THE VASCULAR CONTRIBUTION TO OSTEOGENESIS V. The Vasculature Supplying the Epiphysial Cartilage in Rachitic Rats

Abstract

1. It has been shown that in experimental rickets the well known changes in the epiphysial cartilage which so seriously affect growth are accompanied by severe interference with the progress of the metaphysial vessels into the growth cartilage. 2. Further evidence has been found that, by the repeated increase in their number, the cartilage cells occupying the more distal part of the proliferative segment become more and more affected by their remoteness from the epiphysial vessels, which supply the transudates to these cells. At a given distance these cells are affected and change, becoming hypertrophic, with increasingly large vacuolae, and are rich in glycogen and alkaline phosphatase. 3. The hypertrophic cells alter the nature of the intercellular substance they deposit and this becomes calcifiable. Provided that the metaphysial vessels are situated at an appropriate distance–about three cell capsules away–and that the blood has its necessary components, calcification occurs. 4. Calcification produces the advancing, rigid multitubular structure within which the progressing metaphysial vessels are protected. 5. The interruption of calcification by the withdrawal of fat-soluble vitamins breaks down the whole mechanism of growth and stops the vessels growing into their proper position. The administration of the required vitamins re-establishes the normal sequence of events and allows the vessels to play their decisive role in osteogenesis. 6. Any mechanism which causes the interruption of the vascular progression, whether from metaphysial ischaemia (Trueta and Amato 1960), from severe pressure (Trueta and Trias 1961) or from lack of calcification by withdrawing the fat-soluble vitamins, equally interrupts growth.

A Critical Review of the Classic Metaphyseal Lesion: Traumatic or Metabolic?

“…Ironically, the peripheral pattern of excessive hypertrophic chondrocytes observed in classic metaphyseal lesions is similar to the pattern reported in an experimental model of rickets [34]. Trueta and Buhr [34] observed that the proliferation of hypertrophic chondrocytes in rachitic rodents was most excessive in the peripheral growth plate (Fig. 4C), corresponding to the region of greatest compressive forces.…”

“…A diffuse pattern is seen in active stages of rickets because of the inability of vascular invasion and subsequent resorption of terminal chondrocytes in the absence of mineralized matrix. Ironically, the peripheral pattern of excessive hypertrophic chondrocytes observed in classic metaphyseal lesions is similar to the pattern reported in an experimental model of rickets [34]. Trueta and Buhr [34] observed that the proliferation of hypertrophic chondrocytes in rachitic rodents was most excessive in the peripheral growth plate (Fig.…”

Runx2 Protein Stabilizes Hypoxia-inducible Factor-1α through Competition with von Hippel-Lindau Protein (pVHL) and Stimulates Angiogenesis in Growth Plate Hypertrophic Chondrocytes

“…The ultimate size and structure of each endochondral bone depend on the coordinated regulation of chondrocyte proliferation, maturation, and hypertrophy in response to multiple extracellular signals (6,7). Interestingly, the blood vessel disruption of the growth plate reduces bone mineralization and the replacement of hypertrophic chondrocytes (8,9), suggesting that bone formation is largely dependent on vascularization.…”

Trunk and leg growth in children with paraplegia caused by spinal cord injury

“…These studies show that bone morphology abnormalities are generated by mechanical disorders, but conclude that such abnormalities are in no way responsible for deficient growth in the length of long bones (Trueta, , 1961. Frost (1979) contests the validity of this last conclusion on the grounds of possible interference of regional growth phenomena.…”

“…Other experiments have verified the vital part played in the growth of bone length by insufficient vascularisation (Showing & Celers, 1965;Troupp, 1961;Trueta, 1958Trueta, , 1961Van der Hoeft et at., 1963;Wo & Mittner, 1937), and hypoxia (Person, 1968), and this is why the resulting inequalities were attributed to the vascular effects of neurological damage.…”