Scurvy results in decreased collagen synthesis and bone density in the guinea pig animal model

Kipp, Deborah E.; McElvain, Maureen A.; Kimmel, Donald B.; Akhter, Mohammed P.; Robinson, Roscoe R.; Lukert, Barbara P.

doi:10.1016/8756-3282(95)00481-5

Cited by 76 publications

(60 citation statements)

References 36 publications

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“…Guinea pigs deprived of vitamin C show voluntary decreased food consumption which led to weight loss and even death (Barnes et al, 1973;Odumosu and Wilson, 1973;Kipp et al, 1996). Herein, we observed that the growth rate of capybaras, although lower in experimental compared with the control group, was always positive.…”

Section: Discussionsupporting

confidence: 48%

“…However, higher primates and cavids, like the guinea pig (Cavia porcella) lack this enzyme and thus must receive their vitamin C from an exogenous source. In these species, signs of scurvy (sluggishness, physical discomfort, bleeding gums and noses, loss of teeth, joint weakness, fragile bones, and death) appear when vitamin C is left out of their diet (Barnes et al, 1973;Jones et al, 1973;Odumosu and Wilson, 1973;Kipp et al, 1996). Lack of ascorbic acid also has a negative effect on reproduction, both in males (Chinoy et al, 1986) and females (Clow et al, 1975;Norkus, and Rosso, 1975;Fazleabas et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

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Scurvy in Capybaras Bred in Captivity in Argentine

Cueto

Allekotte

Kravetz

2000

Journal of Wildlife Diseases

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In order to determine if the absence of vitamin C in the diet of capybaras (Hydrochoerus hydrochaeris) causes scurvy, a group of seven young individuals were fed food pellets without ascorbic acid, while another group of eight individuals received the same food with 1 g of ascorbic acid per animal per day. Animals in the first group developed signs of scurvy-like gingivitis, breaking of the incisors and death of one animal. Clinical signs appeared between 25 and 104 days from the beginning of the trial in all individuals. Growth rates of individuals deprived of vitamin C was considerably less than those observed in the control group. Deficiency of ascorbic acid had a severe effect on reproduction of another population of captive capybaras. We found that the decrease in ascorbic acid content in the diet affected pregnancy, especially during the first stages. The results obtained suggest that it is necessary to supply a suitable quantity of vitamin C in the diet of this species in captivity.

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Section: Discussionsupporting

confidence: 48%

Section: Introductionmentioning

confidence: 99%

Scurvy in Capybaras Bred in Captivity in Argentine

Cueto

Allekotte

Kravetz

2000

Journal of Wildlife Diseases

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“…Low dietary intake of ascorbic acid is associated with decreases in bone mass despite greater rates of bone formation and increases in mineralizing surfaces (29). In postmenopausal women, a high intake of ascorbic acid lowers the levels of the bone turnover marker c-telopeptide (30), whereas a low intake of ascorbic acid increases the rate of bone loss (31).…”

Section: Discussionmentioning

confidence: 99%

Follicle-stimulating hormone stimulates TNF production from immune cells to enhance osteoblast and osteoclast formation

