# INBDE practice questions: FK5 — Immunology and host defense Ten original INBDE practice questions on FK5 — Immunology and host defense, each answered on this page with a rationale and a source. Last updated: 2026-08-10. ## Question 1 A 64-year-old woman with painful desquamative gingivitis mentions that both eyes have been red and gritty for months and that nobody has connected the two. Her biopsy shows a subepithelial split with a linear band of IgG and C3 at the basement membrane. What must her treatment plan include? - A. Deferral of all periodontal therapy until the gingival lesions have fully healed - B. Replacement of any amalgam restorations lying against the affected gingival tissue - C. Prompt referral to ophthalmology, since conjunctival scarring can threaten sight - D. Repeat immunofluorescence from the centre of an ulcer to confirm the pattern **Answer C:** Prompt referral to ophthalmology, since conjunctival scarring can threaten sight A subepithelial split with a linear band of IgG and C3 along the basement membrane identifies mucous membrane pemphigoid, in which antibody attacks hemidesmosome components so the full thickness of the epithelium separates from the connective tissue. Its signature oral presentation is exactly her desquamative gingivitis, and the reason to identify it fast is the eye: conjunctival scarring can fuse the eyelid to the globe and cause blindness. A withholds care she needs and offers the eye nothing. B applies the lichenoid contact reaction, a type IV response against an amalgam, to an antibody-mediated disease with a generalised distribution. D repeats a test that is already diagnostic, and samples the ulcer centre, where the epithelium carrying the pattern has been lost. **Common trap:** Managing the mouth and leaving unreferred the ocular disease that carries the worse outcome. Source: Neville, Oral and Maxillofacial Pathology ## Question 2 A 52-year-old woman has a white striated lesion with a central erythematous area on the right buccal mucosa. It lies directly against a large amalgam restoration in the lower right first molar, and the left buccal mucosa is entirely normal. What does this distribution suggest? - A. Reticular oral lichen planus, characteristically bilateral on the buccal mucosa - B. Type I hypersensitivity to mercury released continuously from the restoration - C. Frictional keratosis produced by the restoration margin abrading the mucosa - D. A lichenoid contact reaction to the amalgam, a type IV material response **Answer D:** A lichenoid contact reaction to the amalgam, a type IV material response A lichenoid contact reaction looks like lichen planus but is typically unilateral and sits directly against an amalgam restoration; it is a type IV, T-cell mediated response to the material, and it can resolve when the restoration is replaced. The distribution is the discriminator here. A names the disease it mimics, but the reticular form of oral lichen planus is characteristically bilateral on the buccal mucosa, and this patient's left side is normal. B assigns the wrong mechanism and the wrong clock, since type I reactions are IgE-mediated and produce urticaria, angioedema or bronchospasm within minutes. C would give a uniform keratotic response to friction rather than fine striae with a central erythematous area, and explains neither the pattern nor the material contact. **Common trap:** Calling any striated white lesion lichen planus without checking whether the other side matches. Source: Neville, Oral and Maxillofacial Pathology ## Question 3 A 60-year-old man has had bilateral reticular lichen planus documented for eight years and has been reviewed annually without symptoms. At today's visit one area on the left lateral tongue is firm to palpation and has been ulcerated for six weeks. He asks what happens next. - A. Biopsy the indurated ulcerated area, since this lesion has changed character - B. Reassure him, since the reticular form is asymptomatic and needs no treatment - C. Quote him the published transformation rate so he can weigh the risk himself - D. Excise every striated area in the mouth to remove potentially malignant tissue **Answer A:** Biopsy the indurated ulcerated area, since this lesion has changed character Oral lichen planus is a T-cell mediated attack on basal keratinocytes. The reticular form is often asymptomatic and needs no treatment, but the disease warrants long-term clinical monitoring, and induration with six weeks of ulceration in a previously stable patient is exactly the change that triggers a biopsy. B applies a correct statement about untreated reticular disease to a lesion that has stopped behaving like reticular disease. C rests on a genuinely unresolved disagreement: authorities differ over whether and how often oral lichen planus transforms, and some argue transforming cases were lichenoid dysplasia misdiagnosed at the outset, so no percentage should be quoted as settled fact. D removes asymptomatic striae while leaving the one changed area no better assessed. **Common trap:** Answering a change-in-a-known-lesion question with a transformation percentage instead of a biopsy. Source: Neville, Oral and Maxillofacial Pathology ## Question 4 A 56-year-old woman with rheumatoid arthritis reports two years of dry eyes and dry mouth and difficulty swallowing dry food. Examination shows dry mucosa and six new cervical carious lesions. Anti-SSA/Ro is positive. Which further investigation carries weight in the classification criteria? - A. A parotid sialogram to demonstrate ductal narrowing and glandular destruction - B. A labial minor salivary gland biopsy assessed for focal lymphocytic sialadenitis - C. Serum immunoglobulin electrophoresis to detect a monoclonal band in the gamma region - D. A panoramic radiograph to exclude sialoliths obstructing both submandibular ducts **Answer B:** A labial minor salivary