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Hyperglycemia induced and intrinsic alterations in type 2 diabetes-derived osteoclast function
D L Catalfamo1, T M Britten, D L Storch
1Department of Periodontology, College of Dentistry, University of Florida, Gainesville, FL, USA; Department of Oral Biology, College of Dentistry, University of Florida, Gainesville, FL, USA.
Oral Diseases
|October 2, 2013
Summary
Type-2 diabetes complicates periodontal disease by affecting osteoclasts. This study reveals hyperglycemia impairs osteoclast function, increasing bone loss, while LPS-induced inhibition is lost in diabetic models.
Area of Science:
- Oral biology
- Endocrinology
- Immunology
Background:
- Periodontal disease and type-2 diabetes share a comorbidity of alveolar bone loss.
- The precise role of osteoclasts in this process remains unclear.
Purpose of the Study:
- To investigate osteoclast differentiation and function in type-2 diabetes.
- To explore the impact of hyperglycemia and lipopolysaccharide (LPS) on osteoclast activity.
Main Methods:
- Osteoclasts were derived from bone marrow of db/db mice (type-2 diabetes model) and peripheral blood of humans with type-2 diabetes.
- Evaluated osteoclast differentiation, bone resorption capacity, and expression of soluble mediators.
- Assessed the response to lipopolysaccharide (LPS)-induced deactivation.
Main Results:
- Hyperglycemic db/db mice showed increased osteoclast numbers and size, but similar individual bone resorption compared to controls.
- Osteoclasts from type-2 diabetes individuals exhibited normal differentiation and bone resorption capacity.
- Both murine and human diabetic osteoclasts demonstrated impaired LPS-induced deactivation and elevated pro-osteoclastogenic mediators.
Conclusions:
- Hyperglycemia contributes to abnormal osteoclast differentiation, enhancing bone resorption capacity.
- Osteoclasts from type-2 diabetes models and patients are resistant to LPS inhibition, further increasing bone resorption.
- These findings elucidate mechanisms contributing to alveolar bone loss in type-2 diabetes patients with periodontal disease.
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