Osteoblast function and differentiation

Osteoblast (“Osteo” means bone & “blast” means formation) is an uni-nucleated cell, produced from pluripotent mesenchymal stem cells; osteoblast function is essential for mineralization and synthesis of bone during both bone formation and bone remodeling.

They are found in bone marrow as a single cell or group of cells. Osteoblast latter converted into chondrocytes, muscle cells, and adipocytes.

The matured osteoblast is surrounded by the growing calcified bone matrix; thus, the cell is trapped in a space called a lacuna.

The trapped osteoblast later become a specialized cell called osteocyte, or bone cell. Osteocytes can interconnect with each other as well as with free surfaces of the bone through widespread cytoplasmic progressions that occupy long, meandering channels (canaliculi) via bone matrix.

Osteoblasts contain a smaller number of cell organelles compared to other bone cells (e.g. Osteoclast), which includes lysosomes, mitochondria, and vacuoles.

 

Osteoblast function

The osteoblast can synthesize many cellular molecules including structural proteins, hormones, and enzymes as well as growth factors.

  • Structural protein – Collagen
  • Enzymes – Alkaline phosphatase and collagenase.
  • Hormone – Osteocalcin, (also called as bone gamma-carboxyglutamic acid-containing protein (BGLAP), which is a noncollagenous protein hormone present in bone and dentin).
  • Growth factor – Insulin-like growth factors I and II, transforming growth factor, platelet-derived growth factor, fibroblast growth factor, and bone morphogenetic proteins.
  • Osteoblast also produce the organic unmineralized component of the bone known as osteoid. Osteoid is produced in the form of several specific proteins required for the formation of bone tissue.
Clinical correlation

If there are no sufficient minerals for bone formation or any osteoblast dysfunctions, then the osteoid will not mineralize appropriately, it leads to improper accumulation of osteoid. This condition resulting into emerging various disorders like rickets in children and osteomalacia in adults.

 

Osteoblast differentiation

Recent scientific studies in bone cell biology have significantly changed the conceptions regarding regulatory mechanisms involved in the differentiation of osteoblasts and osteoclasts.

In vertebrates, bone is frequently destroyed and reformed to keep constant bone volume and calcium homeostasis throughout their lives. Osteoblasts and osteoclasts are specialized cells for bone volume maintains. Osteoblast function is required for bone formation, while osteoclasts are responsible for resorption.

In osteoblasts differentiation, bone morphogenetic proteins (BMPs) play critical role. The studies on Smad-mediated signals discovered the particular functions of BMPs in osteoblast differentiation.

Runx2 and Osterix are known transcription factors found to be important molecules for inducing the differentiation of osteoblast cell. Smad transcriptional factors are shown to interact with other transcription regulators, including Runx2.

 

Osteoblast function in osteoclast differentiation 

Recent studies on interactions between Receptor Activator of NF-Kappa B (RANK) and RANK Ligand (RANKL) discovered the well-known hypothesis that osteoblasts play an important role in osteoclast cell differentiation. Osteoblasts express a membrane-associated factor RANKL on their membranes. While, osteoclast precursor cells express a receptor, RANK on their cell membrane. RANKL and RANK interactions (cell-cell interaction) recognize a differentiate of osteoclast precursor cells into osteoclasts. Thus, osteoblast function is also responsible for osteoclast differentiation.

 

Osteoblast-independent differentiation of Osteoclast

Also, recent studies have found that lipopolysaccharide and inflammatory cytokines including tumor necrosis factor receptor-alpha and interleukin-I directly induce the osteoclast differentiation and function, this mechanism is independent of osteoblast function and RANKL-RANK interaction.  Interferon-gamma and transforming growth factor-beta super family members are also found to be important factors for osteoclastogenesis. These studies have provided new areas for analyzing the molecular mechanisms involved in the osteoblast and osteoclast differentiation (Katagiri and Takahashi).

 

 

Data source

Hayden JM1, Mohan S, Baylink DJ. The insulin-like growth factor system and the coupling of formation to resorption. Bone. 1995 Aug;17(2 Suppl):93S-98S.

Baylink DJ, Finkelman RD, Mohan SGrowth factors to stimulate bone formation. J Bone Miner Res. 1993 Dec;8 Suppl 2: S565-72.

Wang DS, Miura M, Demura H, Sato K. Anabolic effects of 1,25-dihydroxyvitamin D3 on osteoblasts are enhanced by vascular endothelial growth factor produced by osteoblasts and by growth factors produced by endothelial cells. Endocrinology. 1997 Jul;138(7):2953-62.

Caetano-Lopes J1, Canhão H, Fonseca JE. Osteoblasts and bone formation. Acta Reumatol Port. 2007 Apr-Jun;32(2):103-10.

Katagiri T, Takahashi N.Regulatory mechanisms of osteoblast and osteoclast differentiation. Oral Dis. 2002 May;8(3):147-59.

Katagiri T1, Takahashi N. Regulatory mechanisms of osteoblast and osteoclast differentiation.Oral Dis. 2002 May;8(3):147-59.

 

 

 

 

 

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