gland biopsy assessed for focal lymphocytic sialadenitis Sjögren disease is lymphocytic destruction of exocrine glands producing dry eyes and dry mouth, often alongside a systemic autoimmune disease such as rheumatoid arthritis or lupus. In the 2016 ACR/EULAR classification criteria, anti-SSA/Ro positivity and a labial salivary gland biopsy showing focal lymphocytic sialadenitis with a focus score of at least 1 focus per 4 mm² each score 3 of the 4 points needed, so with her antibody already positive the labial biopsy is the investigation that carries weight. A and D image the duct system, addressing obstruction rather than the lymphocytic infiltrate the criteria weight. C looks for a plasma cell disorder no criterion in this set names. Her rampant cervical caries is the predictable consequence of salivary loss. **Common trap:** Reaching for an imaging study when the weighted criterion is a tissue diagnosis. Source: [2016 ACR/EULAR classification criteria for primary Sjögren's syndrome](https://pubmed.ncbi.nlm.nih.gov/27785888/) ## Question 5 A 70-year-old man taking three anticholinergic medicines has developed root caries on eight teeth in eighteen months and a sore red palate beneath his denture. He never had decay before. He asks how saliva had been protecting him. Which statement is correct? - A. Secretory IgA lyses cariogenic bacteria, while lactoferrin buffers the acid produced - B. Salivary bicarbonate blocks adherence, while secretory IgA remineralises the enamel - C. Secretory IgA blocks adherence, while lysozyme and histatins do the killing - D. Salivary complement assembles a membrane attack complex on the tooth surface **Answer C:** Secretory IgA blocks adherence, while lysozyme and histatins do the killing Saliva defends mechanically by washing, diluting and clearing, chemically by buffering acid with bicarbonate and phosphate and supplying the calcium and phosphate that let enamel remineralise, and immunologically through secretory IgA — which does not kill bacteria but blocks their adherence, a mechanism called immune exclusion. Lysozyme cleaves bacterial cell wall peptidoglycan, lactoferrin sequesters iron, the peroxidase system generates antibacterial products, and histatins are antifungal peptides active against Candida. A gives secretory IgA a lytic role it does not have and hands lactoferrin the buffering job. B swaps the two functions outright. D moves a plasma cascade onto the tooth surface. Losing saliva removes all of these at once, which is why his caries and denture soreness appeared together. **Common trap:** Assuming the antibody in saliva is what kills the bacteria. Source: [NIDCR — Dry Mouth](https://www.nidcr.nih.gov/health-info/dry-mouth) ## Question 6 A 34-year-old woman has just finished eight weeks of prednisone 40 mg daily for an autoimmune flare. While her medical history is updated before elective treatment, she asks when she can have the varicella vaccine and the tetanus booster her physician mentioned. What applies? - A. Both vaccines should be avoided permanently while she remains on any corticosteroid dose - B. Both vaccines can be given now, because 40 mg daily sits below the high-dose threshold - C. Both vaccines should be deferred until at least three months after the prednisone stops - D. The live varicella vaccine is deferred at least one month after the prednisone stops **Answer D:** The live varicella vaccine is deferred at least one month after the prednisone stops For vaccination purposes, CDC treats 20 mg or more of prednisone per day (or 2 mg/kg per day or more) given for 14 or more consecutive days as high-dose immunosuppressive therapy, and 40 mg daily for eight weeks clears that threshold comfortably. Live attenuated vaccines such as varicella contain organisms that replicate and are generally contraindicated in severe immunosuppression, so live-virus vaccination is deferred at least 1 month after that therapy stops. B misreads the threshold in the wrong direction. A over-restricts: short courses, low-to-moderate doses, alternate-day short-acting regimens, physiologic replacement and topical, inhaled or intra-articular steroids are not contraindications. C invents a longer interval and sweeps in a toxoid, when all non-live vaccines are safe in altered immunocompetence. **Common trap:** Applying the live-vaccine restriction to a non-live product, or inventing a deferral interval. Source: [CDC General Best Practice Guidelines for Immunization — Altered Immunocompetence](https://www.cdc.gov/vaccines/hcp/imz-best-practices/altered-immunocompetence.html) ## Question 7 A 14-year-old girl has 6 to 8 mm probing depths with radiographic bone loss around first molars and incisors. Plaque and calculus are minimal and her brushing is good. Her mother mentions recurrent mouth ulcers and skin boils since infancy. What should this prompt? - A. Evaluation of neutrophil number and function alongside her periodontal treatment plan - B. A course of chlorhexidine and re-evaluation of her brushing technique in three months - C. Testing for latent tuberculosis before any subgingival instrumentation is undertaken here - D. Reassurance, because bone loss around first molars is normal during the growth spurt **Answer A:** Evaluation of neutrophil number and function alongside her periodontal treatment plan A phagocyte defect gives abscesses and, in the mouth, periodontal destruction, and that group announces itself as severe, early periodontal breakdown: leukocyte adhesion deficiency, Papillon–Lefèvre syndrome, Chédiak–Higashi syndrome and cyclic neutropenia all present this way. Aggressive breakdown in a child or adolescent, especially with minimal plaque and a history of recurrent ulcers and skin infections, is a reason to think about the neutrophil rather than only about plaque, and the referral is medical as well as periodontal. B repeats plaque control in a patient whose