Cellular and extracellular matrix of bone, with principles of synthesis and dependency of mineral deposition on cell membrane transport

Abstract

Bone differs from other connective tissues; it is isolated by a layer of osteoblasts that are connected by tight and gap junctions. This allows bone to create dense lamellar type I collagen, control pH, mineral deposition, and regulate water content forming a compact and strong structure. New woven bone formed after degradation of mineralized cartilage is rapidly degraded and resynthesized to impart structural order for local bone strength. Ossification is regulated by thickness of bone units and by patterning via bone morphogenetic receptors including activin, other bone morphogenetic protein receptors, transforming growth factor-β receptors, all part of a receptor superfamily. This superfamily interacts with receptors for additional signals in bone differentiation. Important features of the osteoblast environment were established using recent tools including osteoblast differentiation in vitro. Osteoblasts deposit matrix protein, over 90% type I collagen, in lamellae with orientation alternating parallel or orthogonal to the main stress axis of the bone. Into this organic matrix, mineral is deposited as hydroxyapatite. Mineral matrix matures from amorphous to crystalline hydroxyapatite. This process includes at least two-phase changes of the calcium–phosphate mineral as well as intermediates involving tropocollagen fibrils to form the bone composite. Beginning with initiation of mineral deposition, there is uncertainty regarding cardinal processes, but the driving force is not merely exceeding the calcium-phosphate solubility product. It occurs behind a epithelial-like layer of osteoblasts, which generate phosphate and remove protons liberated during calcium-phosphate salt deposition. The forming bone matrix is discontinuous from the general extracellular fluid. Required adjustment of ionic concentrations and water removal from bone matrix are important details remaining to be addressed.

Aesculetin Accelerates Osteoblast Differentiation and Matrix-Vesicle-Mediated Mineralization

“…Biogenesis of polarized matrix vesicles occurs in selected areas of developing organic matrix of differentiating growth plate chondrocytes, osteoblasts, and odontoblasts [9,25,32]. The apatitic bone mineral crystals are formed within matrix vesicles of mature osteoblasts located at sites of initial calcification in cartilage, bone, and predentin with the assistance of phosphatases and calcium-binding molecules [10,18,32]. Subsequently, preformed hydroxyapatite crystals are exposed to the extracellular space across the matrix vesicle membrane, leading to biomineralization.…”

“…The mature osteoblasts lie adjacent to newly synthesized osteoid and produce the bone mineral hydroxyapatite that is deposited into the organic matrix, forming a dense mineralized matrix [9,10]. Hydroxyapatite crystals present in bone is interspersed in a collagen matrix in a highly regulated manner [11,12].…”

Comparison of Myosepta Development and Transcriptome Profiling between Blunt Snout Bream with and Tilapia without Intermuscular Bones

“…Previous research has demonstrated that IBs may be associated with the regulation of muscle contraction [ 12 , 31 , 32 ]. Bone is isolated by a layer of osteoblasts connected by tight and gap junctions with unique cellular functions and complex molecular composition [ 33 ]. During the formation of the skeleton structure, junction-associated proteins, which only allow the regulated transport and limit the free diffusion of molecules, are expressed in osteoblasts, generating significant resistance across osteoblast monolayers, while gap junctions may play important roles in the communication between cells through connexins as well as in growth, development, and tissue homeostasis [ 34 , 35 , 36 ].…”

Biocompatibility pathways and mechanisms for bioactive materials: The bioactivity zone

“…Bone is a mineralized connective tissue, the properties of which critically depend on its cellular components and the extracellular matrix (ECM), and the interactions between these [ 22 ]. Bone formation occurs during skeletal development and during repair, for example following injury [ 23 ].…”