Your FREE INBDE Flashcards 2026 – 300+ Cards

Masseter, temporalis, medial & lateral pterygoid — all motor from V3 (trigeminal).

Facial nerve (cranial nerve VII).

Facial nerve VII via the chorda tympani.

Lingual nerve (branch of V3).

Glossopharyngeal nerve (CN IX).

V1 ophthalmic, V2 maxillary, V3 mandibular; V3 is the only one carrying motor fibers.

Most often from depositing anesthetic too LOW (below the mandibular foramen).

Posterior, middle, and anterior superior alveolar nerves (branches of V2).

Maxillary nerve (V2) and the pterygopalatine ganglion (parasympathetic to lacrimal/nasal glands).

Parasympathetic secretomotor from the glossopharyngeal nerve (CN IX) via the otic ganglion.

Parasympathetic from the facial nerve (VII) via the chorda tympani and submandibular ganglion.

Mandibular nerve V3.

Maxillary nerve V2.

Muscles of mastication, malleus and incus, trigeminal nerve (V).

Muscles of facial expression, stapes, facial nerve (VII).

~96% inorganic hydroxyapatite; the hardest, most mineralized tissue; no cells, cannot regenerate.

Mineralized tissue with dentinal tubules; formed by odontoblasts; can form throughout life.

Connective tissue with nerves and vessels; odontoblasts line its periphery.

Mineralized layer covering the root; anchors periodontal ligament fibers.

About 5.5 — below this, enamel demineralizes.

Buffering, lubrication, clearance, antimicrobial proteins, and secretory IgA — protects against caries.

Reduced saliva → loss of buffering/clearance → high caries and infection risk.

Promotes calcium and phosphate absorption needed for bone and tooth mineralization.

Parathyroid hormone raises serum calcium; calcitonin lowers it.

Vascular spasm, platelet plug, coagulation cascade, then clot retraction and dissolution.

Glycolysis → Krebs cycle → oxidative phosphorylation in mitochondria yields most ATP.

Buccal nerve (branch of V3) — sensory to the cheek; NOT the same as the facial nerve buccal branch.

Roots of maxillary premolars/molars are close to the floor — oroantral communication risk on extraction.

Osteoblasts build bone; osteoclasts resorb it; osteocytes maintain it.

The maxillomandibular relationship with condyles in the most superior position — a reproducible reference.

Maximum intercuspation — the fully interdigitated bite.

Mesiobuccal cusp of the maxillary first molar in the buccal groove of the mandibular first molar (normal molar relationship).

Mandible/lower molar distal to Class I (retrognathic profile, overjet).

Mandible/lower molar mesial to Class I (prognathic profile, often crossbite).

Overjet = horizontal anterior overlap; overbite = vertical overlap.

Acute unilateral facial nerve (VII) paralysis; the forehead is involved (lower-motor-neuron lesion).

0–14; 7 is neutral; lower is more acidic; each unit is a 10-fold change in H+ concentration.

7 (neutral).

A solution that resists pH change; bicarbonate is a major physiologic and salivary buffer.

An acid donates H+ (proton); a base accepts H+.

Oxidation is loss of electrons; reduction is gain (OIL RIG).

Net movement of molecules from high to low concentration; passive, no energy.

Movement of water across a semipermeable membrane toward higher solute concentration.

Cells swell and can lyse — why water is the worst avulsed-tooth storage medium.

Equal solute concentration; no net water shift (e.g., normal saline).

Weak attraction giving water its high surface tension and solvent properties.

Covalent = shared electrons; ionic = transferred electrons (electrostatic attraction).

Lowers activation energy and speeds a reaction without being consumed.

A system at equilibrium shifts to counteract an imposed change (e.g., pH affecting LA ionization).

Relates pH and pKa to the ratio of ionized to non-ionized drug — explains LA behavior.

Cohesive force at a liquid surface; relevant to wetting of impression materials.

Difference in concentration driving passive transport (diffusion, osmosis).

