Fluoride Action Network

Skeletal Fluorosis: The Misdiagnosis Problem

F.A.N. | May 2012 | By Michael Connett

Skeletal fluorosis, even in its most advanced crippling phase, can be easily misdiagnosed as another type of bone disease if doctors fail to test for fluoride. As the studies below show, doctors in the U.S. have repeatedly failed to detect even the most severe, crippling forms of fluorosis, resulting in years of prolonged suffering  for their misdiagnosed patients. There are four factors that explain this failure:

The first is that symptoms of joint pain and stiffness can precede the development of detectable bone changes. This “pre-skeletal” phase of the disease is extremely difficult to diagnose, as the symptoms are “non-specific” and indistinguishable from the joint pains of common arthritic conditions.

The second factor is that, even when bone changes do occur, they may not look like the classic form of skeletal fluorosis, in which the first and most prominent bone change is “axial osteosclerosis” (increased density of the spine, pelvis, and ribs).  Some fluorosis victims, for example, may experience osteophytes (bone spurs) and interosseus membrane calcification in the peripheral skeleton without signs of osteosclerosis in the spine. (Wang 2007; Savas 2001). In other fluorosis victims, the bone changes may display primarily as  osteomalacia, osteoporosis, secondary hyperparathyroidism, or combinations thereof. In short, the x-ray picture of skeletal fluorosis is not uniform, and can vary quite significantly between individuals. To the extent, therefore, that doctors consider axial osteosclerosis to be a pre-requisite finding for a diagnosis fo fluorosis, some patients with skeletal fluoride poisoning will fall through the cracks.

Third, even when the bone changes typical of classical fluorosis are present, they can mimic the appearance of other diseases, including osteoarthritis, spondylosis, DISH, renal osteodystrophy, Paget’s Disease, osteopetrosis, and bony metastasis. As noted by a team of American doctors who treated a woman with crippling skeletal fluorosis: “Our case report illustrates dramatically that fluorosis can lead to severe disability while closely mimicking a wide variety of other disorders… We believe increased awareness of this unusual disease is needed to enable physicians to make the proper diagnosis.” (Fisher 1989).

The fourth factor explaining the frequency of misdiagnosis is that current medical understanding of skeletal fluorosis has been shaped by longstanding, but now scientifically discredited, notions that the levels of fluoride necessary to produce fluorosis (as measured by the daily dose or water/urine/blood/bone fluoride content) are uniform across the poplation and far higher than the vast majority of individuals in western populations ever receive.

As a result of these four factors, it is a virtual certainty that individuals in the general population who have some form of skeletal fluorosis are being misdiagnosed as suffering from more commonly known conditions (e.g., osteoarthritis, spondylosis, etc). Proof that this is the case can be found in the following case reports of skeletal fluorosis written by doctors in the U.S. and other western countries. As can be seen, a recurring feature of these reports is that the fluorosis patients–even those with crippling skeletal fluorosis–were misdiagnosed for years, often by multiple teams of doctors, due to a failure to consider fluoride as a possible cause of their disease. As these reports also document, the failure to identify fluoride as the cause of the disease, results in years of ineffective treatments and unnecessary pain. This is because the only known way to alleviate the symptoms of fluorosis is to identify and discontinue the source of fluoride causing the problem. Thus, until the source of excessive fluoride “identified and discontinued,” the symptoms will not improve, and will generally worsen.  (Hallanger-Johnson 2007).

published Case Reports where skeletal Fluorosis was Misdiagnosed:

Izuora, et al. (2011): A 48-year old Georgia woman had drank large volumes of tea brewed in fluoridated water (1 to 2 gallons/day) since the age of 12. By the age of 30, she developed kyphosis (i.e., pokerback), and she experienced “worsening, throbbing, severe bone and joint discomfort” since her late 30’s. “Painful areas included her elbows, wrists, hips, knees, and ankles.” Despite having severe pokerback for up to 18 years, intense joint pain for over a decade, and bone changes “typical of phase 3 (crippling skeletal fluorosis),” her doctors failed to diagnose her condition as fluorosis. It wasn’t until the authors of this study (specialists in the field of fluorosis) examined her that the diagnosis was made. Moreover, as the authors of this study note, the woman’s paternal grandfather and aunts also had kyphosis and, as with the woman, each had drank large volumes of tea throughout their lives. The woman, however, “had not been given an explanation” for what caused her grandfather’s and aunts’ “kyphosis.”
SOURCE: Izuora K, et al. (2011). Skeletal fluorosis from brewed tea. J Clin Endocrinol Metab. 96(8):2318-24.

Kumar, et al. (2011): A 40-year old taxi-driver in India “with a history of continuous pain in his back for one year and knee and elbow joints for nine months” who was experiencing “difficulty in walking,” was diagnosed as having “seronegative spondyloarthropathy with peripheral joint involvement was made.”  After x-ray examination revealed increased bone density in the pelvis and interosseuous membrane calcification in the forearm and leg, doctors inquired whether the patient had been exposed to excessive fluoride. After finding high levels of fluoride in the patient’s water supply, the doctors diagnosed the condition as fluorosis. Skeletal fluorosis, the doctors note, “can easily be mistaken for other conditions such as rheumatoid arthritis, osteoarthritis or seronegative spondyloarthropathy.”
SOURCE: Kumar S, et al. (2011). Skeletal fluorosis mimicking seronegative spondyloarthropathy: a deceptive presentation. Tropical Doctor 41:247-48.

Hallanger-Johnson, et al. (2007): A 50-year old American woman who consumed large quantities of tea developed diffuse bone pain and mild thoracic “kyphosis” (hunchback). Her primary physician diagnosed her as having “arthritis” and treated her with analgesics. The treatment proved ineffective, and four years later, the woman “developed chronic pain and stiffness in her lower back that progressed to include bilateral hip and knee pain.” Her doctor changed the diagnosis to “Paget’s disease of bone,” and prescribed 5 mg/kg of etidronate daily. After 18 months, the symptoms had still not improved and the etidronate dosage was increased to 40 mg/day. Six months later, with symptoms still not improving, the etidronate dosage was increased to 80 mg/day. This again proved ineffective, and over the course of the next year, “her pain progressed to an incapacitating level.” It wasn’t until the woman visited specialists at the Mayo Clinic — seven years after her initial diagnosis of “arthritis” and four years after her diagnosis of “Paget’s Disease” — that her condition was correctly diagnosed as skeletal fluorosis. After significantly reducing her tea consumption, the patient’s bone pain “improved markedly.” As the Mayo Clinic doctors note: “Fluoride toxicity can present in an insidious manner, and clinicians may overlook its signs and symptoms. Unless recognized and the source of excessive fluoride identified and discontinued, fluoride toxicity can be both progressive and crippling.”
SOURCE: Hallanger Johnson JE, et al. (2007). Fluoride-related bone disease associated with habitual tea consumption. Mayo Clinic Proceedings 82(6):719-24.

Whyte, et al. (2005): A 52-year-old American woman who drank large volumes of instant tea developed significant bone and joint pain. Between 1993 and 1998, she sought medical assistance to reduce the pain. Although x-rays showed “marked osteosclerosis” in her spine, pelvis, and ribs, doctors failed to diagnose her as having skeletal fluorosis. Instead, she was considered to have a form of “disc disease.” Five years after seeking medical help, the woman’s “skeletal discomfort intensified” and “included new neck and scapular pain and elbow and knee arthralgias.” She was then referred to a specialist who suspected skeletal fluorosis based on her “bone and joint pains, acquired axial osteosclerosis, well water, . . . and periodontal disease.” Upon learning of her tea-drinking habit, and after testing the fluoride levels in tea and urine, the bone density of her spine, and a sample of her iliac crest bone, the specialists diagnosed her as suffering from fluorosis. After sharply reducing her tea intake, her bone density remained unchanged over the next three years, but she felt “completely well” within five years.
SOURCE: Whyte MP, et al. (2005). Skeletal fluorosis and instant tea. American Journal of Medicine 118:78-82.