plaque control is already good. C borrows a screening step that belongs to tumour necrosis factor inhibitor therapy. D describes a physiological event that does not exist, since bone loss is never a normal feature of growth. **Common trap:** Explaining destruction by the visible plaque when the destruction is far out of proportion to it. Source: Newman and Carranza's Clinical Periodontology and Implantology ## Question 8 A 49-year-old woman with generalised periodontitis and 5 to 7 mm pockets asks what is actually removing the bone around her teeth, since she has been told that her plaque control is only moderately poor. Which mechanism explains her bone loss? - A. Bacterial collagenase dissolving alveolar bone directly at the base of each pocket - B. Inflammation raising RANKL relative to osteoprotegerin, so osteoclasts mature and resorb - C. Osteoprotegerin binding RANK on osteoclast precursors and driving them to resorb bone - D. Antibody against the periodontal organisms cross-reacting with the bone matrix proteins **Answer B:** Inflammation raising RANKL relative to osteoprotegerin, so osteoclasts mature and resorb Bacteria start periodontitis, but the host response causes most of the tissue and bone destruction. Macrophages and fibroblasts release IL-1β, TNF-α, IL-6 and prostaglandin E2, which drive matrix metalloproteinase production and connective tissue breakdown, and bone loss runs through one axis: RANKL, expressed by activated immune cells and osteoblast-lineage cells, binds RANK on osteoclast precursors and drives them to mature and resorb bone, while osteoprotegerin is a decoy receptor that mops up RANKL and stops that signal. Health is a low RANKL-to-OPG ratio; inflammation raises it. C reverses the two proteins, giving the decoy the activating role. A skips the host entirely. D invents a cross-reactive antibody, when antibody against periodontal organisms does not reliably resolve the disease. **Common trap:** Reversing RANKL and osteoprotegerin, or crediting the bacteria with the resorption directly. Source: Newman and Carranza's Clinical Periodontology and Implantology ## Question 9 A 57-year-old man whose father died of a myocardial infarction has read that gum disease causes heart attacks. He has moderate periodontitis and asks whether completing his periodontal treatment will prevent one. How should the dentist answer him? - A. Yes, because completing periodontal treatment has been shown to reduce cardiovascular events - B. No, because the two conditions share no biological or inflammatory connection of any kind - C. The link is an association; treatment improves oral health, not proven cardiac outcomes - D. Yes, provided he also takes a course of systemic antibiotics alongside the treatment **Answer C:** The link is an association; treatment improves oral health, not proven cardiac outcomes The honest statement is that the link between periodontitis and systemic conditions such as cardiovascular disease is an association. Periodontal treatment improves oral health and some intermediate biological markers, but a causal reduction in cardiovascular events has not been established, so the wording is "associated with," not "causes." That framing leaves him a real reason to complete treatment without selling him an outcome nobody can promise. A asserts the causal claim the evidence does not support. B overcorrects into denying an association that is real and biologically plausible, given the inflammatory mediators the host response generates. D adds systemic antibiotics to a treatment whose value here is mechanical and inflammatory control, and no source makes antibiotics the route to a cardiac benefit. **Common trap:** Answering an oral–systemic link question with either a promised cure or a flat denial. Source: Newman and Carranza's Clinical Periodontology and Implantology ## Question 10 A 38-year-old man brings a letter from his physician reporting a CD4 count of 150 cells/µL, a CD4 percentage of 18%, and no opportunistic illness to date. He needs three restorations. How is his HIV infection classified under the CDC surveillance case definition? - A. Not stage 3, because the CD4 percentage of 18% remains above 14% - B. Not stage 3, because no opportunistic illness has been documented - C. Stage 3 only once an opportunistic illness is documented as well - D. Stage 3, because the CD4 count is already below 200 cells/µL **Answer D:** Stage 3, because the CD4 count is already below 200 cells/µL Under the CDC surveillance case definition, HIV infection is classified as stage 3 when the CD4 count falls below 200 cells/µL, or the CD4 percentage of total lymphocytes falls below 14%, or a stage-3-defining opportunistic illness is documented. The three are alternatives, not a checklist, so a count of 150 cells/µL settles the classification on its own. A and B each read one unmet criterion as a veto over one that is met. C inverts the relationship, since a documented opportunistic illness classifies a patient as stage 3 regardless of a higher CD4 count, which makes it sufficient rather than required. What the classification changes is the differential you carry and the questions you put to his physician, not your infection control. **Common trap:** Treating the three stage-3 criteria as conditions that must all be satisfied together. Source: [CDC Revised Surveillance Case Definition for HIV Infection — United States, 2014](https://www.cdc.gov/mmwr/preview/mmwrhtml/rr6303a1.htm) ## Next step [Take the free INBDE practice test](https://dentovio.com/inbde/free-practice-test) Official reference: [JCNDE — Integrated National Board Dental Examination](https://jcnde.ada.org/inbde). Original exam-style questions written for study, never recalled exam content. Independent educational preparation, not clinical advice, and not affiliated with or endorsed by the Joint Commission on National Dental Examinations.