Age at menarche and urbanization in Cameroon: current status and secular trends.

Status quo data on the age at menarche were obtained on samples of Cameroonian girls living in urban (Yaoundé) (n = 205), suburban (n = 505) and rural areas (n = 201). Mean ages at menarche, estimated by probit analysis, are 13.18 years (SD 1.08) in Yaoundé, 13.98 years (SD 1.55) in the suburban area, and 14.27 years (SD 1.65) in the rural area. The early menarcheal age observed in Yaoundé girls attending 'privileged schools' (12.72 years, SD 1.18) substantiates the hypothesis that in good environmental conditions Africans are as early-maturing as Asiatic or Mediterranean populations. Comparison with retrospective data on age at menarche during previous decades reveals the presence of a clear secular trend towards earlier maturation, at a rate of 2.5-3.2 months per decade, only in the main cities of the country (Yaoundé/Douala) and a lack of temporal variation in rural areas. The degree of urbanization influences maturational age and its evolution, probably through improvements in the nutritional standards.

PIP: "Status quo data on the age at menarche were obtained on samples of Cameroonian girls living in urban (Yaounde) (n=205), suburban (n=505) and rural areas (n=201).... Comparison with retrospective data on age at menarche during previous decades reveals the presence of a clear secular trend towards earlier maturation, at a rate of 2.5-3.2 months per decade, only in the main cities of the country (Yaounde/Douala) and a lack of temporal variation in rural areas. The degree of urbanization influences maturational age and its evolution, probably through improvements in the nutritional standards." (EXCERPT)

Alkaline phosphatase inhibition by levamisole prevents 1,25-dihydroxyvitamin D3-stimulated bone mineralization in the mouse.

To determine the relationship between alkaline phosphatase (AP), 1,25(OD)2D3 and bone formation in vivo, we have examined the effects of levamisole, a stereospecific inhibitor of AP on bone formation and on 1,25(OH)2D3-stimulated bone mineralization in the mouse. Normal mice were injected daily with levamisole at doses of 40 and 80 mg/kg/b.w. The compound was given alone or in combination with 1,25(OH)2D3 infusion (0.05 micrograms/kg/d) for 7 days. Treatment with levamisole alone inhibited the serum AP activity (mainly of skeletal origin in mice) by 18.4 and 61.3% for the low and high dose respectively. No deleterious effect on body growth, tibia length, and bone cells population was detected. The moderate inhibition of AP activity produced by the lower dose of levamisole alone (18.4%) or in combination with 1,25(OH)2D3 (37.9%) was associated with a reduced endosteal matrix apposition rate (MaAR) determined by double 3H-proline labeling method. This effect was related to a levamisole-induced fall in serum phosphate. Despite the moderate inhibition of AP activity, the mineral apposition rate (MiAR) determined by the double tetracycline labeling method remained normal. Moreover, 1,25(OH)2D3 infusion still resulted in increased MiAR which was stimulated to the same extent as in the absence of levamisole. By contrast, the more severe inhibition of AP activity induced by 80 mg/kg of levamisole alone (61.3%) or in combination with 1,25(OH)2D3 (45.8%) inhibited both the MaAR and the MiAR and prevented the stimulatory effect of 1,25(OH)2D3 on bone mineralization. The data show that AP activity affects the bone matrix and mineral apposition rates in vivo and that severe inhibition of AP activity inhibits the 1,25(OH)2D3-induced stimulation of bone mineralization in the mouse.

Contrasting effects of 1,25-dihydroxyvitamin D3 on bone matrix and mineral appositional rates in the mouse.

In order to determine the effects of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) on bone matrix appositional rate (Ma AR) and bone mineral appositional rate (Mi AR), three doses (0.06, 0.13 and 0.20 microgram/kg/d) of 1,25(OH)2D3 were continuously infused for seven days in young mice. Histologic parameters of bone formation and resorption were evaluated by morphometric and autoradiographic methods. All doses of 1,25(OH)2D3 increased serum calcium and produced a dose-related increase in the metaphyseal osteoclastic surface and in the number of acid phosphatase-stained osteoclasts. The Mi AR evaluated by double tetracycline labeling was enhanced at all dosage levels. By contrast the Ma AR evaluated by double 3H-proline labeling was decreased at the two highest doses of 1,25(OH)2D3 which also produced growth impairment. We concluded that the continuous administration of 1,25(OH)2D3 in the mouse produces contrasting effects on bone matrix synthesis and calcification, resulting in a dose-related reduction in the amount of osteoid.

Inhibition by aminohydroxypropylidene bisphosphonate (AHPrBP) of 1,25(OH)2 vitamin D3-induced stimulated bone turnover in the mouse.

