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Problems of vertebral growth plate metabolism regulation at different stages of ontogenesis are insufficiently covered in the literature. However, the study of function mechanism of provisional cartilage of vertebral growth plate is a practical and theoretical basis of pathogenesis model of idiopathic scoliosis and Scheuermann’s disease both associated with growth disorders.

Objective: To investigate the function mechanism of vertebral growth plate structural components during formation and growth.

Materials and methods: Fifty vertebral body specimens of children at the age from 1 to 14 years obtained from the forensic medicine department were studied by methods of morphohistochemistry, biochemistry, and ultra-structural analysis. The expression of five proteoglycan genes and their albuminous products was investigated by RT-PCR method.

Results: The process of growth represents a sequence of morphogenetic movements ongoing up to the achievement of sexual maturity. But morphofunctional organization and regulation of growth are different in different periods of ontogenesis. Early postnatal growth of vertebral bodies is governed by a radially located zone of growth. The cell population in a just-formed cartilage growth plate is non-uniform: from poorly differentiated chondroblast through the form of highly differentiated ones to degrading chondrocyte. This period of the spine development is characterised by the presence of vessels in provisional cartilage tissue. The concept of “chondro/hematic barrier” suggested and validated by A.M Zaidman explains a conservation of homeostasis at a stage of vertebral bodies differentiation. The process of chondrogenic differentiation of prechondroblasts in the early postnatal period is inducted by the chorda influence. In the late postnatal period (12–14 years) the laws of structural and functional organization of cartilage growth plate of vertebral body remain the same: phenotypic heterogeneity, polarity, and zonality of cells. A metabolic centre of complex architectonics of cartilage tissue is chondroblast. Chondroblast is functioning at the level of chondron which is a functional unit of vertebral growth plate. Chondroblast (chondrocyte) is located in the centre of chondron and surrounded by pericellular matrix presented by diffuse aggrecan molecules, or growth plate aggregates.

Due a peculiar architectonics, growth plate molecules have inner spaces comparable in size with Golgi’s vesicles. Metabolites, small molecules, and water freely penetrate through these molecules. Diffuse molecules together with type II thin collagenic fibres, minor collagenes, and structure-forming growth plates perform barrier function. Besides barrier function, diffuse molecules perform information function inside a chondron, forming a kind of information field. Signals of this field are perceived by chondroblast receptors, and the cell gene apparatus expression is carried out through second messengers. Thus, either stimulation of proliferative activity with subsequent differentiation during intensive growth, or interruption of these processes (period of growth delay) occurs. Single chondrons unite into chains in proliferation zones. Cell interaction inside chondron occurs due transmembrane structures, as a contact coordination of functions of cells with inherent high specificity. Concentration of diffuse molecules of growth plate (aggrecan) in proliferation zones is the highest on evidence of histochemical and ultrastructural assays. Besides, diffuse molecules are the short-distance regulators of DNA synthesis the mechanism of action of which is realised through the system of receptors on a cellular membrane. Hence, contact intercellular interactions are one of the mechanisms controlling cell division. These are so-called extracellular factors of chondroblast proliferation regulation.

Thus, the process of growth represents a complex two-stage mechanism of proliferation and differentiation of chondroblasts, and adequate osteogenesis. All three processes provide harmonious spine formation, and disturbance of one of them results in pathology development.

Correspondence should be addressed to Jeremy C T Fairbank at The Nuffield Orthopaedic Centre, Windmill Road, Headington, Oxford OX7 7LD, UK