Читать книгу Bone and Soft Tissue Augmentation in Implantology - Группа авторов - Страница 13

These cells originate from pluripotent mesenchymal stem cells through the activation of a series of transcription factors⁶² partially involving members of the bone morphogenetic protein superfamily.^81,99 Osteoblasts are present in layers on the bone surface. In all active bone-formation sites, they are responsible for extracellular matrix production (osteoid) and subsequent mineralization. Osteoblasts are polarized cells with a mineral-facing side through which the matrix is extruded. Once osteoid production stops, some osteoblasts are trapped in the extracellular matrix and differentiate into osteocytes, which are located in the bone lacunae. On the one hand, neurocranial bones,²¹ including the mandible (except the mandibular condyle) and maxilla as well as part of the clavicle, are formed by membranous ossification. This is a direct ossification without a cartilaginous phase, where differentiated osteoblasts lead to osseous matrix formation through mesodermal and ectomesodermal cellular condensation. On the other hand, the appendicular and axial skeleton follows an endochondral ossification route. A temporary cartilaginous scaffold is produced by chondrocytes, which mature and hypertrophy in a second stage. In a third stage, this cartilaginous matrix becomes mineralized. Finally, a vascularization is established that allows, at first, the arrival of osteoclasts (or chondroclasts), which lead to the resorption of the calcified cartilaginous matrix and, following that, the differentiation of osteoblasts that will replace the cartilaginous scaffold by a bony matrix. This matrix will lead to the formation of the trabecular structure of the long bones.⁹¹

Osteoblasts can produce three types of bone: woven bone, primary parallel-fibered bone, and lamellar bone. The difference between these bone types is related to the orientation of the collagen fibrils: In woven bone, the fibrils are three-dimensionally and randomly distributed due to the rapidity of osteoid deposition and mineralization (Fig 1-1). Compared with mature lamellar bone, this bone is more elastic and mechanically less consistent due to the low level of mineralization and the lack of a specific orientation of the collagen fibers. In adults, this type of bone is produced during healing processes, and it is the only bone able to grow in the absence of a pre-existing mineralized tissue. Woven bone forms ridges and roots between and around the blood vessels (Fig 1-2). Primary parallel-fibered bone is characterized by a more parallel distribution of the collagen fibrils, and is typically produced during periosteal and endosteal bone apposition. The mechanical properties are as weak as those of woven bone. Lamellar bone is a well-organized mineralized tissue. Collagen fibrils are distributed in parallel layers that have a thickness of 3 to 5 µm. Osteoid production is slow (1 to 2 µm per day) compared with woven bone, and it takes about 10 days to be mineralized at a well-defined mineralization front. Lamellar bone needs a pre-existing bone surface to be produced by osteoblasts, which means that, unlike woven bone, it is not able to bridge gaps.

Fig 1-1 Osteoblasts produce bone on the surface of a host bone. Bone formation occurs on the surface of existing bone (pink). New bone (dark purple) is lined by seams of osteoblasts and arranged in osteonal structures. Osteoid (barely stained) is bone that is not yet mineralized. The direction of new bone formation can be anticipated by the sprouting of extension into the defect area. [The image is of pig bone.]

Fig 2-1 Osteoblast seams during the early stages of bone formation. Bone formation is the consequence of osteoblast activity. Osteoblasts dominate the scene, and non-mineralized bone (osteoid) is visible. [The image is of pig bone.]

When not active in osteoid production, osteoblasts can differentiate into bone-lining cells. This particular conformation determines a flat distribution of osteoblasts over the bone surface, creating a barrier-like layer between the bone and the extracellular space that seems to be responsible for ion exchange. The bone lining cells may also be responsible for bone resorption through two mechanisms: the first is determined by cell contraction and subsequent bone surface exposition; the second is defined by the direct secretion of osteoclast activating factors.