Background: Osteoporosis (OP) is the most common metabolic bone disorder which can increase risk of fracture. Glucocorticoid (GC) is the most common cause of secondary osteoporosis. Methyl sulfonyl methane (MSM) is an organosulfur molecule that is used as a precursor for synthesis of many amino acids and maintaining normal connective tissues.
Aim of the Work: The current work aimed to explore the possible protective potency of MSM on glucocorticoid induced osteoporosis in adult male albino rat model.
Materials and Methods: Thirty adult male albino rats were divided into three groups; control, glucocorticoid treated (7 mg/kg, once/week dexamethasone I.M injection) and MSM treated groups (400 mg/kg/day, orally). The blood samples were subjected to biochemical tests (calcium, phosphorus and alkaline phosphatase levels). Sections from rat tibia were examined histologically, immunohistochemically for the expression of osteopontin (OPN), Receptor activator of nuclear factor- kappa B ligand (RANKL), and d-Transferase-Biotin-dUTP nick end labeling (TUNEL) and by scanning electron microscope .
Results: Glucocorticoid caused significant reduction in both serum calcium of and phosphorus levels with significant elevation in the level of alkaline phosphatase, compared to the control group. In addition, it produced marked increase in thickness of periosteum, and marked thinning of compact bone of the diaphysis with many fissures, degenerated osteoblasts and osteoporotic cavities. Significant upregulation of (RANKL), (TUNEL),and (OPN), markers for bone resorption, apoptosis and bone formation respectively were noticed. Co-administration of MSM improved osteoporosis in glucocorticoid induced rat model.
Conclusion: Glucocorticoid induced osteoporosis in adult male rats. Marked improvement was achieved by co-administration of MSM.