Fluoride stimulation of the rat parathyroid gland: An ultrastructural study

Ream, Larry J.; Principato, Robert

doi:10.1002/aja.1001620305

Cited by 6 publications

(2 citation statements)

References 27 publications

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“…PTH is an important early step in osteoclastogenesis. It is also worth noting that there have been repeated associations between increased fluoride intake and increases in circulating PTH and hyperparathyroidism (Sivakumar and Krishnamachari, 1976;Ream and Principato, 1981;Gupta et al, 2001;Chadha and Kumar, 2004). Stronger evidence of enhanced osteoclastogenesis is the increase in the number of osteoclasts along the bone surfaces in C3H mice.…”

Section: Bone and Bone Biology Studies Involving Inbred Strains Of Micementioning

confidence: 99%

Fluoride’s Effects on the Formation of Teeth and Bones, and the Influence of Genetics

2010

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Fluorides are present in the environment. Excessive systemic exposure to fluorides can lead to disturbances of bone homeostasis (skeletal fluorosis) and enamel development (dental/enamel fluorosis). The severity of dental fluorosis is also dependent upon fluoride dose and the timing and duration of fluoride exposure. Fluoride's actions on bone cells predominate as anabolic effects both in vitro and in vivo. More recently, fluoride has been shown to induce osteoclastogenesis in mice. Fluorides appear to mediate their actions through the MAPK signaling pathway and can lead to changes in gene expression, cell stress, and cell death. Different strains of inbred mice demonstrate differential physiological responses to ingested fluoride. Genetic studies in mice are capable of identifying and characterizing fluoride-responsive genetic variations. Ultimately, this can lead to the identification of at-risk human populations who are susceptible to the unwanted or potentially adverse effects of fluoride action and to the elucidation of fundamental mechanisms by which fluoride affects biomineralization.

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Section: Bone and Bone Biology Studies Involving Inbred Strains Of Micementioning

confidence: 99%

Fluoride’s Effects on the Formation of Teeth and Bones, and the Influence of Genetics

2010

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“…1967;Baylink et al, 1970b;Belanger. 1964;Rich and Feist, 1970], Serum PTH was reported to be tem porarily increased by a single dose of fluo ride in humans [Larsen et al" 1978], Others found parathyroid hyperplasia in fluoridetreated sheep [Faccini and Care, 1965] and rats [Ream and Principato, 1981], There is also a theoretical basis for suspecting sec ondary hyperparathyroidism in fluorosis. Accordingly, the increment in bone forma tion rate induced by fluoride treatment would tend to lower serum calcium and thereby induce increased PTH secretion.…”

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Monofluorophosphate Physiology: The Effects of Fluoride on Bone

Baylink¹,

Duane²,

Farley³

et al. 1983

Caries Res

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Fluoride is an effective agent in the treatment of osteoporosis and is the only available agent that is capable of producing a large increment in bone mass. Fluoride stimulates bone formation largely through its action to increase osteoblast number. In vitro work suggests that the effect of fluoride to increase osteoblast number is due to a direct action of fluoride to stimulate the proliferation of osteoblast precursors. In fluoride-treated patients the increase in bone formation leads to an increase in bone mass as manifested by an increase in X-ray density, which in turn leads to a decrease in bone pain and a decrease in fracture rate. These positive effects are limited to the axial skeleton and are not observed in the appendicular skeleton in the dose used. The increase in bone formation is reflected by an increase in serum total alkaline phoshatase activity, which is due to an increase in the bone isoenzyme and which can be used to assess serially the action of fluoride on bone. Serum total alkaline phosphatase activity measurements indicate that, during 2 years of fluoride treatment, about 80% of patients respond and that the magnitude of the response is quite variable. The major disadvantages of fluoride in the treatment of osteoporosis include: (1) All patients do not exhibit a response. (2) Fluoride treatment causes gastric and joint side effects in a significant proportion of patients.

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Histomorphometric analysis of iliac crest bone biopsies in placebo-treated versus fluoride-treated subjects

et al. 1995

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In a 4-year controlled, prospective trial, histomorphometric analysis was used to compare the tissue-level skeletal effects of fluoride therapy in 43 postmenopausal women (75 mg NaF/day) with those of 35 matching placebo subjects; all subjects received 1500 mg/day elemental calcium supplement. In addition to an initial, baseline biopsy, a second biopsy was obtained after 6, 18, 30 or 48 months. Measurements were made on a third biopsy obtained from 8 subjects following at least 72 months of fluoride therapy. The change in cancellous bone volume or trabecular thickness in fluoride-treated subjects was not different from a change in placebo-treated subjects. However, paired analysis in the fluoride-treated subjects indicated that bone volume was increased between the first and second biopsies (p < 0.005). Both osteoid length and width were significantly increased in fluoride compared with placebo subjects; however, only the osteoid surface increased linearly (r = 0.63, p < 0.001). The mineral apposition rate and relative tetracycline-covered bone surface were not different between fluoride and placebo treatment, although they were decreased in both groups in the second biopsy. The tetracycline-covered bone surface returned to normal in the third biopsy. Definitive evidence for osteomalacia is a prolonged mineralization lag time, which following fluoride treatment was found to be increased 9-fold in the second biopsy and 4-fold in the third biopsy. Further evidence for osteomalacia was increased osteoid thickness by 6 months, evidence of focal areas of interstitial mineralization defects, and broad tetracycline labels of low fluorescence intensity. In the third biopsies, osteoclastic resorption was observed beneath osteoid seams. Fluoride therapy increased the cortical width compared with placebo treatment (p < 0.02), and increased the osteoid surface in Haversian canals, but did not change the osteoid width, resorption surface or cortical porosity. After an initial rise, serum fluoride levels remained constant, and the urine values fell slightly. The bone fluoride concentration rose throughout the treatment period, and was correlated with the change in osteoid-covered bone surface (r = 0.56, p < 0.001). Although we found definitive evidence for osteomalacia, the cause of the osteomalacia was not determined in this study. On the other hand, the presence of bone resorption beneath unmineralized osteoid and of osteocyte halos is suggestive of hyperparathyroidism. Thus, it is possible that the strong stimulus for bone formation brought about by fluoride therapy resulted in relative calcium deficiency.

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Fluoride stimulation of the rat parathyroid gland: An ultrastructural study

Cited by 6 publications

References 27 publications

Fluoride’s Effects on the Formation of Teeth and Bones, and the Influence of Genetics

Fluoride’s Effects on the Formation of Teeth and Bones, and the Influence of Genetics

Monofluorophosphate Physiology: The Effects of Fluoride on Bone

Histomorphometric analysis of iliac crest bone biopsies in placebo-treated versus fluoride-treated subjects

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