Calcium Metabolism and Oxidative Stress in Bone Fractures: Role of Antioxidants

Abstract

Calcium ion is an essential structural component of the skeleton. There is growing evidence for the importance of nutrition in the maintenance of bones and joints health. Nutritional imbalance combined with endocrine abnormalities may be involved in osteoporosis. For example, essential fatty acids and their metabolites were reported to have beneficial action in osteoporosis. The mechanism by which fatty acids prevent osteoporosis may involve inhibition of pro-inflammatory cytokines, which are known to have a major role in osteoporosis through induction of oxidative stress which had adverse effects on the skeleton. Other risk factors for osteoporosis, such as smoking, hypertension and diabetes mellitus are also associated with increased oxidative stress and free radicals levels. When bone fracture occurs, a remarkable yield of free radicals is generated by the damaged tissues. However, controlled production of free radicals by normally functioning osteoclasts could accelerate destruction of calcified tissues and assist bone remodeling. Enhanced osteoclastic activity observed in bone disorders may have been responsible for increased production of reactive oxygen species [ROS] in the form of superoxide, which is evident by increased levels of serum malondialdehyde [MDA] levels. One of the most damaging effects of ROS is lipid peroxidation, the end product of which is MDA which also served as a measure of osteoclastic activity. Inhibition of the antioxidant enzymes activities, such as superoxide dismutase and glutathione peroxidase, was found to increase superoxide production by the osteoclasts which represented by increased levels of MDA. Therefore, oxidative stress is an important mediator of bone loss since deficiency of antioxidant vitamins has been found to be more common in the elderly osteoporotic patients. It is concluded from this review that increased free radical production overwhelms the natural antioxidants defense mechanisms, subjecting individuals to hyperoxidant stress and thus leading to osteoporosis. In addition, administration of antioxidants might protect bones from osteoporosis and also might help in the acceleration of healing of fractured bones.

Current Evidence on the Association of Dietary Patterns and Bone Health: A Scoping Review

“…It also acts as a cofactor for osteoblast differentiation and collagen formation (66,67). Carotenoids and other antioxidants also affect bone health by reducing oxidative stress (68). Vitamin K is involved in bone matrix formation, where mineralization happens (69).…”

Calcium and Vitamin D status in Premenopausal and Postmenopausal Women

“…Nutrition imbalance with endocrine abnormalities may be involved in osteoporosis [25]. Calcium and Vitamin D is widely used therapies for Osteoporosis.…”

Contribution of methylglyoxal to delayed healing of bone injury in diabetes

“…Decreased and delayed bone formation was observed with the reduction of growth factor levels in diabetic animals (36,37). Dysregulation of the transition from cartilage to bone has also been observed due to chondrocyte apoptosis, premature removal of cartilage, reduced osteoblast differentiation, and insufficient vascularization (7,(10)(11)(12)38,39). Supernormal osteoclast activity was reported to disturb remodeling of the osseous callus (7).…”

“…Several mechanisms, including insulin insufficiency, hyperglycemia, and oxidative stress, are considered to delay fracture healing in type 1 and type 2 diabetes via the reduction of osteoblast differentiation, increased osteoclast activity, and induction of apoptosis in chondrocytes and osteoblasts (7,(10)(11)(12). Of these, chronic and sustained hyperglycemia is known to enhance the glycation reaction, and ultimately results in the formation of advanced glycation end-products (AGEs).…”