Cornelius von Wilmowsky, Karl Andreas Schlegel, Christoph Baran, Emeka Nkenke, Friedrich Wilhelm Neukam, Tobias Moest
The study aims to establish a peri-implant dehiscence-type bone defect in a diabetic animal model of human bone repair and to quantify the influence of diabetes on peri-implant bone regeneration.
Material and methods
Experimental diabetes was induced in three domestic pigs by streptozotocin. Three animals served as healthy controls. After 12 months four standardized peri-implant dehiscence bone defects were surgically created in the ramus mandibulae. The animals were sacrificed after 90 days. Samples were histologically analyzed to quantify new bone height (NBH), bone-to-implant-contact (BIC), area of newly formed bone (NFB), bone-density (BD), and bone mineralization (BM) in the prepared defect (- D) and in a local control region (-L).
After 90 days, diabetic animals revealed a significantly lower BIC (p=0.037) and BD (p=0.041) in the defect area (-D). NBH and BM-D differences within the groups were not significant (p>0.05). Significant more NFB was measured in the healthy control group (p=0.046). In the region of local bone BIC-L was significant less in the diabetic group (p=0.028). In the local control region BD-L and BM-L was lower in the diabetic group compared to the healthy control animals (p>0.05).
Histological evidence indicates impaired peri-implant defect regeneration in a diabetic animal model.
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