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Studies on the pathogenesis of avian rickets II. Necrosis of perforating epiphyseal vessels during recovery from rickets in chicks caused by vitamin D3 deficiency.

This study involved comparison of the distribution and integrity of perforating epiphyseal and marrow vessels with the stage of development and integrity of chondrocytes and the distribution of insoluble calcium in the proximal tibial growth plate of 3-week-old vitamin-D3-deficient hypocalcemic chicks and 3-week-old D3-deficient chicks 12, 36, 72, and 120 hours after an oral dose of 10,000 units vitamin D3. The aim was to clarify the mechanisms responsible for chondrocyte hypertrophy and cartilage calcification in the avian growth plate. Within 12 hours after administration of vitamin D3, serum calcium levels rose to normocalcemic levels. The following morphologic changes were first recognizable at the times indicated. Distal portions of previously elongated perforating epiphyseal vessels and adjacent proliferative and maturing chondrocytes underwent necrosis by 12 hours. Chondrocyte necrosis was not preceded by hypertrophy. By 36 hours, vascular and chondrocyte necrosis involved large portions of the thickened proliferating and maturing zone, and perforating epiphyseal vessels were shortened to a normal length. By 72 hours, chondrocyte hypertrophy and calcification resumed around the shortened epiphyseal vessels. By 120 hours, marrow had removed the necrotic cartilage, and morphologically normal growth plate was restored, with perforating epiphyseal and marrow vessels, both ending in a narrow hypertropic cartilage zone. The results indicate that proximity of chondrocytes to perforating epiphyseal vessels is necessary for their viability, but loss of these vessels does not cause hypertrophy. Since hypertrophy and calcification both occur in the proximity of perforating epiphyseal vessels in normocalcemic animals but not in hypocalcemic animals, it is likely that the vessels influence hypertrophy and calcification by delivering calcium to chondrocytes.

Animals↗

Calcium absorption in Nigerian children with rickets.

BACKGROUND: Nutritional rickets is common in Nigerian children and responds to calcium supplementation. Low dietary calcium intakes are also common in Nigerian children with and without rickets. OBJECTIVE: The objective was to assess intestinal calcium absorption in Nigerian children with rickets. DESIGN: Calcium absorption was assessed in 15 children with active rickets (2-8 y of age) and in 15 age- and sex-matched children without rickets by using a dual-tracer stable-isotope method. The children with rickets were supplemented with calcium for 6 mo; calcium absorption was reevaluated 12 mo after the baseline study. Fractional calcium absorption could be determined in 10 children with rickets and in 10 children without rickets. RESULTS: The children with and without rickets had dietary calcium intakes of approximately 200 mg/d. Compared with the control children, the children with rickets had lower serum 25-hydroxyvitamin D and calcium concentrations and greater 1,25-dihydroxyvitamin D and parathyroid hormone concentrations. In fact, there were 15 rachitic and 15 control children in the study. Mean (+/-SD) fractional calcium absorption did not differ between those with (61 +/- 20%) and without (63 +/- 13%) rickets (P = 0.47). Calcium absorption was not associated with serum concentrations of calcium, alkaline phosphatase, 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, or parathyroid hormone. Mean fractional calcium absorption was significantly greater after (81 +/- 10%) than before (61 +/- 20%) calcium supplementation for the treatment of rickets (P = 0.035). CONCLUSIONS: In Nigerian children with rickets, the capacity to absorb calcium is not impaired; however, fractional calcium absorption increases after the resolution of active disease. Calcium absorption may be inadequate to meet the skeletal demands of children with rickets during the active phase of the disease, despite being similar to that of control children.

Calcium↗