Fluoride's Effects on Bone - Dr. John Lee's Site

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Fluoride's Effects on Bone - Dr. John Lee's Site

JoAnn Guest Dec 17, 2004 17:55 PST

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Fluoride's Effects on Bone as read from Dr. John Lee's Site

 

http://www.johnleemd.net/breaking_news/fluoridation_02.html

 

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Fluoride's Effect on BONE - and some related considerations

T.C. Schmidt – 12 March 2000

 

Foreword. Except for the introductory sentence (from a textbook);

one CDC document; two FDA documents; and the NIOSH RTECS (as referenced

in the text per se.)

 

the technical basis for this review has been LIMITED on purpose ONLY to

those citations which are retrievable on-

line from the National Library of Medicine (PubMed MEDLINE and/or

Internet Grateful Med TOXLINE).

 

Introduction

 

Bone tissue has long been recognized as a key accumulation site for

some toxic substances –

" bones also serve a " detoxicating " function,

elements such as lead, radium, fluorine and arsenic being removed

from circulation and deposited into bones and teeth " (The

Physiological Basis of Medical Practice, 1961).

 

That is, fluoride 'accumulates' in skeletal tissue, concentrating in the

surface layers of the lacunae and canaliculae -- thus helping to clarify

the pathogenesis of the osseous lesions seen in skeletal fluorosis

(Smith, 1985a).

 

Bone samples from cadavers show that fluoride content of trabecular bone

correlates with that of the drinking water --

 

with histomorphic bone changes becoming markedly increased when water

fluoride content exceeds 1.5-ppm (Alrnala, et al. 1985).

 

Thus, daily intake of fluoride that is deemed beneficial to developing

teeth, if ingested throughout adult life,

 

may lead to skeletal " fluorosis' of varying degrees, plus certain

disorders that are now becoming common

in both the middle-aged and elderly (Smith, 1985b).

 

This was more recently substantiated in a review (Diesendorf, et al.

1997) -- showing " a consistent pattern of evidence " .

 

Osteoporosis in the long bones may provide the earliest radiographic

indicator of fluorosis (Lian and Wu, 1986); with clinical radiological

aspects including

" calcification " and/or ossification of the attachments of the 'soft-

tissue' structures to bone, osteosclerosis, osteopenia, growth lines,

and metaphyseal osteomalactic zones (Wang, et al. 1994).

 

More subtle changes as stained section and microradiograph include

interstitial mineralization defects and mottled eperiosteocytic lacunae

(Boivin,

et al. 1989) and CT/MR imaging are very helpful in early diagnosis

(Reddy, et al. 1993).

 

Lessons-Learned from Therapy

 

Water fluoridation proponents like to tout that fluoride is used as

a " treatment " for osteoporosis.

Despite more than several decades of research, the

efficacy " remains controversial " (Kopp and Roby, 1990;

inter-alia);

and it has NOT been approved as a treatment by FDA.

 

Even adherents now recommend restricting prospective clinical trials to

axial skeleton only -- provided that the patient has good peripheral

bone density, renal function and vitamin-D status (Dequeker and

Declerck, 1993).

 

However, unless the patients receiving fluoride are also closely

monitored for the onset of osteo-fluorosis, there are

examples (Tollefsen, et al. 1995; Mrabet, et al. 1995)

contraindicating this treatment approach, even for such very select

cases.

 

Side effects include gastro-intestinal problems and " painful

lower extremity syndrome " -- and " experience has taught that denser

bones are not necessarily better bones " (ibid, 1995).

 

This is consistent with earlier findings (Stein and Granik, 1980)

that although increased bulk might offset the reduced static

compressive strength of vertebral bone which presented as a function

of the fluoride content, it may also become more brittle, thus

rendering it more likely to fracture on impact.

 

Similarly, based on small-angle x-ray scattering and backscattered

electron imaging of the vertebrae of mini-pigs treated with fluoride

(Fratzl, et al.

1996) changes in the mineral/collagen composite were evident, which

helped explain the reduction in the bio-mechanical properties due to

fluoride treatment that were found in earlier studies.

 

These reductions were comparable to the vertebral bone strength results

found in rats after fluoride treatment (Sogaard, et al. 1995a), which

concluded " the increase in bone mass during fluoride treatment does

not translate into an improved bone strength -- rather, bone quality

declines " .

