Journal of periodontal research · 2023
Hyperlipidemia impairs bone regeneration of closed bone defects and tooth extraction wounds in mice.
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Liu Wenchuan, Yang Jing, Li Shanshan, Ye Xin, Yang Pishan, Zhang Jin
Аннотация
OBJECTIVES: To evaluate the effect of hyperlipidemia on the healing of bone defects.
MATERIALS AND METHODS: Apolipoprotein E (ApoE)-deficient mice and wild-type (WT) C57BL/6J mice were fed with an atherogenic high-fat diet (HFD) or a standard chow diet (as control) for 6 weeks. Blood samples were collected to evaluate serum lipid levels. Closed bone defects and open tooth extraction wounds were then created in the mandibles of these animals. One or two weeks after surgery, animals were euthanized. Micro-CT analysis and histomorphometric analysis were conducted to evaluate the healing of bone defects and the alveolar ridge resorption.
RESULTS: Bone regeneration of closed bone defects was considerably delayed in the hyperlipidemic Apoe-/- mice and WT mice. No obvious difference was detected in the new bone formation of the tooth extraction wounds. The HFD-fed mice showed more prominent reduction in the lingual alveolar ridge height of the tooth extraction wounds when compared with the control group.
CONCLUSIONS: Hyperlipidemia results in delayed bone regeneration in large closed bone defects. Although tooth extraction wounds are small and normally regenerated in a hyperlipidemic microenvironment, the prominent reduction in the alveolar ridge height is also a challenge for future restoration of the dentition.
MATERIALS AND METHODS: Apolipoprotein E (ApoE)-deficient mice and wild-type (WT) C57BL/6J mice were fed with an atherogenic high-fat diet (HFD) or a standard chow diet (as control) for 6 weeks. Blood samples were collected to evaluate serum lipid levels. Closed bone defects and open tooth extraction wounds were then created in the mandibles of these animals. One or two weeks after surgery, animals were euthanized. Micro-CT analysis and histomorphometric analysis were conducted to evaluate the healing of bone defects and the alveolar ridge resorption.
RESULTS: Bone regeneration of closed bone defects was considerably delayed in the hyperlipidemic Apoe-/- mice and WT mice. No obvious difference was detected in the new bone formation of the tooth extraction wounds. The HFD-fed mice showed more prominent reduction in the lingual alveolar ridge height of the tooth extraction wounds when compared with the control group.
CONCLUSIONS: Hyperlipidemia results in delayed bone regeneration in large closed bone defects. Although tooth extraction wounds are small and normally regenerated in a hyperlipidemic microenvironment, the prominent reduction in the alveolar ridge height is also a challenge for future restoration of the dentition.