"The effect of fluoride on osteoclasts is less well understood
than its effect on osteoblasts, and is complicated
by a possible effect of fluoride-induced secondary hyperparathyroidism."
SOURCE: Chachra D, et al. (1999). The effect
of fluoride treatment on bone mineral in rabbits. Calcified
Tissue International 64:345-351.
"The toxic effects of fluoride were
more severe and more complex and the incidence of metabolic bone
disease (rickets, osteoporosis, parathyroid
hormone bone disease) and
bony leg deformities was greater (>90%) in children
with calcium deficiency as compared to in children with adequate
calcium who largely had osteoslcerotic form of skeletal fluorosis..."
SOURCE: Teotia M, Teotia SP, Singh KP. (1998). Endemic chronic
fluoride toxicity and dietary calcium deficiency interaction syndromes
of metabolic bone disease and deformities in India: year 2000.
Indian Journal of Pediatrics 65:371-81.
In the fluoride-treated bone "we observed osteoclasts resorbing
bone beneath osteoid seams, and fragments
of osteoid isolated in the bone marrow. This type of resorption
beneath unmineralized bone matrix is often observed in osteomalacia,
particularly that caused by renal
abnormalities and associated secondary
hyperparathyroidism."
SOURCE: Lundy MW, et al. (1995). Histomophometric analysis of
iliac crest bone biopsies in placebo-treated versus fluoride-treated
subjects. Osteoporosis International 5:115-129.
"Although some authors have suggested
that the resorption observed in skeletal
fluorosis is due to secondary hyperparathyroidism in
humans and in fluoride-treated animals, others have found
no effect of fluoride on parathyroid mass or serum parathyroid
levels in animal studies."
SOURCE: Lundy MW, et al. (1995). Histomophometric analysis of
iliac crest bone biopsies in placebo-treated versus fluoride-treated
subjects. Osteoporosis International 5:115-129.
"Other diseases simulating radiographic
features of fluorosis are Paget's
disease, parathyroid hormone disorders,
osteopetrosis, chronic renal failure, myelofibrosis,
hypophosphatemic osteomalacia, and diffuse blastic metastases."
SOURCE: Fisher RL, et al. (1989). Endemic fluorosis with spinal
cord compression. A case report and review. Archives of Internal
Medicine 149: 697-700.
"Secondary hyperparathyroidism
has been suggested as a possible mechanism by which fluoride produces
changes in bone, and hyperparathyroidism has been found
in some humans and experimental animals exposed to fluoride. The
experimental pigs examined in the present study, however, showed
no signs of hyperparathyroidism."
SOURCE: Kragstrup J, et al. (1989). Effects of fluoride on cortical
bone remodeling in the growing domestic pig. Bone 10:421-424.
"A combination of osteosclerosis,
osteomalacia and osteoporosis
of varying degrees as well as exostoses formation characterzes
the bone lesions (of skeletal fluorosis).
In a proportion of cases secondary hyperparathyroidism
is observed with associated characteristic bone changes."
SOURCE: Krishnamachari KA. (1986). Skeletal fluorosis in humans:
a review of recent progress in the understanding of the disease.
Progress in Food and Nutrition Sciences 10(3-4):279-314.
"Metabolic bone disease occurred more frequently in residents
of endemic (fluorosis) areas than in residents
of nonendemic areas whose nutritional status was comparable. Common
metabolic bone disorders, associated with endemic skeletal fluorosis,
were osoteoporosis (bone
resorption), rickets, osteomalacia,
and parathyroid bone disease."
SOURCE: Teotia SPS, et al. (1984). Environmental fluoride and
metabolic bone disease: an epidemiological study (fluoride and
nutrient interactions). Fluoride 17: 14-22.
"Fluoride, by the nature of its incorporation into bone
crystals and by its direct cytotoxic effect on bone resorbing
cells, reduces the availability of calcium from bone. It appears
that fluoride ingestion during lactation created a heightened
state of calcium homeostatic stress. As a result, bone mineral
was mobilized by resorption of the endosteal surface and by cavitation
of the interior of the cortex. Secondary
hyperparathyroidism is thought
to play an integral part (in skeletal fluorosis) in an attempt
to maintain calcium homeostasis."
SOURCE: Ream LJ, et al. (1983). Fluoride ingestion during multiple
pregnancies and lactations: microscopic observations on bone of
the rat. Virchows Arch [Cell Pathol] 44: 35-44.
"The inhibition of resorptive function together with the
decreased level at which bone and serum calcium equilibrate after
the incorporation of fluoride would lead
to a fall in serum calcium and a compensatory increase in parathyroid
hormone secretion. This rise in serum parathyroid hormone
would stimulate the differentiation of progenitor cells into both
osteoblasts and osteoclasts."
SOURCE: Ream LJ. (1983). Scanning electron microscopy of the rat
femur after fluoride ingestion. Fluoride 16: 169-174.