 

Not only does this approach not exhibit any efficacy for

the axial skeleton based on vertebral fracture incidence (Hillier,

et al. 1996) but to make matters worse this is " achieved at the expense

of bone-mineral in the peripheral cortical skeleton " .

 

That is, in prospective clinical trials comparing fluoride treatment vs

a placebo, not only was there was no decrease in vertebral fracture

rate, but there was an increase in non-vertebral (hip) fractures

(Riggs, et al. 1990; Riggs, et al. 1994).

 

Per FDA Consumer (April,

1991) that study included the use of calcium and resulted in a 35%

increase in bone mass but " the new bone was weak and structurally

abnormal " .

 

Indeed, the difference in rate of hip fractures for fluoride treated

patients vs non-treated is ten-times higher than

would normally be expected (Hedlund and Gallagher, 1989).

 

Likewise, fluoride treatment was found to result in a nine-fold

increase in definitive osteomalacia (Lundy, et al. 1995) which was

attributed to a prolonged mineralization lag time, as well as a

resultant relative calcium deficiency.

 

Although the latter might be expected to be ameliorated by

incorporating calcium supplements, such

a double-blind clinical trial (Kleerekoper, et al. 1991) showed this

to be no more effective than placebo in retarding the progression of

spinal osteoporosis.

 

Similarly, fluoride with both calcium and vitamin-D, is no more

effective than calcium and vitamin-D alone (Meunier, et al. 1998).

 

That fluoride cannot be recommended as a

prophylactic agent for the fractures that are the primary adverse

health outcome of osteoporosis (Melton, 1990) is supported by

patient bone biopsies (Sogaard, et al. 1994; Sogaard, et al. 1995b) in

which bone fluoride level increased significantly after 1-year and 5-

years - - however, after 5-years of " treatment " decreases in trabecular

bone

strength and quality were 45% and 58%, respectively.

 

Whereas bone mass and architecture in all appendicular and most

axial sites is normally controlled by loading history, the new bone

formed

as a result of artificially stimulated bone remodeling using

fluoride is exclusively appositional, with no creation of new trabeculae

(Balena, et al. 1998).

 

It has an " abnormal texture " that is less

strong (Lips, 1998), and the loss in trabecular strength due to the

adverse influence of fluoride treatment altering the normal control

has been calculated (Carter and Beaupre, 1990).

 

Although the increased fragility has been attributed to both hypo- and

hyper- mineralization, the net result is " identical to that of heavy

fluorosis " (Fratzl, et al. 1994) -- characterized by the presence of

additional large crystals, located outside the collagen fibrils.

 

These large crystals (calcium-fluoride) which are not present in

either controls or osteoporotic bone before the fluoride treatment

contribute to increased mineral density with no improvement in

mechanical properties (ibid, 1994).

 

Again, even for the select case of axial vertebral fracture, U.S.

randomized double-blind study shows no beneficial effect (Zeigler, 1991)

-- such that the subsequent FDA

Guidelines for Preclinical and Clinical Evaluation of Agents Used in

the Prevention of Treatment of Postmenopausal Osteoporosis (1994;

pub. 1997) states " the relation between increased bone mass density

and reduced fracture risk has been validated for patients receiving

estrogens, but not fluoride " .

 

Yet, the fluoride proponents still keep on trying (e.g., Gitomer, et

al. 2000) to show what does NOT exist --

 

an efficacious balance between increased bone mass and deterioration

of the bone material properties.

 

Similarly, an issue of Journal of

Dental Research (Turner, et al. 1995) states that fluoride affects

bone strength more severely in older animals – but the " responsible

mechanism " is unknown.

 

Etiology

 

During prolonged exposure of adult bone to fluoride,

the early uptake is variable and depends on the remodeling activity.

Regardless of whether or not the rate of uptake into bone stabilizes

at a maximum level following an initial period of increasing

rapidity (Boivin, et al. 1988), the effect is as follows. While simple

in-

vitro soaking reduces rigidity with a 45% decrease in torsional

strength (Silva and Ulrich, 2000), the remodeling process is changed

by altering the normal balance between resorption and formation,

accompanied by a retardation of subsequent mineralization (Ream,

1981; Grynpas, 1990; Mohr, 1990; Dequeker and Declereck, 1993;

Kleerekoper, 1996).

 

That the net result is reduced strength per unit

of bone has been confirmed based on fracture stress and x-ray

diffraction, even if no fluorosis or osteomalacia is observed

histologically (Turner, et al. 1997).

