Vitamin K2 inhibits glucocorticoid-induced bone loss partly by preventing the reduction of osteoprotegerin (OPG)

• Published in: Journal of bone and mineral metabolism Vol. 23; no. 1; pp. 41 - 47
• Main Authors: SASAKI, Nobuhiro, KUSANO, Eiji, TAKAHASHI, Hideaki, ANDO, Yasuhiro, YANO, Kazuki, TSUDA, Eisuke, ASANO, Yasushi
• Format: Journal Article
• Language: English
• Published: Tokyo Springer 2005; Springer Nature B.V
• Subjects: Acid Phosphatase - blood; Adult; Alkaline Phosphatase - blood; Biological and medical sciences; Biomarkers; Bone density; Bone Density - drug effects; Bone Resorption - blood; Bone Resorption - prevention & control; Bone Resorption - urine; Bones; Diseases of the osteoarticular system; Female; Glomerulonephritis; Glucocorticoids - adverse effects; Glycoproteins - blood; Humans; Investigative techniques, diagnostic techniques (general aspects); Isoenzymes - blood; Male; Medical sciences; Nephrology. Urinary tract diseases; Nephropathies. Renovascular diseases. Renal failure; Osteoarticular system. Muscles; Osteocalcin - blood; Osteogenesis - drug effects; Osteoporosis; Osteoporosis. Osteomalacia. Paget disease; Osteoprotegerin; Parathyroid Hormone - metabolism; Radiodiagnosis. Nmr imagery. Nmr spectrometry; Receptors, Cytoplasmic and Nuclear - blood; Receptors, Tumor Necrosis Factor; Tartrate-Resistant Acid Phosphatase; Vitamin K 2 - pharmacology; Glomerulonephritis; Alkaline phosphatase; Suppression; Diseases of the osteoarticular system; Vitamin; Phosphoric monoester hydrolases; Esterases; Bone remodeling; Menatetrenone; Glucocorticoid; Prevention; Osteoporosis; Serum; Vitamin K; Kidney disease; Human; Osteocalcin; Urinary system disease; Group treatment; Enzyme; Resorption; Metabolism; Parathormone; Chronic; Parathyroid hormone; Hydrolases; Bone mineral density; Bone; Formation
• ISSN: 0914-8779; 1435-5604
• DOI: 10.1007/s00774-004-0539-6

We have recently demonstrated that glucocorticoid (GC) suppresses bone formation and enhances bone resorption, with resultant bone loss. This altered bone turnover is not due to the action of parathyroid hormone (PTH), but appears to be related to the suppression of osteoprotegerin (OPG). As vitamin K2 (menatetrenone) has been used for the treatment of osteoporosis, the present study was carried out to evaluate the effect of vitamin K2 on GC-induced bone loss. Twenty patients with chronic glomerulonephritis treated with GC for the first time were chosen for this study. Ten patients received GC alone (group A) and the other 10 patients each received 15 mg of vitamin K2 per day in addition to GC (group B). Markers of bone metabolism, including serum OPG, osteocalcin (OC), bone-specific alkaline phosphatase activity (BAP), PTH, tartrate-resistant acid phosphatase (TRAP), and bone mineral density (BMD), were measured before and during the treatment. OPG was significantly decreased in group A (P < 0.001), while no significant change was seen in group B. TRAP was markedly increased in both groups, more particularly in group A (P < 0.01). PTH was decreased in group A, but was increased in group B. OC was decreased at month 1 but subsequently increased until month 12 in both groups. BAP had decreased at month 3 in group A (P < 0.05), but not in group B. BMD of the lumbar spine was significantly reduced after 6 months (P < 0.01), and 12 months (P < 0.001) of treatment in group A, whereas there was no remarkable change in group B. The present study demonstrated that the inhibition exerted by vitamin K2 of the reduction in OPG induced by GC may, at least in part, play a role in the prevention and treatment of GC-induced bone loss.