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Diabetes mellitus is a group of metabolic disorder characterize by and absolute or partial insulin deficiency. Diabetic hyperglycemia is produce by the effect of homeostasis between proteolytic enzymes, their inhibitors and the antioxidants defense that protect and repair vital tissues and molecular components. Bone consist of both component and trabecular bone tissue. Organic matrix and albumin form part of noncollagenous of bone .Initiation of mineralization and collagen fibrils form the phase of mineral matrix. Calcium flux into and out of bone depend of osteoclastic and osteoblastic activity. The remodeling is initiated by resorption and new bone formation at the resorption site. Diabetic complication is a critical factor for bone pathology and could start early inflammatory stage even before hyperglycemia. Diabetic produces bone loss from reduce osteoblast activity. Partly insulin deficiency   produce defective bone remodeling indirect by oxidative stress. The current treatment for defective bone in diabetes state include biophosphonate and cinaciguat. Biphosphonate inhibit bone resorption, but may worsen bone quality. A novel type of activation of sGMP is cinaciguat an NO independent activator of oxidative GC, increase c GMP synthesis on diabetic and restore proliferation and survival of osteoblasts. Chronic hyperglycemia interferes with the oseointegration of implants in diabetics. Both diabetic and aging plays a role in abnormal differentiation of osteroblasts. In diabetic patients may improve the oral health to have a positive impact if optimal glycemic control is emphasized. However with cinaciguat present as a novel paradigm enhancing bone formation under hyperglycemia and protect bone implants.

Diabetic oxidative stress and bone loss complications