 

That bone uptake as calcium-

fluoride in-vitro (Okazaki, et al. 1985) occurs in-vivo with a

concomitant reduction in strength has been confirmed (Kotha, et. al.

1998).

 

And, the premise that this calcium-fluoride may effect the

interface bonding between the bone mineral and the organic matrix of

the bone tissue (ibid, 1998) is basically the same as the contention

(Walsh, et al. 1994) that the reduction in both the tensile and

compressive properties is attributable to " a constituent interfacial

de-bonding mechanism " .

 

That is, after initial octacalcium-phosphate

nucleation (Bodier-Houlle, et al. 1998), a cartilaginous type matrix

results from abnormal mineralization during the matrix maturation

(Susheela and Jha, 1983), most likely due to the effects on

glycosaminoglycan and proteoglycan synthesis (Waddington and

Langley,

1998).

 

Epidemiology

 

Fluoride is a cumulative " toxin " , adversely affecting the homeostasis of

bone mineral metabolism.

 

Total ingested fluoride is the most important factor determining the

clinical course of osteo-fluorosis,

which is on the increase world-wide (Krishnamachari, 1986).

 

A level of 4-10 ppm in drinking water causes progressive ankylosis of

various joints and crippling deformities irrespective of other variables

–

as evidenced by skeletal radiology and scintigraphy, cross-correlated

with urinary and serum fluoride levels (Gupta, et al. 1993).

 

At greater than 4-ppm for longer than 10-years (Haimanot, 1990) there is

generalized osteophytosis and sclerosis with reduction in diameter of

nter-vertebral foramina and spinal clonal. Animal studies (Turner, et

al. 1996) showed fluoridated water equivalent to only 3-ppm in humans

results in reduced bone strength after 6-months -- when

accompanied by renal deficiency.

 

Similarly, comparison of a control

community having a fluoride content of 1-ppm and that of another

with a 4-ppm level (Sowers, et al. 1991) showed a 95%

confidence-interval (CI) for the 5-year relative risk (RR) for women of

any fracture of 1.0-4.4 -- and for wrist, spine or hip it was 1.1-4.7.

 

That such increase in risk correlates with fluoride accumulation was

corroborated based on a study of toenail fluoride concentration in

more than 64,000 women (Feskanich, et al. 1998) -- comparing the

highest quartile against the lowest quartile provided a 95% CI 0.2-

4.0 for hip fracture RR, and 0.8-3.1 for forearm fracture.

 

That detrimental accumulation occurs due to water fluoridation at

the " public health goal " was shown by comparing fluoridated and non-

fluoridated areas (Alhava, et al. 1980) with the highest

accumulations being in women with severe osteoporosis.

 

That reduction in bone strength presents clinically at the " public

health goal " -- the 95% CI RR for hip fracture of fluoridated vs

non-fluoridated

(Jacobsen, et al. 1992) was 1.06-1.10 for women and 1.13-1.22 for

men. Similarly, for femoral neck fracture the 95% CI of RR was 1.08-

1.46 for women and 1.00-1.81 for men (Danielson, et al. 1992) -- and

a study (Kurttio, et. al. 1999) showed a 95% CI for hip fracture

among younger women of 1.16-3.76.

 

Related Considerations

 

During treatment with fluoride for spinal osteoporosis, some

patients suffered spontaneous bilateral hip fractures (Gerster, et al.

1983)

with histological examination revealing severe osteo-fluorosis --

attributed to excessive retention of fluoride due to renal

insufficiency.

 

Fluoride is " nephrotoxic " , causing lesions of kidney

tubule (Kassabi, et al. 1981).

 

Acute renal failure results from accidental industrial exposure to

fluoride (Usada, et al. 1998); with the nephrotoxic effects related to

serum fluoride level.

 

Not only does this result in " aluminum deposition " into bone (Ittel, et

al.

