Deep pockets and a rising HbA1c

Correct answer: A. Scaling and root planing with oral hygiene instruction and risk factor control

• A. Correct. Non-surgical therapy is always step one. Scaling and root planing with oral hygiene instruction, smoking cessation support and liaison with her physician about glycaemic control comes first, and the tissues are then re-evaluated at four to six weeks to see what residual disease actually needs surgery.
• B. Surgery before non-surgical therapy operates on inflamed, infected tissue with unknown response potential. Re-evaluation after initial therapy typically shrinks the surgical need considerably.
• C. Antibiotics cannot penetrate a mature biofilm. Without mechanical disruption they achieve very little, and adjunctive systemic antibiotics are reserved for specific situations rather than used routinely.
• D. Pockets of 5 to 6 mm without mobility are treatable. Extraction at this stage is indefensible.

Correct answer: A. Interleukin-1 beta

• A. Correct. IL-1 beta is a principal pro-inflammatory mediator in periodontitis. It stimulates matrix metalloproteinase production, drives RANKL expression and therefore osteoclastic bone resorption, and amplifies the local inflammatory response. It acts alongside TNF-alpha, IL-6 and prostaglandin E2.
• B. IL-12 drives Th1 differentiation and matters in antimicrobial defence, but it is not the central mediator of periodontal tissue breakdown.
• C. IL-10 is anti-inflammatory and regulatory. It suppresses pro-inflammatory cytokine production and is protective rather than destructive.
• D. IL-4 is a Th2 cytokine that promotes B-cell responses and downregulates macrophage activation.

Correct answer: B. Enterococcus faecalis

• A. Fusobacterium nucleatum is a key bridging organism in plaque maturation, linking early gram-positive colonisers to late gram-negative pathogens.
• B. Correct, and this is the exception. Enterococcus faecalis is a gut commensal whose oral significance is in persistent endodontic infection and failed root canal treatment, not in the developing gingival biofilm.
• C. Prevotella intermedia appears in gingivitis and increases markedly in pregnancy and puberty gingivitis, where steroid hormones substitute for its vitamin K requirement.
• D. Actinomyces species are among the earliest colonisers and dominate in the shift from health to gingivitis.

Note: Tannerella forsythia, which the recall listed, is a red complex organism of established periodontitis rather than early gingivitis, so it would also be defensible as an exception. The unambiguous outlier is Enterococcus faecalis.

Correct answer: C. Predominantly anaerobic gram-negative rods

• A. Facultative gram-positive rods such as Actinomyces belong to early colonisation, before the anaerobic shift occurs.
• B. Aerobic gram-positive cocci such as streptococci dominate healthy supragingival plaque, which is the opposite end of the ecological shift.
• C. Correct. The deepened pocket is an anaerobic, protein-rich niche that selects for gram-negative rods. The red complex of Porphyromonas gingivalis, Tannerella forsythia and Treponema denticola, along with Prevotella and Fusobacterium, are all gram-negative and largely rod or spirochaete in form.
• D. Veillonella is an anaerobic gram-negative coccus present in plaque, but cocci are not the dominant morphotype of the periodontitis flora.

Correct answer: D. Anaerobic gram-negative organisms similar to those in periodontitis

• A. Candida may be recovered from some peri-implantitis lesions but is not the predominant organism.
• B. Lactobacilli are acidogenic organisms of the caries process and are not central to peri-implant disease.
• C. Gram-positive aerobic cocci characterise healthy peri-implant tissue, not disease.
• D. Correct. The peri-implant microbiota closely mirrors that of periodontitis, dominated by anaerobic gram-negative species. This is why a patient with untreated periodontitis carries a substantially raised risk of peri-implantitis; the pathogens translocate from teeth to implant surfaces.

Correct answer: D. Smoking

• A. Age alone is not a risk factor for implant failure; healthy older patients osseointegrate well.
• B. Surface texture influences the rate of integration, but it does not outweigh smoking and poorly controlled diabetes as a cause of failure.
• C. Oestrogen therapy is not an established cause of implant failure. Antiresorptive agents such as bisphosphonates are the drug class of concern for the jaws.
• D. Correct. Smoking is the single strongest modifiable risk factor for implant failure and peri-implantitis. Nicotine causes vasoconstriction, carbon monoxide impairs oxygen delivery, and neutrophil function and fibroblast activity are both depressed, so wound healing and osseointegration suffer. Her uncontrolled diabetes compounds it.

Correct answer: D. Hyperglycaemia amplifies the inflammatory response and impairs healing, and periodontal inflammation in turn worsens glycaemic control

• A. The association is well established, biologically explained and bidirectional.
• B. Microvascular change contributes, but reducing the whole relationship to vessel thinning misses the dominant inflammatory and immune mechanisms.
• C. Raised glucose in gingival crevicular fluid alters the local environment, but it is a minor part of a much larger picture.
• D. Correct. The relationship is bidirectional. Advanced glycation end products accumulate and bind RAGE receptors, driving cytokine release; neutrophil chemotaxis and phagocytosis are impaired; collagen turnover is disturbed. In the other direction, the systemic inflammatory burden of periodontitis increases insulin resistance, and treating periodontitis produces a measurable fall in HbA1c.