistic), betel/areca nut, HPV-16, and sun exposure (lip). Most common intraoral site is the lateral/ventral border of the tongue; floor of mouth is also high-risk.

Differentiate pemphigus vulgaris from mucous membrane (cicatricial) pemphigoid.

Pemphigus vulgaris: intraepithelial (suprabasal) acantholytic blisters, anti-desmoglein 3, positive Nikolsky, 'tombstone' basal cells, fragile bullae. Pemphigoid: subepithelial blister, antibodies to basement membrane (hemidesmosomes), more stable blisters, desquamative gingivitis.

Distinguish recurrent aphthous stomatitis (minor) from primary herpetic gingivostomatitis.

Aphthous ulcers: non-keratinized movable mucosa only, no vesicle stage, not viral, recurrent shallow ulcers with erythematous halo. Herpetic: HSV-1, preceded by vesicles, affects keratinized AND movable mucosa plus attached gingiva, fever/systemic signs, first episode in children.

What are the histologic and clinical hallmarks of oral lichen planus?

Clinically: bilateral white Wickham's striae (reticular form) or erosive lesions. Histologically: hyperkeratosis, saw-tooth rete ridges, band-like (lichenoid) subepithelial lymphocytic infiltrate, and basal cell (liquefactive) degeneration.

What is the most common salivary gland neoplasm overall, its most common location, and key behavior?

Pleomorphic adenoma (benign mixed tumor) — most common in the parotid gland; benign but recurs if incompletely excised and has small risk of malignant transformation (carcinoma ex pleomorphic adenoma).

Name the most common malignant salivary gland tumor and the malignancy noted for perineural invasion.

Mucoepidermoid carcinoma is the most common salivary gland malignancy (mucous + epidermoid cells). Adenoid cystic carcinoma is notorious for perineural invasion, pain, and late distant metastases ('Swiss-cheese' cribriform pattern).

Differentiate a mucocele from a ranula.

Both are mucus extravasation/retention phenomena. Mucocele: most common on the lower lip from minor salivary gland duct rupture (often trauma). Ranula: a mucocele of the floor of the mouth involving the sublingual/submandibular gland, producing a bluish 'frog-belly' swelling.

What is sialolithiasis, which gland is most often affected and why?

Sialolithiasis is a salivary calculus (stone) obstructing a duct, causing painful swelling at mealtimes. The submandibular gland (Wharton's duct) is most affected due to its thick mucous secretion and the upward, against-gravity course of its duct.