Iqbal

Sun

Kumar

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

192

135

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Declining estrogen production after menopause causes osteoporosis in which the resorption of bone exceeds the increase in bone formation. We recently found that mice deficient in the ␤-subunit of follicle-stimulating hormone (FSH␤) are protected from bone loss despite severe estrogen deficiency. Here we show that FSH␤-deficient mice have lowered TNF␣ levels. However, TNF␣-deficient mice are resistant to hypogonadal bone loss despite having elevated FSH, suggesting that TNF␣ is critical to the effect of FSH on bone mass. We find that FSH directly stimulates TNF␣ production from bone marrow granulocytes and macrophages. We also explore how TNF␣ up-regulation induces bone loss. By modeling the known actions of TNF␣, we attribute the high-turnover bone loss to an expanded osteoclast precursor pool, together with enhanced osteoblast formation. TNF␣ inhibits osteoblastogenesis in the presence of ascorbic acid in culture medium, but in its absence this effect becomes stimulatory; thus, ascorbic acid reverses the true action of TNF␣. Likewise, ascorbic acid blunts the effects of TNF␣ in stimulating osteoclast formation. We propose that hypogonadal bone loss is caused, at least in part, by enhanced FSH secretion, which in turn increases TNF␣ production to expand the number of bone marrow osteoclast precursors. Ascorbic acid may prevent FSH-induced hypogonadal bone loss by modulating the catabolic actions of TNF␣.postmenopausal osteoporosis ͉ TNF␣ ͉ bone ͉ ascorbic acid ͉ hypogonadal P ostmenopausal osteoporosis is a leading cause of morbidity and mortality in the increasingly aging population, with fracture rates exceeding the combined incidence of breast cancer, stroke, and heart attacks in postmenopausal women (1). Traditionally, this bone loss has been attributed solely to declining estrogen levels. However, we recently showed that the pituitary hormone folliclestimulating hormone (FSH), the secretion of which is under estrogenic feedback, directly enhances osteoclast formation and function. The deletion of its ␤-subunit (FSH␤) protects against bone loss despite severe hypogonadism (2). This finding indicates that FSH is a requirement for hypogonadal bone loss and, although awaiting definitive proof, suggests strongly that elevated FSH contributes to the genesis of postmenopausal osteoporosis.However, enhanced osteoclastogenesis, a consequence of the direct action of FSH on its G i -coupled receptor on osteoclast precursors, does not fully explain hypogonadal bone loss. There are accompanying alterations in bone and bone marrow, notably enhanced bone formation, increased T lymphocyte production, and macrophage activation. The alterations in immune function have been attributed to an increase in TNF␣ production that is thought to arise solely from estrogen deficiency. However, because TNF inhibits osteoblast differentiation in vitro, the increased bone formation has not been attributed to TNF␣. Thus, the genesis of enhanced bone formation, an essential component of the highturnover bone loss, has remained unclear.Ablat...

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“…Recently, a strain of scorbutic Osteogenic Disorder Shionogi (ODS) rat was established and was found to be suitable for in vivo investigations of AsA deficiency (Mizushima et al, 1984). Scorbutic guinea pig results in low levels of bone formation in leg bones and collagen synthesis in articular cartilage (Kipp et al, 1996), and leads to decreased expression of mRNAs for osteocalcin, alkaline phosphatase, and type I collagen, and to increased osteopontin expression in calvarial bone (Mahmoodian et al, 1996). Scorbutic rats are characterized by low body weight, small craniofacial size, and low concentrations of plasma alkaline phosphatase (Tsunenari et al, 1991;Miyajima et al, 1995;Togari et al, 1995).…”

mentioning

confidence: 99%

Morphological influence of ascorbic acid deficiency on endochondral ossification in osteogenic disorder Shionogi rat

Sakamoto

Takano

2002

Anat. Rec.

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The influences of chronic deficiency of L-ascorbic acid (AsA) on the differentiation of osteo-chondrogenic cells and the process of endochondral ossification were examined in the mandibular condyle and the tibial epiphysis and metaphysis by using Osteogenic Disorder Shionogi (ODS) rats that bear an inborn deficiency of L-gulonolactone oxidase. Weanling male rats were kept on an AsA-free diet for up to 4 weeks, until the symptoms of scurvy became evident. The tibiae and condylar processes of scorbutic rats displayed undersized and distorted profiles with thin cortical and scanty cancellous bones. In these scorbutic bones, the osteoblasts showed characteristic expanded round profiles of rough endoplasmic reticulum, and lay on the bone surface where the osteoid layer was missing. Trabeculae formation was deadlocked, although calcification of the cartilage matrix proceeded in both types of bone. Scorbutic condylar cartilage showed severe disorganization of cell zones, such as unusual thickening of the calcification zone, whereas the tibial cartilage showed no particular alterations (except for a moderately decreased population of chondrocytes). In condylar cartilage, hypertrophic chondrocytes were encased in a thickened calcification zone, and groups of nonhypertrophic chondrocytes occasionally formed cell nests surrounded by a metachromatic matrix in the hypertrophic cell zone. These results indicate that during endochondral ossification, chronic AsA deficiency depresses osteoblast function and disturbs the differentiation pathway of chondrocytes. The influence of scurvy on mandibular condyle cartilage is different from that on articular and epiphyseal cartilage of the tibia, suggesting that AsA plays different roles in endochondral ossification in the mandibular condyle and long bones. Anat Rec 268: 93-104, 2002.

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Scurvy results in decreased collagen synthesis and bone density in the guinea pig animal model

Cited by 76 publications

References 36 publications

Scurvy in Capybaras Bred in Captivity in Argentine

Scurvy in Capybaras Bred in Captivity in Argentine

Follicle-stimulating hormone stimulates TNF production from immune cells to enhance osteoblast and osteoclast formation

Morphological influence of ascorbic acid deficiency on endochondral ossification in osteogenic disorder Shionogi rat

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