Periodontal and systemic relationships practice questions for the periodontics Qualifying Exam
This domain covers both directions of the link: systemic conditions that change the periodontium, and what periodontitis and its treatment do to systemic health. Precision about the strength of evidence matters.
2027 ABP blueprint domain: Periodontal and Systemic Relationships
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37questions on this domain in the bank
What the blueprint covers
The 2027 Qualifying Exam blueprint lists these objectives for this domain:
Systemic diseases and conditions that affect the periodontium
The effect of periodontal diseases on systemic health
High-yield areas
Diabetes both ways, and HbA1c change after periodontal therapy
Cardiovascular disease: association, mechanisms and what trials have and have not shown
Pregnancy outcomes and periodontal treatment during pregnancy
Genetic and immune disorders that cause early, severe periodontitis
Association versus causation in the consensus reports
How to study it
For each link, learn what kind of evidence exists, how strong it is and what the consensus papers concluded. Questions often turn on the difference between an association and a proven effect of treatment.
Free practice questions: Periodontal and systemic relationships
4 questions from the bank, with the full rationale and source. Pick your answer, then open the rationale.
Question 1 of 4 · moderatePeriodontal and Systemic Relationships
A 50-year-old man who smokes 25 cigarettes per day has generalized probing depths of 5 to 7 mm with subgingival calculus, but bleeding on probing is recorded at only 12% of sites. A resident suggests that the low bleeding score shows that his disease is largely inactive. Which interpretation is most appropriate?
Low bleeding reliably indicates stability, so supportive care alone is sufficient
Smoking suppresses bleeding on probing in a dose-dependent way, masking inflammation
Low bleeding indicates pseudopockets from gingival overgrowth rather than attachment loss
Smoking normally increases bleeding, so the low score points to a probing technique error
Low bleeding in heavy smokers reflects reduced plaque accumulation on the root surfaces
Show answer and rationale
Answer: B. Smoking suppresses bleeding on probing in a dose-dependent way, masking inflammation
A (incorrect): A low bleeding score is usually reassuring, but smoking suppresses the bleeding response, so in this patient it no longer reflects disease activity reliably. Treating him as stable would leave deep, calculus-bearing pockets untreated.
B (correct): In a large NHANES III analysis, smoking had a strong, chronic and dose-dependent suppressive effect on gingival bleeding, strongest in those smoking more than 10 cigarettes per day and smallest in former smokers. Deep pockets with calculus that bled readily in never-smokers bled much less in heavier smokers, so a low score here underestimates disease activity.
C (incorrect): The stem describes deep probing depths in a periodontitis context with calculus, not drug-induced or inflammatory overgrowth. Pseudopockets do not explain the low bleeding, and attachment levels must still be measured.
D (incorrect): The direction is reversed: smoking reduces, not increases, bleeding on probing. Blaming technique would lead the clinician to distrust valid measurements.
E (incorrect): Bleeding suppression in smokers was seen even at healthy sites without calculus or deep pockets (odds ratio 0.56 in heavier smokers), so it reflects an effect of smoking on the host response rather than cleaner root surfaces. In this patient, calculus is present anyway.
Source: Dietrich T, Bernimoulin JP, Glynn RJ. The effect of cigarette smoking on gingival bleeding. J Periodontol. 2004;75(1):16-22. doi:10.1902/jop.2004.75.1.16. Abstract, Results and Conclusion. https://pubmed.ncbi.nlm.nih.gov/15025212/
Question 2 of 4 · hardPeriodontal and Systemic Relationships
Histologic examination of a primary incisor that exfoliated prematurely in a child with confirmed hypophosphatasia shows a root surface lacking normal acellular cementum, with poorly attached periodontal ligament fibers. Which mechanism best explains the defect?
Excess alkaline phosphatase activity depletes the local phosphate needed for mineralization
Inorganic pyrophosphate, a mineralization inhibitor, accumulates when TNAP is deficient
Neutrophil serine proteases remain inactive, allowing bacteria to destroy the cementum
Periodontal ligament collagen is degraded by unregulated activation of complement C1
Odontoclasts resorb the cementum early to make way for the erupting successor tooth
Show answer and rationale
Answer: B. Inorganic pyrophosphate, a mineralization inhibitor, accumulates when TNAP is deficient
A (incorrect): Hypophosphatasia results from loss-of-function variants that reduce, not increase, alkaline phosphatase activity. The direction of the enzyme defect is reversed in this option.
B (correct): Tissue-nonspecific alkaline phosphatase (TNAP) normally lowers local levels of inorganic pyrophosphate, a potent inhibitor of hydroxyapatite formation. When TNAP is deficient, pyrophosphate accumulates and acellular cementum fails to form properly, so the periodontal ligament cannot anchor the tooth, which explains early exfoliation of teeth with intact roots and little inflammation.
C (incorrect): Inactive neutrophil serine proteases describe cathepsin C deficiency in Papillon-Lefevre syndrome, where tooth loss is driven by severe inflammatory periodontitis. Cementum aplasia is not the mechanism.
