Implants · single question
How does poorly-controlled diabetes mellitus contribute to peri-implantitis and impaired osseointegration?
Show answer and explanation
Correct answer: D. It inhibits osteoblast activity and reduces bone formation
- A. Incorrect. The opposite occurs — osteoclastic resorption is INCREASED via the AGE/RAGE pathway and elevated RANKL, accelerating peri-implant bone loss.
- B. Incorrect. Diabetes DECREASES collagen synthesis and increases collagenase activity, which is exactly why wound healing and soft-tissue attachment are compromised.
- C. Incorrect. Diabetes affects both compartments: microvascular disease and neutrophil dysfunction impair the soft tissue seal, while AGE accumulation impairs the bone response.
- D. Correct. Chronic hyperglycaemia and the accumulation of ADVANCED GLYCATION END-PRODUCTS (AGEs) suppress OSTEOBLAST differentiation and function, reducing osteoid production and impairing bone-to-implant contact. At the same time RANKL-driven osteoclastic activity is up-regulated, so formation falls while resorption rises — a net negative bone balance around the implant.