Conduction, convection, and radiation.

A fluid's resistance to flow; affects impression and cement handling.

How much solute dissolves in a solvent; low solubility is desired for cements in the mouth.

A substance that dissociates into ions and conducts electricity in solution.

Strong, durable, technique-tolerant, not bonded, poor esthetics; contains mercury alloyed with silver.

Esthetic, bonded resin with filler; undergoes polymerization shrinkage — place incrementally.

Chemically bonds to tooth and releases fluoride; lower strength; good for root caries and high-risk patients.

Glass ionomer with resin added — better strength while keeping fluoride release.

Polysulfide, condensation silicone, addition silicone (PVS), and polyether.

Accurate, dimensionally stable impression material; the fixed-prosthodontics workhorse.

Composite shrinks toward the curing light, risking marginal gaps; managed by incremental placement.

Phosphoric acid creates micro-porosities in enamel for micromechanical bonding of resin.

How much a material expands with heat; a large mismatch with tooth causes microleakage.

Plaster and dental stone (calcium sulfate hemihydrate) used for casts and dies.

Forms acid-resistant fluorapatite and promotes remineralization; mostly a topical effect.

0.7 ppm (parts per million).

Enamel mottling from excess fluoride during tooth development.

Probably toxic dose ~5 mg/kg — warrants medical evaluation.

Stress = force per area applied; strain = the resulting deformation.

Stiffness of a material; higher modulus = more rigid (less flexible).

Current between two dissimilar metals (e.g., amalgam touching gold) causing a brief pain.

Trituration mixes alloy with mercury; the gamma-2 phase is the weakest/most corrosion-prone (minimized in modern alloys).

Dentin bonding is harder due to moisture and the smear layer; needs a hybrid layer.

A resin (or glass ionomer) flowed into pits and fissures to prevent caries.

Fixed (crown/bridge) is cemented and not patient-removable; removable (denture/partial) is taken out.

The artificial tooth that replaces a missing tooth in a fixed bridge.

The tooth (or implant) that supports a fixed or removable prosthesis.

Direct bone-to-titanium contact; the basis of implant stability.

Hereditary defective ENAMEL formation; thin/pitted/discolored enamel on all teeth.

Hereditary defective DENTIN; opalescent blue-gray teeth; often with osteogenesis imperfecta.

Absent/hypoplastic clavicles, delayed sutures, many supernumerary and unerupted teeth.

Colonic polyps (malignant potential) with osteomas and supernumerary/impacted teeth.

Multiple basal cell carcinomas and multiple odontogenic keratocysts.

Macroglossia, delayed eruption, periodontal disease, class III tendency.

Cleft lip = failed fusion of medial nasal & maxillary processes; cleft palate = failed palatal shelf fusion.

One mutant allele causes disease; affected in every generation; 50% offspring risk.

Two mutant alleles needed; often skips generations; carriers unaffected.

Mainly affects males; no male-to-male transmission (e.g., hemophilia).

Congenitally missing teeth; most commonly third molars, then maxillary lateral incisors and second premolars.

Extra tooth, classically between the maxillary central incisors.

Fusion = two tooth germs unite (usually fewer teeth); gemination = one germ splits (usually normal count).

Invagination of enamel into the tooth; high caries/pulp risk; common in maxillary lateral incisors.

Enamel hypoplasia from trauma or infection of the predecessor primary tooth.

Localized developmental defect with thin enamel/dentin and a faint radiographic outline.

Defect of ectodermal structures — hypodontia/anodontia, conical teeth, sparse hair, reduced sweating.

A mutation alters DNA sequence; a polymorphism is a common variant (>1% of population).

First permanent molar (~age 6) — the '6-year molar.'

Natal teeth are present at birth; neonatal teeth erupt within the first 30 days.

Light continuous force → bone resorption (pressure side) and apposition (tension side).

20 primary teeth.

32 permanent teeth (including third molars).

Appliance that preserves arch space after early loss of a primary tooth.