"unopposed fluoride may lead to hyperparathyroidism"
SOURCE: Vigorita VJ, Suda MK. (1983). The microscopic morphology
of fluoride-induced bone. Clinical Orthopaedics and Related
Research 177:274-282.
"The mechanism leading to the hyperfunction
of the parathyroid glands in skeletal
fluorosis is not clear. Studies on growing rabbits
have suggested that fluoride, probably by producing a more stable
fluorapatite, reduced the resorption of the fluoride containing
bone with a resultant increase in the resorption of normal non-fluoride
containing bone and that the hyperfunction of the parathyroids
is, therefore, a compensatory mechanism which, probably, develops
to maintain the plasma calcium and to overcome the physical effects
of the more stable and less reactive fluoroapatite crystals. Jowsey
et al (1972) argue that the secondary hyperparathyroidism seen
in fluorosis is due to the fact that fluoride directly stimulates
osteoblastic activity and that the calcium intake is insufficient
to mineralise the rapidly forming new bone tissue. They cite evidence
for this from the report of a decreased incidence of radiologically-recognised
endemic fluorosis in areas with a high calcium content in the
drinking water. More significantly, Jowsey and her co-workers
(1972) have found that by combining vitamin D and calcium supplements
with fluoride they were able to stimulate bone growth in osteoporotic
patients wtihout producing a, concomitant, increase in bone resorption."
SOURCE: Faccini JM, Teotia SPS. (1974). Histopathological assessment
of endemic skeletal fluorosis. Calcified Tissue Research
16: 45-57.
"the increased production of (parathyroid
hormone) is strongly suggested by the marked increase in the
number of trabecular resorption surfaces and the pattern of tunnelling
resorption observed."
SOURCE: Faccini JM, Teotia SPS. (1974). Histopathological
assessment of endemic skeletal fluorosis. Calcified Tissue
Research 16: 45-57.
"The increased bone resorption stimulated
by fluoride administration may be due to excessive parathyroid
activity."
SOURCE: Riggins RS, et al. (1974). The effects of sodium fluoride
on bone breaking strength. Calcified Tissue Research 14:
283-289.
"Fluoride administration in both man
and animals has been shown to stimulate new bone formation. However,
the bone is poorly mineralized, and osteomalacia
and secondary hyperparathyroidism frequently occur."
SOURCE: Jowsey J, et al. (1972). Effect of combined therapy with
sodium fluoride, vitamin D and calcium in osteoporosis. The
American Journal of Medicine 53: 43-49.
"[T]here are a number of similarities
between the effects of excess parathyroid hormone and the
administration of fluoride on bone... In the present study
secondary hyperparathyroidism would be a reasonable explanation
for the observed increase in endosteal bone resorption, endosteal
resorbing surface, and the linear rate of bone resorption (in
the fluorotic animals)."
SOURCE: Baylink D, et al. (1970). Effects of fluoride on bone
formation, mineralization, and resorption in the rat. In: TL Vischer,
ed. (1970). Fluoride in Medicine. Hans Huber, Bern. pp. 37-69.
"The frequent description in the literature
of large resorption cavities with fibrous tissue replacement suggested
to me that the parathryoids were overactive in skeletal
fluorosis, and this was demonstrated by an electron-microscopic
study of the parathyroid glands from fluorotic sheep
and a concomitant immunoassay of the amount of circulating
parathyroid hormone, which was found to be as much as five times
higher than resting levels and control levels."
SOURCE: Faccini JM. (1969). Fluoride and bone. Calcified Tissue
Research 3:1-16.
"The demonstrable hyperactivity
of the parathyroid glands in fluorotic rabbits and sheep in
the presence of this inhibition of resorption suggests that it
is a compensatory phenomenon to maintain the serum calcium at
a constant level."
SOURCE: Faccini JM. (1969). Fluoride and bone. Calcified Tissue
Research 3:1-16.
"Osteosclerosis from chronic
renal disease associated with secondary hyperparathyroidism
may produce similar changes (as skeletal fluorosis), and
indeed may have intensified the findings (of fluorosis) in one
of our patients."
SOURCE: Morris JW. (1965). Skeletal fluorosis among indians of
the American Southwest. American Journal of Roentgenology,
Radium Therapy & Nuclear Medicine 94: 608-615.
"While some authors consider the (fluorosis) lesion to be
a form of osteosclerosis, others attribute it to mineral deficiency
characterized by an increase of osteoid formation. Some
consider the osseous condition a response to parathyroid hyperfunction
or intoxication; others have reported the aggravating
effects of a calcium deficient diet. Studying young dogs, Kellner
reported a gross similarity between the bony changes in fluorosis
and rickets."
SOURCE: Belanger LF, et al. (1958).
Rachitomimetic effects of fluoride feeding on the skeletal tissues
of growing pigs. American Journal of Pathology 34: 25-36.
Back to top
