Vitamin B₆deficiency experimentally-induced bone and joint disorder: microscopic, radiographic and biochemical evidence

Abstract

In the present study the effect of pyridoxine deficiency on the ultrastructure and morphology of bone and its metabolism was examined in the rapidly growing chick. Pyridoxine-deficient animals had tibias of reduced dry weight and cortical thickness. Histomorphometry demonstrated a disproportionately high eroded surface, lower amount of osteoid tissue and reduced mineralized trabecular width. Anteriorposterior radiographs of the tibiotarsometatarsal joint showed reduced secondary ossification centres and coarse trabeculation. Decalcified metaphyseal cartilage showed irregular trabeculas and a markedly reduced amount of Fast-green counterstain matrix suggesting that there is less collagen present and in turn less availability for matrix to be laid down for later calcification. Plasma activity of the bone alkaline phosphatase isoenzyme (EC 3.1.3.1) was decreased. Plasma Ca and PO, levels did not vary. The present bone study referring to a pseudo-lathyritic state in which collagen maturation is not completely achieved supports the hypothesis that pyridoxine is an essential nutrient for the connective tissue matrix.

Chemical and biomechanical characterization of hyperhomocysteinemic bone disease in an animal model

“…In animals receiving aminoacetonitrile, a less toxic analog of BAPN, electron microscopy of long bones shows significant enlargement of Type I collagen fibrils while a similar but less severe abnormality is observed in vitamin B 6 -deficiency and in hyperhomocysteinemia induced by hCySH added to the diet [13]. Changes in collagen solubility and collagen cross-linking are hallmarks of connective tissue changes associated with these dietary manipulations [14-16]. …”

“…In growing chicks fed a B 6 -deficient diet, there were no changes in bone length, bone diameter, or moment of inertia, but mechanical performance was altered. Moreover, histomorphometric and radiological studies showed low-turnover osteopenia [14]. …”

B vitamins, homocysteine, and bone disease: Epidemiology and pathophysiology

“…Interestingly, although McKusick [15] suggested that homocysteine impairs collagen cross-links, vitamin B 6 is an essential coenzyme for lysyl oxidase, a collagen cross-link precursor [33]. Investigations using chick models found that vitamin B 6 may be important for collagen cross-linking and formation [30,34,35], and that alterations of the collagen matrix due to B 6 deficiency may degrade bone biomechanical properties [36]. In the previously mentioned study by Saito et al [18], the plasma vitamin B 6 concentration in the fracture group was half that of the controls (26.4 vs 49.8 nmol/L).…”

“…Animal studies suggest that vitamin B 6 may influence bone turnover, as deficiencies in this nutrient have been associated with decreased concentrations of plasma alkaline phosphatase [29,30] and osteocalcin [31]. In one study among humans, Reynolds et al [32] found that patients with hip fracture had lower serum vitamin B 6 than controls.…”

B-6 vitamers and 4-pyridoxic acid in the plasma, erythrocytes, and urine of postmenopausal women

“…Studies in chicks and rats showed the essential role of vitamin B-6 in the structural integrity of collagen molecules in connective tissue, biomechanical properties (strength), and healing of bone whose organic matrix is composed primarily of collagen (5-7). Vitamin B-6 -deficient bone is more fragile because of osteoporosis-type lesions and uncoupling (ie, there is too much resorption for the newly formed bone) (8,9). Reynolds et al (10) reported that half of their hip fracture patients were vitamin B-6 deficient (plasma PLP: 13 nmol/L).…”