Immediate, non-specific, no memory — barriers, neutrophils, complement, saliva.

Slower, specific, with memory — B cells/antibodies and T cells.

IgE-mediated; immediate (anaphylaxis, allergy).

Antibody (IgG/IgM)-mediated against cell-surface antigens (e.g., transfusion reaction).

Immune-complex deposition (e.g., serum sickness, lupus).

Delayed, T-cell-mediated (contact dermatitis to latex/metals, TB skin test).

IgM (then class-switch to IgG).

IgG — crosses the placenta and provides long-term immunity.

IgA — protects mucosal surfaces; found in saliva and other secretions.

IgE.

Opsonization, inflammation, and membrane-attack-complex lysis of pathogens.

First responders; phagocytose bacteria; dominant in acute inflammation and the periodontal pocket.

Phagocytosis and antigen presentation; dominant in chronic inflammation.

Coordinates the immune response; the target of HIV.

Kills virus-infected and tumor cells.

Active = your own response (infection/vaccine, lasting); passive = transferred antibodies (e.g., maternal, temporary).

Saliva flow, mucosal barrier, antimicrobial proteins (lysozyme, lactoferrin), and normal flora.

Pemphigus vulgaris and mucous membrane pemphigoid cause oral blistering/erosions.

Redness, heat, swelling, pain, and loss of function.

Acute = neutrophils; chronic = lymphocytes, plasma cells, macrophages.

True allergy is an immune (often type I) reaction; intolerance/side effect is not immune-mediated.

Autoimmune destruction of salivary/lacrimal glands → dry mouth and dry eyes; high caries risk.

Granulation tissue at the apex of a NON-vital tooth; the most common periapical radiolucency.

Identical on radiograph; distinguished only on histology (cyst has epithelial lining).

Inflammatory cyst from an epithelialized periapical granuloma; on a non-vital tooth.

Develops around the CROWN of an unerupted tooth (commonly third molar).

Aggressive, recurrence-prone developmental cyst; multiple OKCs suggest Gorlin syndrome.

Benign but locally aggressive odontogenic tumor; multilocular 'soap-bubble' radiolucency at the mandibular angle.

Fibrous dysplasia.

Osteosarcoma.

Multiple myeloma.

Sickle cell disease (or thalassemia).

A white patch that cannot be rubbed off or attributed to another condition; potentially premalignant.

A red patch; higher malignant potential than leukoplakia — biopsy.

Squamous cell carcinoma; classic high-risk site is the lateral/ventral tongue and floor of mouth.

Painful recurrent ulcer with a yellow-gray base and erythematous halo on non-keratinized mucosa; not infectious.

Involves a VITAL tooth; do NOT treat endodontically.

Involves VITAL teeth, mostly anterior mandible in middle-aged women; no treatment needed.

Necrosis = uncontrolled cell death with inflammation; apoptosis = programmed death without inflammation.

Externalized phosphatidylserine flags the cell for phagocytosis without a scar.

Hydropic (vacuolar) swelling is reversible; irreversible injury includes membrane damage and nuclear changes.

New connective tissue and capillaries in healing; not the same as a granuloma.

Organized collection of macrophages (epithelioid cells), classic of TB and foreign-body reactions.

Disordered, abnormal cell growth and maturation; a premalignant change.

Reversible change of one mature cell type to another (e.g., smoker's respiratory epithelium).

Hyperplasia = more cells; hypertrophy = larger cells.

Benign bony exostoses (palate / lingual mandible); no treatment unless interfering with prosthesis.

Most common benign reactive oral growth; smooth nodule from chronic irritation.

Red, friable, vascular growth that bleeds easily; common on gingiva, often in pregnancy.

Most common salivary gland tumor; benign, usually in the parotid.

Mucus-extravasation lesion, commonly on the lower lip from a severed minor salivary duct.

Wickham striae — lacy white lines on buccal mucosa; T-cell mediated.

