Evangelia Kalaitzoglou1,2, Iuliana Popescu3, R Clay Bunn3,4, John L Fowlkes3,4, Kathryn M Thrailkill3,4. 1. UK Barnstable Brown Diabetes Center, University of Kentucky College of Medicine, 830 S. Limestone St., Lexington, KY, 40536, USA. evangelia.kalaitzoglou@uky.edu. 2. Department of Pediatrics, University of Kentucky College of Medicine, Lexington, KY, 40536, USA. evangelia.kalaitzoglou@uky.edu. 3. UK Barnstable Brown Diabetes Center, University of Kentucky College of Medicine, 830 S. Limestone St., Lexington, KY, 40536, USA. 4. Department of Pediatrics, University of Kentucky College of Medicine, Lexington, KY, 40536, USA.
Abstract
PURPOSE OF REVIEW: To describe the effects of type 1 diabetes on bone cells. RECENT FINDINGS: Type 1 diabetes (T1D) is associated with low bone mineral density, increased risk of fractures, and poor fracture healing. Its effects on the skeleton were primarily attributed to impaired bone formation, but recent data suggests that bone remodeling and resorption are also compromised. The hyperglycemic and inflammatory environment associated with T1D impacts osteoblasts, osteocytes, and osteoclasts. The mechanisms involved are complex; insulinopenia, pro-inflammatory cytokine production, and alterations in gene expression are a few of the contributing factors leading to poor osteoblast activity and survival and, therefore, poor bone formation. In addition, the observed sclerostin level increase accompanied by decreased osteocyte number and enhanced osteoclast activity in T1D results in uncoupling of bone remodeling. T1D negatively impacts osteoblasts and osteocytes, whereas its effects on osteoclasts are not well characterized, although the limited studies available indicate increased osteoclast activity, favoring bone resorption.
PURPOSE OF REVIEW: To describe the effects of type 1 diabetes on bone cells. RECENT FINDINGS:Type 1 diabetes (T1D) is associated with low bone mineral density, increased risk of fractures, and poor fracture healing. Its effects on the skeleton were primarily attributed to impaired bone formation, but recent data suggests that bone remodeling and resorption are also compromised. The hyperglycemic and inflammatory environment associated with T1D impacts osteoblasts, osteocytes, and osteoclasts. The mechanisms involved are complex; insulinopenia, pro-inflammatory cytokine production, and alterations in gene expression are a few of the contributing factors leading to poor osteoblast activity and survival and, therefore, poor bone formation. In addition, the observed sclerostin level increase accompanied by decreased osteocyte number and enhanced osteoclast activity in T1D results in uncoupling of bone remodeling. T1D negatively impacts osteoblasts and osteocytes, whereas its effects on osteoclasts are not well characterized, although the limited studies available indicate increased osteoclast activity, favoring bone resorption.
Entities:
Keywords:
Bone cells; Osteoblasts; Osteoclasts; Osteocytes; Type 1 diabetes
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