D (incorrect): Abnormal intracellular autoactivation of mutant complement C1r is the mechanism proposed for periodontal Ehlers-Danlos syndrome. It does not explain a primary defect of cementum mineralization.
E (incorrect): Physiologic root resorption precedes normal exfoliation, but these teeth were lost with complete roots and no resorption. The defect lies in attachment, not in accelerated resorption.
Source: Lira dos Santos EJ, Mohamed FF, Kramer K, Foster BL. Dental manifestations of hypophosphatasia: translational and clinical advances. JBMR Plus. 2025;9(2):ziae180. doi:10.1093/jbmrpl/ziae180. Introduction; section on the role of periodontists. https://pmc.ncbi.nlm.nih.gov/articles/PMC11770227/
Question 3 of 4 · easyPeriodontal and Systemic Relationships
A 29-year-old woman at 26 weeks of gestation reports gingival bleeding and swelling that began early in the second trimester. Her plaque scores are similar to those recorded at a recall visit 1 year ago, probing depths are 2 to 4 mm, and there is no clinical attachment loss. Which explanation is most consistent with the evidence?
Pregnancy increases gingival inflammation without a matching rise in plaque levels
Pregnancy gingivitis is driven mainly by a large increase in the mass of dental plaque
Gingival inflammation in pregnancy peaks in the first trimester and then resolves
The findings indicate periodontitis triggered by the hormonal changes of pregnancy
The bleeding most likely reflects gestational thrombocytopenia rather than inflammation
Show answer and rationale
Answer: A. Pregnancy increases gingival inflammation without a matching rise in plaque levels
A (correct): A systematic review found a significant rise in gingival index through pregnancy, higher in the second and third trimesters than in the first and higher than post partum or in nonpregnant women, with only small changes in plaque. Sex steroid hormones modify the gingival response to a similar plaque burden, which fits her presentation.
B (incorrect): Plaque remains the initiating factor, but the evidence shows only small changes in plaque levels during pregnancy. The exaggerated inflammation reflects a hormonally modified host response rather than a large plaque increase.
C (incorrect): Gingival inflammation was lower in the first trimester than in the second or third. The timeline is reversed, and inflammation tends to decline after delivery rather than during pregnancy.
D (incorrect): She has no clinical attachment loss, so the diagnosis is plaque-induced gingivitis modified by sex steroid hormones, not periodontitis. Labeling it periodontitis would misclassify a reversible condition.
E (incorrect): A bleeding disorder would not explain the swelling and the localized inflammatory pattern on a normal plaque burden. The well-documented hormonal effect on the gingiva is the far more likely cause.
Source: Figuero E, Carrillo-de-Albornoz A, Martin C, Tobias A, Herrera D. Effect of pregnancy on gingival inflammation in systemically healthy women: a systematic review. J Clin Periodontol. 2013;40(5):457-473. doi:10.1111/jcpe.12053. Abstract, Results and Conclusion. https://pubmed.ncbi.nlm.nih.gov/23557432/
Question 4 of 4 · easyPeriodontal and Systemic Relationships
A 4-year-old girl has red, thickened, scaling skin on her palms and soles. Her primary teeth show severe gingival inflammation with deep pockets, and several are mobile in the same order in which they erupted. Her parents are first cousins and are both clinically unaffected. A mutation in which gene is most likely responsible?
ALPL
ITGB2
C1R
ELANE
CTSC
Show answer and rationale
Answer: E. CTSC
A (incorrect): ALPL mutations cause hypophosphatasia, in which primary teeth are lost early with intact roots and little inflammation because cementum is deficient. Palmoplantar hyperkeratosis is not a feature.
B (incorrect): ITGB2 encodes CD18, the common subunit of beta-2 integrins, and its mutation causes leukocyte adhesion deficiency type 1. That condition causes severe early periodontitis and recurrent infections, but not palmoplantar keratoderma.
C (incorrect): C1R mutations cause periodontal Ehlers-Danlos syndrome, an autosomal dominant disorder with absent attached gingiva, easy bruising and pretibial pigmentation. Unaffected parents and palmoplantar keratoderma argue against it.
D (incorrect): ELANE mutations cause cyclic or severe congenital neutropenia, presenting with recurrent fevers, oral ulcers and periodontitis. The skin findings here are not explained by neutropenia.
E (correct): Papillon-Lefevre syndrome is an autosomal recessive disorder caused by mutations in CTSC, which encodes the lysosomal protease cathepsin C. Palmoplantar hyperkeratosis with periodontitis destroying the primary teeth in eruption sequence, beginning between ages 1 and 4, is the classic picture, and heterozygous carrier parents (here, consanguineous) are clinically unaffected.
Source: Adamski Z, Burchardt D, Pawlaczyk-Kamienska T, Borysewicz-Lewicka M, Wyganowska-Swiatkowska M. Diagnosis of Papillon-Lefevre syndrome: review of the literature and a case report. Postepy Dermatol Alergol. 2020;37(5):671-676. doi:10.5114/ada.2020.100480. Abstract; Introduction; Pathogenesis section. https://pmc.ncbi.nlm.nih.gov/articles/PMC7675075/
For exam preparation only, not clinical advice.
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