1992); as fluoride elimination is via the kidney (Kono, 1994) and

decreased kidney function results in increasing serum fluoride, a

vicious cycle is not unlikely (Marumo and Li; 1996). Elevated PTH is

not uncommon in fluorosis (Srivastava, et al. 1989) and is a uremic

toxin playing a major role in nervous system dysfunction

(Smogorzewski and Massry, 1995) and development of hypertension

(Uchimoto, et al. 1995). Also, there is evidence that detrimental

effects on kidney function may occur at fluoride levels associated

with the " misuse " of fluoridated dentifrice by children (Borke and

Whitford; 1999). Finally, while CDC calls for a normal control range

for school fluoridation systems of up to 6.5-ppm (Water

Fluoridation:

A manual for water plant operators; 1994) the following relate the

deleterious renal and other effects caused by a bottled mineral

water

at 8.5-ppm (Alexandra, et al. 1984; Arlaud, et al. 1984; Noel, et

al.

1985; Camous, et al. 1986; Boivin, et al. 1986; Lantz, et al. 1987;

Welsch, et al. 1990; Haettich, et al. 1991; Nicolay, et al. 1997 and

1999).

 

Some epidemiological studies indicate that men may have a greater

susceptibility to the detrimental effects of fluoride on bone

strength (Karagas, et al. 1996; inter-alia); a comparison of

fluoridated and non-fluoridated areas revealed a significant

increase

in osteosarcoma among males under 30-years of age (Mahoney, et al.

1991); the animal model also produces male osteosarcomas (Bucher, et

al. 1991); and a gender-specific physiologically based pharmokinetic

model has been developed to describe the absorption, distribution

and

elimination of fluoride (Rao, et al. 1995). Testosterone deficiency

is a major risk factor for male osteoporosis (Katznelson, 1998); and

fluoride correlates with decreased testosterone levels (Susheela and

Jethanandani, 1996), as well as reduced sperm count and motility

(Narayana and Chinoy, 1994). In most likelihood, this is the

causative factor for reduced fertility rate in areas of the U.S.

having fluoride levels of at least 3-ppm (Freni, 1994). That is,

based on the deleterious testicular effects in three different

animal

models (Chinoy and Sequeira, 1989; Sushella and Kumar, 1991;

Krasowski and Wlostowski, 1992; Kumar and Sushella, 1994 and 1995)

this decrease in the total fertility rate due to ingested fluoride

is

paternal in nature. As CDC now " celebrates " the fifty-years of water

fluoridation as being one of the greatest public health advances of

the century, the following have documented very significant

(approximately 50%) decrease in human semen quality (both seminal

volume and mean sperm density) concomitant with a very significant

(300-400%) increase in testicular cancer over the past fifty-years –

(Carlsen, et al. 1992; Giwercman, et al. 1993; Carlsen, et al. 1995;

Skakkebaek, et al. 1998; Medras and Jankowska, 1999; Sinclair,

2000).

While those references assert that this must be due to some (albeit

undetermined) environmental pollutant, the previous mentioned study

showing decreased total fertility rate in the areas of the U.S. with

water fluoride levels of at least 3-ppm (ibid, 1994) has a consensus

p-value of 0.0002 - 0.0004.

 

In addition to being a " reproductive effector " (due to both paternal

and maternal effects) the compound descriptors for sodium-fluoride

in

the NIOSH Registry of Toxic Effects of Chemical Substances (RTECS)

also include " tumorigen " and " mutagen " . The latter is based on more

than 40 positive results including the following -- unscheduled DNA

synthesis and DNA inhibition of human fibroblast; cytogenic analysis

of human fibroblast, human lymphocyte, and other human cells;

mutation in human lymphocyte; and DNA inhibition in human lung.

Similarly, another review of genetic toxicity (Zeiger, et al. 1993)

states that gene mutations in human cells were produced in the

majority of cases, and " the weight of the evidence leads to the

conclusion that fluoride does result in increased chromosome

aberrations " .

 

The " painful lower extremity syndrome " from fluoride treatment has

been attributed (O'Duffy, et al. 1986) to stress fractures. An

associated fibromyalgia however, should not be dismissed out of

hand.

It is associated with " chronic fatigue syndrome " , and there is a

relationship between chronic fatigue and pineal gland calcification

(Sandyk and Awerbuch, 1994) with the latter consisting of apatite

crystals similar in size and structure to dentin and bone (Nakamura,

et al. 1995). Thus, fluorides potential to acerbate soft-tissue

pathologies in general, deserves further consideration. Similarly,

the cognitive difficulties that result from exposure to fluoride

(Spittle, 1994) are accompanied by general malaise and fatigue;

intolerance to low levels of environmental chemicals is a

polysymptomatic sequela of chronic fatigue, fibromyalgia, etc.

resulting from an immunological and/or a neurogenic triggering of

somatic symptoms and inflammation (Bell, et al. 1998); and the

earliest subjective symptoms of osteo-fluorosis are arthritic in

nature.

