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Osteoblast

Osteoblasts are responsible for synthesis, deposition and mineralization of the bone matrix. Osteoblast secrete type I collagen, the main component of the organic bone matrix. Mineralization is affected by the deposition of tiny crystals of calcium phosphate. Osteoblasts are 15-30 micron across. They are found mainly at the surfaces of a mature bone were they form a monolayer. Within the bone matrix, osteoblast are found in regions that undergo remodeling (a renewal of the bone tissue). Osteoblasts have an extensive granularendoplasmic reticulum, a large golgi complex and numerous secretory vesicles. Their plasma membranes have many extensions, some contacting neighboring osteoblasts and osteocytes. In the process of bone matrix formation the osteoblasts become embedded in the matrix and transform into osteocytes.

Osteocytes maintain the bone tissue. Some potential functions of osteocytes include a mechanical and/or metabolic pump for the bone lymphatic system, regulation of bone mineralization and the measurement of stress. Osteocytes have numerous extensions which they send through the surrounding matrix. The extensions of neighboring cells make contact creating a continuous metabolic and information pathway. The inner structure of osteocytes is characteristic of non active cells with a little granular endoplasmic reticulum, few ribosomes and a small Golgi apparatus. The average life span of an osteocyte is very long - up to 25 years.

Osteoclasts

Osteoclasts are responsible for the bone removal by demineralization and destruction of the bone matrix. The exact mechanism is not understood yet. Osteoclasts arise by the fusion of mononuclear cells that originate in the bone marrow and bear similarity to macrophages. This is in contrast to osteoblast which resemble fibroblasts and developed from mesenchymal cells. Osteocytes contain numerous mitochondria, vacuoles and lysosomes. The lysosomes are acid phosphate positive and mostly located under ruffed membrane, in the area were bone resorption occurs. Bone resorption occurs normally concurrently with bone deposition. Both osteoblasts and osteocytes cooperate in the remodeling process. This process is on going through most of our live and ensures the vitality of the bone tissue. Overactive osteoclast may lead to osteoporoses.

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Osteoclast inhibitory effects of vitamin K2 alone or in combination with etidronate or risedronate in patients with rheumatoid arthritis: 2-year results.

Morishita M, Nagashima M, Wauke K, Takahashi H, Takenouchi K.

J Rheumatol. 2008 Mar;35(3):407-13. Epub 2008 Feb 1. Department of Joint Disease and Rheumatism, Nippon Medical School, Tokyo, Japan.

OBJECTIVE: To investigate the effects of vitamin K2 (Vit K2) alone or in combination with etidronate and risedronate on bone loss, osteoclast induction, and inflammation in patients with rheumatoid arthritis (RA).

METHODS: Subjects comprised 79 patients with RA who were receiving prednisolone, divided into 3 groups: Group K, Vit K2 alone; Group KE, Vit K2 plus etidronate; and Group KR, Vit K2 plus risedronate. During a 24-month treatment and followup period, levels of N-terminal telopeptide of type I collagen (NTx) and bone alkaline phosphatase were measured. Bone mineral density (BMD) of the 3 groups was measured using dual-energy x-ray absorptiometry. Damage score to fingers on radiographic findings were measured according to the Larsen method. Serum levels of receptor activator of nuclear factor-kappaB ligand (RANKL) and osteoprotegerin (OPG) were measured.

RESULTS: Falls in rate of change of BMD decreased after 18 months in groups KR and KE. Larsen damage scores indicated a significant difference between Group KE and other groups. Significant decreases in serum NTx were observed in groups KE and KR at all timepoints, but not in Group K. Levels of RANKL decreased significantly in all 3 groups.

CONCLUSION: Vit K2 alone or in combination with bisphosphonates for treatment of osteoporosis in patients with RA may inhibit osteoclast induction via decreases in levels of RANKL.

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