Generalised deep pockets in type 2 diabetes

Correct answer: D. Type 2 diabetes mellitus

• A. Hypercholesterolaemia and statin therapy have no meaningful negative periodontal effect. If anything, statins have been studied for a modest anti-inflammatory benefit.
• B. Hypertension does not itself affect periodontal healing. Some antihypertensives matter for other reasons — calcium channel blockers cause gingival enlargement — but valsartan, an angiotensin receptor blocker, does not.
• C. Fatty liver contributes to systemic inflammation and is part of the metabolic syndrome, but it has no direct established effect on periodontal outcome.
• D. CORRECT. Diabetes is the systemic condition with the strongest, best-documented effect on periodontal prognosis. Hyperglycaemia impairs NEUTROPHIL chemotaxis and phagocytosis, drives accumulation of advanced glycation end products that stiffen collagen and amplify inflammatory cytokine release, and causes microvascular disease that reduces tissue perfusion and healing. Glycaemic control, more than any other single variable here, determines the response to periodontal therapy.

Note: The relationship is bidirectional: periodontal treatment produces a measurable HbA1c reduction of roughly 0.3 to 0.4 percent, comparable to adding a second oral hypoglycaemic. That is worth saying to the patient.

Correct answer: A. The removable partial denture

• A. CORRECT as the exception. A removable partial denture does not reduce salivary output. It may make a dry mouth FEEL worse, because retention depends on a salivary film and a dry denture becomes uncomfortable and unstable, but the prosthesis is not a cause of hyposalivation — it is a casualty of it.
• B. Antihypertensives are among the commonest drug causes of xerostomia. Diuretics reduce fluid volume, and several classes have anticholinergic or sympatholytic effects on salivary flow.
• C. Uncontrolled diabetes causes xerostomia by two mechanisms: osmotic diuresis from glycosuria produces dehydration, and diabetic autonomic neuropathy impairs salivary gland stimulation.
• D. Mouth breathing dries the mucosa directly, and reduced fluid intake compounds the dehydration.

Note: When you meet an 'all cause xerostomia EXCEPT' item, run the four categories: drugs, systemic disease (diabetes, Sjögren, HIV), radiation to the head and neck, and dehydration. Whatever falls outside those four is your answer.

Correct answer: D. It increases glucagon production

• A. Suppressing hepatic gluconeogenesis is metformin's PRINCIPAL action, mediated through AMP-activated protein kinase. This is why it lowers fasting glucose so effectively.
• B. Reducing intestinal glucose absorption is a recognised, if secondary, contributor and helps explain the gastrointestinal side effects.
• C. Increasing peripheral insulin sensitivity, chiefly in skeletal muscle, is a genuine metformin mechanism — it improves glucose uptake without stimulating insulin secretion.
• D. CORRECT as the exception. Metformin DECREASES glucagon signalling rather than increasing it. Glucagon is the counter-regulatory hormone released in starvation to RAISE blood glucose by driving hepatic glycogenolysis and gluconeogenesis. A drug that increased glucagon would raise blood sugar, which is the opposite of what metformin does.

Note: Because metformin does not stimulate insulin release, it does not cause hypoglycaemia on its own — which is why a metformin-only patient does not need appointment timing adjusted around meals the way a sulphonylurea or insulin patient does. The serious rare adverse effect is lactic acidosis in renal impairment.