 

Side-effects of fluoride treatment also include gastro-intestinal

problems simply referred to as -- " symptoms " (Riggs, et al.

1990); " intolerance " (Dequeker and Declerick, 1993);

and " complaints "

(Lips, 1998). In two separate studies, the comparative results

between patients receiving fluoride treatment for 3-12 months (Das,

et al. 1994) and those having documented osteo-fluorosis (Dasarathy,

et al. 1996) were identical - 70% endoscopic abnormalities, 70-90%

histologic chronic atrophic gastritis; and 100% microscopic

abnormalities such as loss of microvilli.

 

Moreover, these affects were also qualitatively similar to a study

(Gupta, et al. 1992) that

correlated non-ulcer dyspepsia with ingested fluoride level. As

expected, symptoms occurring at the (RTECS) human acute TDLo dosage

of only 214 ug/kg are gastrointestinal.

 

Similar to curing osteoporosis, fluoride has been proposed as a

preventive measure (sic) against Alzheimer's Disease (AD) based on

the presumption that by direct competition in the gut, fluoride

would

decrease aluminum uptake (Kraus and Forbes, 1992). Rather, such

antagonism (Li, et al. 1990) is due to the formation of aluminum-

fluoride complex (Li, et al. 1991). That fluoride potentiates neuro-

toxicity of aluminum has been substantiated (van der Voet, et.al.

1999) -- consisting of interference with neuronal cytoskeleton

metabolism.

 

Aluminum accumulations have been found in nuclei of the

paired-helical filament (PHF) containing neurons in the brains of

both AD patients and elderly normal controls (Shore and Wyatt, 1983)

but as no elevations of aluminum were found in serum or

cerebrospinal

fluid of AD patients, aluminum alone is not the cause – rather,

aluminum in PHF bearing neurons is simply a " marker " . Fluoride had

been deemed to be a potent stimulator of bone formation (Farley, et

al. 1983), but most recent work indicates that the mitogenic effect

on osteoblasts is due to fluoro-aluminate (Caverzasio, et al. 1997;

Susa, et al. 1997) -- while another model claims the mitogenic

action

is non-specific (Lau and Baylink,1998). In the animal model, 0.5-ppm

aluminum-fluoride for one-year resulted in decreased neuronal

density

and " necrotic-like " brain-cells (Varner, et al. 1998). Also,

fluoride

decreases protein content of brain tissue (Shashi, et al. 1994) with

7-months of 30-ppm fluoride resulting in a 10% decrease in total

brain phospholipid content (Guan, et.al. 1998) – as well as

(biphasic) changes in brain levels of coenzyme-Q (Wang, et al.

1997).

Osteo-fluorosis is endemic in certain regions of China (Dasheng and

Cutress, 1996) with detrimental effects of fluoride on the IQ of

children now being documented (Yang, et al. 1994; Li, et al. 1995).

 

Just as ingested fluoride has a deleterious effect on bone, the same

is true for developing teeth. Dental fluorosis (enamel hypoplasia)

is

a form of lesion (Limeback, 1994; Fejerskov, et al. 1994) now having

an incidence (Clark, 1994) of 35-60% in fluoridated areas of N.

America. Most studies (Wiktorsson, et al. 1991; Kobayashi, et al.

1992; Frencken, et al. 1992; Ismail, et al. 1993; Vignarajah, 1993;

Hartshorne, et al. 1994; Cisternas, et al. 1994; Akpata, et al.

1997;

Ibrahim, et al. 1997; Wang and Riordan, 1999; Angelillo, et al.

1999)

show no statistically significant decrease in the incidence of

dental

caries from ingested fluoride. Indeed, caries in permanent dentition

increase with increasing dental fluorosis (Mann, et al. 1990); the

odds ratio for developing dental fluorosis increases with decreasing

age of exposure (Ismail and Messer, 1996); caries decrease after

cessations of water fluoridation (Seppa, et al. 1998; Kunzel and

Fischer, 1997 and 2000); and incidence correlates with elevated

blood

lead levels (Moss, et al. 1999) with the heavily fluoridated North-

Eastern U.S. having a greater incidence than the less fluoridated

Western portions. As the caries decrease over the past 50-years is

NOT due to water fluoridation (Miyazaki and Morimoto, 1996; Evans,

et

al. 1996; Einarsdottir and Bratthall, 1996; de Liefde, 1998) general

consensus attributes it to fluoridated dentifrice. The extent of

that

is now being questioned however (Nadanovsky and Sheiham, 1995;

Haugejorden, 1996); with speculation as to the actual cause

including

changes in oral microbial flora (Einarsdottir and Bratthall, 1996)

and antibiotics (de Liefde, 1998).