White plaques that wipe off leaving erythema; Candida albicans; risk with immunosuppression/inhaled steroids.

Recurrent vesicles on keratinized/attached mucosa (lips, hard palate, gingiva).

Cheese-like necrosis, classic of tuberculosis.

Increased hydrostatic pressure or decreased oncotic pressure shifting fluid into tissues.

Gingivitis = reversible inflammation, no attachment loss; periodontitis = irreversible attachment and bone loss.

The true measure of periodontitis severity (from the CEJ), not just pocket depth.

Periodontitis is staged (I–IV, severity/complexity) and graded (A–C, rate of progression).

Bone loss between multi-rooted tooth roots; worsens prognosis.

Nonsurgical removal of plaque, calculus, and biofilm from root surfaces — first-line perio therapy.

Healthy sulcus is about 1–3 mm; ≥4 mm with bleeding suggests disease.

Mineralized plaque (tartar); a plaque-retentive factor, not the direct cause of inflammation.

Hormones exaggerate the gingival inflammatory response (pregnancy gingivitis / pyogenic granuloma).

Pain to stimulus that stops quickly; pulp is salvageable — remove the cause.

Lingering or spontaneous pain; requires root canal therapy or extraction.

A non-vital tooth fails to respond to cold/electric pulp testing.

Bacteria/toxins from a necrotic pulp inflaming the periapical tissues.

Rapid-onset swelling and severe pain from a necrotic pulp; treat with drainage and removing the source.

Remove infected pulp, disinfect and shape the canals, and obturate to seal them.

Reimplant ASAP; handle by crown, do not scrub the root; store in milk or HBSS, never water.

Do NOT reimplant — risk to the developing permanent successor.

Painful loss of the extraction blood clot ~3–5 days post-op; manage with irrigation and a medicated dressing.

An opening into the maxillary sinus after extraction of a maxillary posterior tooth.

Rapidly spreading bilateral submandibular/sublingual cellulitis — an airway emergency.

Midface fracture patterns I (horizontal), II (pyramidal), III (craniofacial separation).

Pulpotomy removes coronal pulp; pulpectomy removes all pulp tissue (primary teeth).

Rampant caries in young children, classically from prolonged bottle/sippy use with sugary liquids.

Tobacco and alcohol (synergistic); HPV for oropharyngeal SCC.

Benign replacement of bone by fibro-osseous tissue; classic 'ground-glass' radiograph.

Disordered bone remodeling; 'cotton-wool' radiopacities and hypercementosis; high alkaline phosphatase.

Benign migratory glossitis — shifting red patches with white borders; usually asymptomatic.

Streptococcus mutans — acidogenic, aciduric; ferments sugar into enamel-demineralizing acid.

Advance established (deep) caries lesions; acidogenic, aciduric.

Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola.

Aggregatibacter actinomycetemcomitans (A. a.).

A structured biofilm of bacteria in a matrix adhering to tooth surfaces.

Organized community more resistant to antimicrobials than free-floating bacteria.

Gram-positive retain crystal violet (thick peptidoglycan); gram-negative have an outer membrane with endotoxin.

Lipopolysaccharide of gram-negative outer membrane; triggers inflammation/septic shock.

Bacteria are cells; viruses are not — they need a host cell to replicate.

Fusobacterium and spirochetes; acute necrotizing ulcerative gingivitis with punched-out papillae and pain.

Fungus causing oral candidiasis (thrush); opportunistic with immunosuppression or antibiotics.

Filamentous bacteria causing 'lumpy jaw' with sulfur granules.

Causes primary herpetic gingivostomatitis and recurrent herpes labialis.

Obligate aerobes need oxygen; obligate anaerobes are killed by it; facultative use either.

Sterilization kills ALL microbes including spores; disinfection reduces but may spare spores.

Steam under pressure, commonly 121°C at 15 psi for ~15–20 minutes; the standard for instrument sterilization.

Bacterial spores used to verify a sterilizer actually killed resistant organisms.