The purpose of this study was to evaluate whether the 1,25(OH)2D3-induced increased bone mineralization in the mouse occurs in response to stimulation of bone resorption. In order to inhibit bone resorption, 35-day-old mice were given 16 mumol/kg/day of (3-amino-1-hydroxypropylidene)-1, 1-bisphosphonate (AHPrBP) for 10 days, the first injection occurring 3 days prior to the continuous infusion of 0.06, 0.13, or 0.20 micrograms/kg/day of 1,25(OH)2D3 for 7 days. Two groups of mice were treated with AHPrBP or 1,25(OH)2D3 alone. The skeletal changes were assessed by histomorphometric study of caudal vertebrae after double 3H-proline and double tetracycline labelings for evaluation of the matrix apposition rate (MaAR) and mineral apposition rate (MiAR), respectively. Treatment with AHPrBP alone or combined to 1,25(OH)2D3 decreased the number of acid phosphatase-stained osteoclasts and reduced the endosteal MaAR and MiAR and the amount of osteoid. When given alone, 1,25(OH)2D3 increased serum calcium above normal, enhanced the number of histochemically active osteoclasts, and stimulated the endosteal MiAR. Pretreatment with AHPrBP blocked both the increase in serum calcium and the stimulation of the MiAR induced by 1,25(OH)2D3 infusion though serum 1,25(OH)2D3 levels rose according to the dose given. The results show that 1) the serum calcium and the bone resorbing responses to 1,25(OH)2D3 infusion are prevented by pretreatment with AHPrBP, and 2) the stimulatory effect of 1,25(OH)2D3 on the mineralization rate is blocked when bone resorption is inhibited.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of low doses of stable strontium on bone metabolism in rats.

The effects of low doses of oral stable strontium (0.19-0.40% of strontium chloride) on mineral and bone metabolism were examined in normal rats using biochemical and histomorphometrical methods. The strontium levels in serum and bone rose according to the intake of the element. Oral strontium supplementation did not produce deleterious effects on body growth or on mineral homeostasis except a transitory slight decrease in serum calcium. At the dosage level of 0.40% however, strontium induced a slight defective bone mineralization. At lower levels, treated rats showed stimulated bone formation evidenced by increased amount of osteoid and increased extent of tetracycline double-labelled surface while the mineralization lag time remained normal. The osteoclastic surface and the number of acid phosphatase-stained chondroclasts and osteoclasts remained unchanged. Stimulation of bone formation without apparent change in bone resorption resulted in a 10% increase in the trabecular calcified bone volume. The strontium-induced increased osteogenesis was not associated with changes in circulating levels of 1,25(OH)2 vitamin D or in parathyroid hormone effects. The results show that small doses of oral strontium may stimulate bone formation without altering bone resorption in the rat.

Inhibition of bone matrix apposition by (3-amino-1-hydroxypropylidene)-1,1-bisphosphonate (AHPrBP) in the mouse.

To elucidate the mechanism of action of (3-amino-1-hydroxypropylidene)-1,1-bisphosphonate (AHPrBP, formerly APD) on bone metabolism, we have studied the influence of low doses of AHPrBP on bone resorption and formation in the mouse. Thirty-five-day-old mice were given daily injections of 0.16, 1.6, or 16 mumol/kg BW per day of AHPrBP for 10 days. At sacrifice biochemical parameters were measured in serum and bone ash, and histomorphometric parameters of bone formation and resorption were determined on undecalcified sections of caudal vertebrae after double 3H-proline and double tetracycline labelings. Serum calcium and 1,25-dihydroxyvitamin D levels remained normal at all dosage levels. Compared to controls, AHPrBP at doses of 1.6 and 16 mumol/kg per day increased the number of osteoclasts and the number of nuclei per osteoclast but markedly decreased the number of acid phosphatase-stained osteoclasts. Thus, AHPrBP appears to inhibit osteoclastic activity in vivo in part through reduction of acid phosphatase activity. At doses of 1.6 and 16 mumol/kg per day AHPrBP reduced serum alkaline phosphatase and the osteoblastic surface and decreased the endosteal osteoid surface and thickness. Both the matrix apposition rate and the mineral apposition rate were progressively reduced at the endosteal level, although they were not significantly changed at the periosteal level. Greater inhibition of bone resorption than bone formation resulted in increased endosteal bone density and bone mineral content. AHPrBP at a dose of 0.16 mumol/kg per day did not alter either the osteoclastic bone resorption or the mineral and matrix apposition rates.

Carence en iode et reproduction chez les femmes de l'Adamaoua

La malnutrition est aggravee par les deficiences en oligo-elements et l'une des formes les plus connues est la carence en iode qui donne des troubles divers. Cette carence atteint environ 160 millions de personnes en Afrique contre 300 millions en Chine; 200 millions en Inde; 100 millions en Indinesie; 60 millions en Amerique et quelques millions de cas en Europe. Les troubles dus a la carence en iode (TDCI) sont un probleme general qui touche 12de la population mondiale. Au Cameroun; l'enquete nationale sur les TDCI montre que 6 millions de personnes sur 11 millions sont atteintes; de meme que toutes les 10 provinces mais a des taux differentes de prevalence. Ainsi une forte endemicite est signalee a l'Extreme-Nord (Doukoula 75); au Nord-Ouest (64a Oshie et 59a Jakiri); dans l'Adamaoua (45dans Vina); dans Ouest (58dans le Noun) et une endemicite moindre dans l'Est (14a Batouri)