 

Peer Review Journal References Cited in the Text – with more than

80%

of them being published within the past ten-years

 

Akapa, et al. (1997). Dental fluorosis in 12-15-year-ol rural

children exposed to fluorides from well drinking water in the Hail

region of Saudi Arabia. Community Dent Oral Epidemiol; 25(4): 324-

327.

 

Alexandre, et al. (1984). Fluoride poisoning caused by Vichy Saint-

Yorre water. [title only; article in French]. Presse Med; 13(16);

1009.

 

Alhava, et al. (1980). The effect of drinking water fluoridation on

the fluoride content, strength and mineral density of human bone.

Acta Orthop Scand; 51(3): 413-420.

 

Angelillo, et al. (1999). Caries and fluorosis prevalence in

communities with different concentrations of fluoride in the water.

Caries Res; 33(2):114-122.

 

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Fluoride & Osteoporosis: Endemic Fluorosis Studies

 

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Fluoride & Osteoporosis: Endemic Fluorosis Studies

 

http://www.slweb.org/fluoride-bone.html#5

 

Krishnamachari KA, Krishnaswamy K. (1973). Genu valgum and

osteoporosis in an area of endemic fluorosis.

 

The Lancet. 2(7834):877- 879.

 

" Anteroposterior views of the cervicothoracic and lumbodorsal spine

showed the presence of osteosclerosis in all but two patients.

 

The most striking radiological feature, however, was severe osteoporosis

 

of the lower end of the femur and upper ends of the tibia and fibula

and rarefaction of the metacarpal bones.

 

In some patients, rarefaction of pelvic bones, femoral neck, and lower

ends of radius and ulna was also observed. "

 

Christie DP. (1980). The spectrum of radiographic bone changes in

children with fluorosis. Radiology. 136(1):85-90.

 

" Painful, crippling deformities in Tanzanian children from an area of

endemic fluorosis reported... Combinations of osteomalacia,

osteoporosis, and osteosclerosis result in a spectrum of bone changes

from an early age. "

 

Lian ZC, Wu EH. (1986). Osteoporosis--an early radiographic sign of

endemic fluorosis. Skeletal Radiol. 15(5):350-3.

 

" Radiological investigation of skeletal fluorosis was carried out

among the inhabitants from two areas where the fluoride content of

water was high, using both conventional radiography and radiographic

measurements of bone mineral content (BMC)...

 

It is very interesting to observe that in the majority of our cases,

osteosclerosis in the

spine and pelvis was always combined with osteoporosis of the long

bones. It might be an indication that the axial skeleton undergoes a

quite different pathological process from the appendicular

skeleton... "

 

Mithal A, et al. (1993). Radiological spectrum of endemic fluorosis:

relationship with calcium intake. Skeletal Radiol. 22(4):257-61.

 

" Skeletal fluorosis continues to be endemic in many parts of India.

 

Osteosclerosis and interosseous membrane calcification have long been

regarded as hallmarks of this disease.

 

Our study showed in addition a wide variety of radiological patterns:

coarse trabecular pattern, axial osteosclerosis with distal osteopenia

and diffuse osteopenia.

 

Wang Y, et al. (1994). Endemic fluorosis of the skeleton:

radiographic features in 127 patients. Am J Roentgenol. 162(1):93-8.

 

This study examines the radioagraphic features of 127 patients with

skeletal fluorosis. It is reported that 54% of the patients have

osteosclerosis, while 40% have osteopenia (osteoporosis, 22% &

osteomalacia, 18%).

 

According to the authors: " Two different

osteopenic patterns were defined: an osteoporotic pattern with

overall decreased bone density and an osteomalacic pattern that

combines the features of osteoporosis with bone deformity. "

 

The authors note how, in the past, skeletal fluorosis was " thought to

result merely in osteosclerosis " but that " later, various radiologic

features were found, including osteosclerosis, osteomalacia, and

osteoporosis. "

_________________

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