Vertically transmitted, often from caregiver to infant ('window of infectivity').

S. mutans glucosyltransferase converts sucrose into sticky insoluble glucan that aids plaque adhesion.

Needs host/tooth + cariogenic bacteria + fermentable sugar + time.

Bloodborne; high occupational risk in dentistry — vaccination is standard for staff.

Take the LOWEST of the weight-based limit, the absolute cap, and the epinephrine ceiling.

mg per cartridge = % × 10 × 1.8 mL (standard 1.8 mL cartridge).

2 × 10 × 1.8 = 36 mg of lidocaine per 1.8 mL cartridge.

7 mg/kg, absolute cap 500 mg (with vasoconstrictor).

6.6 mg/kg, absolute cap 400 mg; available as 3% plain (no vasoconstrictor).

8 mg/kg, cap 600 mg; risk of methemoglobinemia.

~2 mg/kg, cap ~90 mg; longest-acting and most cardiotoxic — avoid in children.

Metabolized largely in plasma (by plasma esterases), unlike other amides.

0.2 mg in a healthy patient; 0.04 mg in a cardiac patient (often the limiting factor).

0.01 mg/mL × 1.8 mL ≈ 0.018 mg of epinephrine per cartridge.

Vasoconstriction → slows absorption, prolongs anesthesia, reduces bleeding and systemic toxicity.

CNS excitation/convulsions FIRST, then CNS and respiratory depression.

Low (acidic) pH shifts the weak base to its ionized form, so less non-ionized base crosses the nerve.

Amides (lidocaine, articaine) metabolized in liver/plasma; esters (procaine) by plasma cholinesterase, higher allergy risk.

Esters metabolize to PABA, the usual cause of true local-anesthetic allergy.

Amoxicillin 2 g adult (50 mg/kg child), single dose 30–60 min before the procedure.

Removed as an alternative in 2021 due to C. difficile risk.

Cephalexin, azithromycin, clarithromycin, or doxycycline (avoid cephalosporins if anaphylaxis to penicillin).

Prosthetic valve/repair material, prior IE, transplant with valvulopathy, certain congenital heart disease.

Mitral valve prolapse, rheumatic heart disease, bicuspid aortic valve, routine prosthetic joints.

Inhibit cyclooxygenase (COX) → less prostaglandin; first-line for acute dental pain.

Acetaminophen has analgesic/antipyretic but little anti-inflammatory effect; safer with bleeding/ulcer risk.

MRONJ — medication-related osteonecrosis of the jaw, especially after extractions.

Unopposed alpha effect → hypertension with reflex bradycardia.

Agonists at mu opioid receptors; reserved for severe pain; risk of respiratory depression and dependence.

Opioid antagonist that reverses opioid overdose (respiratory depression).

Benzodiazepine antagonist that reverses benzodiazepine oversedation.

Minimal sedation; rapid onset/offset; give 100% oxygen at the end to prevent diffusion hypoxia.

Causes intrinsic tooth discoloration and enamel hypoplasia if given during tooth development; avoid <8 yr & in pregnancy.

Inhibits vitamin-K-dependent clotting factors (II, VII, IX, X); monitored by INR.

Irreversibly inhibits COX-1 → impaired platelet aggregation for the platelet's lifespan (~7–10 days).

Vasoconstriction (raises blood pressure).

Increases heart rate and contractility.

Bronchodilation and vasodilation in skeletal muscle.

Immunosuppression and impaired healing; possible adrenal suppression requiring steroid coverage.

An NSAID (e.g., ibuprofen), unless contraindicated.

Ratio of toxic dose to effective dose; a narrow index means a small margin of safety.

Both effective; articaine is popular for infiltration; both are amides.

Impaired healing, higher infection and periodontitis risk; assess control (HbA1c) before surgery.

Usually continue therapy for routine dentistry; check INR for warfarin; use local hemostatic measures.

Chronic steroid use can blunt the stress response — consider steroid coverage for major procedures.

Avoid elective bone surgery when possible; greatest risk with IV bisphosphonates.

Second trimester is safest for elective dental care; avoid teratogenic drugs.

Defer elective care and refer for very high readings (e.g., ≥180/110 mmHg).

Many drugs (anticholinergics, antihistamines, antidepressants) reduce saliva and raise caries risk.

Sudden, severe, brief electric facial pain in a trigeminal distribution; carbamazepine is first-line.

Professionally applied topical fluoride to prevent and arrest caries, including in young children.

Antiseptic mouthrinse that reduces plaque bacteria; side effect is tooth/restoration staining.

Topical nystatin or clotrimazole; systemic fluconazole for resistant/extensive cases.

Antiviral for herpes simplex infections.

Autonomy, nonmaleficence, beneficence, justice, veracity.

Respect for the patient's right to self-determination; basis of informed consent.

Do no harm.

Act in the patient's best interest.

Fairness in the distribution of care.

Truthfulness; honest disclosure to the patient.

Autonomy (NOT beneficence — a classic trap).

A competent patient's autonomy overrides the dentist's beneficence.

Disclosure of risks/benefits/alternatives to a patient with capacity, given voluntarily; revocable anytime.

Elimination → substitution → engineering → administrative → PPE (PPE is last).

Treat all blood and body fluids as potentially infectious for every patient.

Percutaneous sharps injury.

Federal law protecting the privacy and security of patient health information.

Requires exposure control plan, PPE, hepatitis B vaccination, and sharps safety.

ASA I healthy → ASA VI brain-dead; estimates pre-treatment medical risk.

Suspected child or elder abuse/neglect must be reported (dentists are mandated reporters).

Duty, breach of the standard of care, causation, and damages.

What a reasonably prudent practitioner would do under similar circumstances.

Ending the dentist-patient relationship without notice during active treatment.

Battery = treating without consent; negligence = falling below the standard of care.

Ability to understand information and appreciate consequences; minors usually need a guardian.

Tell-show-do, positive reinforcement, voice control; nonpharmacologic methods preferred first.

Behavior change depends on perceived susceptibility, severity, benefits, and barriers.

Disclosure allowed when required by law (e.g., reportable abuse or communicable disease).

Overriding a patient's wishes for their perceived good — conflicts with autonomy.

Of the truly diseased, the fraction the test correctly identifies; a test property (prevalence-independent).

Of the truly healthy, the fraction the test correctly clears; prevalence-independent.

Of those who test positive, the fraction truly diseased; changes with prevalence.

Of those who test negative, the fraction truly healthy; changes with prevalence.

Rules OUT (SnNOut) — a negative result is trustworthy.

Rules IN (SpPIn) — a positive result is trustworthy.

Used in COHORT studies; ratio of risk in exposed vs unexposed.

Used in CASE-CONTROL studies; ratio of the odds of exposure.

Patients you must treat to prevent one bad outcome = 1 / absolute risk reduction.

Systematic reviews and meta-analyses, then RCTs.

Follows exposed vs unexposed groups forward in time; can give incidence and relative risk.

Compares diseased vs non-diseased looking backward for exposure; uses the odds ratio.

Random assignment to intervention vs control; the strongest single study design for causation.

A snapshot at one time point; measures prevalence.

A third variable distorting the apparent association between exposure and outcome.

Systematic error from how subjects are chosen, making the sample unrepresentative.

Keeping participants/investigators unaware of group assignment to reduce bias.

Mean = average; median = middle value; mode = most frequent; median resists outliers.

Type I = false positive (reject a true null); Type II = false negative (miss a real effect).

Result is statistically significant — less than a 5% chance it arose by chance alone.

Incidence = new cases over time; prevalence = all existing cases at a point.

Integrates best research evidence, clinical expertise, and patient values/preferences.

Reliability = consistent/repeatable; validity = measures what it intends to.

Absolute = simple difference in risk; relative = proportional reduction (can look bigger).