Khamees, et al. (1995): A 70-year-old farmer from Yemen had suffered from “progressive skeletal stiffness” for six years, until becoming entirely “dependent for ambulation and many other self-care activities.” A doctor diagnosed him as suffering from “osteoarthritis of both knees” and referred him to specialists “for preoperative rehabilitation procedures.” Upon inspection, the specialists found “quadriparesis resulting from compression of the spinal cord and nerve roots at multiple levels.” X-rays revealed a “uniform increase in bone density” and “calcification of interosseuous membrane and ligaments” in the pelvis, dorso-lumbar spines, and right forearm. Based on these bone changes, and the finding of  slightly elevated fluoride levels in the man’s water supply and urine, the specialists changed the diagnosis from osteoarthritis to crippling skeletal fluorosis. As noted by the specialists, the fluoride level in the man’s water was “relatively low when compared  to the standards put down by the WHO and many other authors to cause crippling skeletal fluorosis.”
SOURCE: Khamees MF, et al. (1995). An uncommon presentation of fluorosis. Electroencephalography & Clinical Neurophysiology 97(4):S229.

Roschger, et al (1995): The difficulty of differentiating between osteoarthritis and skeletal fluorosis was further highlighted in a 1995 study by Austrian doctors. In the study, the doctors conducted x-rays of a woman who had received high-dose (23 mg/day) fluoride for 6 years as an experimental treatment for osteoporosis. After the woman sustained multiple spontaneous fractures, the doctors x-rayed her skeleton and measured her bone density. According to the doctors, “radiographs of the skeleton and bone scintigraphy showed degenerative osteoarthritis,” but none of the traditional signs of skeletal fluorosis.  As the doctors noted, “Interestingly, laboratory findings, skeletal radiographs and bone densitometry, gave no indication for abnormalities of bone metabolism or mineralization.” It wasn’t until the doctors performed a bone biopsy that they were able to detect the presence of fluorosis. As the doctors noted, “Without bone biopsy we would have failed the correct diagnosis.” Based on this experience, the doctors concluded that “invasive investigation of the skeleton (bone biopsy, histomorphometry, BSEI plus SAXS) is the only diagnostic tool, when skeletal fluorosis is suspected.”
SOURCE: Roschger P, et al. (1995). Bone mineral structure after six years fluoride treatment investigated by backscattered electron imaging (BSEI) and small angle x-ray scattering (SAXS): a case report. Bone 16:407. 

Boyle & Chagnon (1995): A 58-year-old Quebec man, in good health, installed a new well on his farm. Unbeknowst to the man, the well water contained 25 mg/L of fluoride. Within six years, the man “began suffering from severe pain and stiffness in his joints and difficulty in breathing.” His wife, who drank less of the water than him, developed “mild pain in her hands and wrists.” The man sought medical help. “After almost a year of examinations and symptomatic treatments by his local doctor,” the man “was informed that his illness was serious but idiopathic.” The man was then transferred to rheumatology specialists in Quebec City who diagnosed him with fluorosis after finding increased bone density on x-ray and elevated fluoride in his urine. After discontinuing consumption of the well water, the man’s joint pain subsided.
SOURCE: Boyle DR, Chagnon M. (1995). An incidence of skeletal fluorosis associated with groundwaters of the maritime carboniferous basin, Gaspe region, Quebec, Canada. Environmental Geochemistry and Health 17: 5-12.

Bruns (1988) & Fisher (1989): A 65-year-old Mexican woman living in Oklahoma, with a history of well-water use in Mexico, developed “progressive lower extremity weakness and intermittent urinary incontinence” over the course of 1 to 2 months. Approximately one week before visiting the doctor, “her legs had become so weak she was no longer able to ambulate” (i.e., walk). At her appointment with the doctors, “she reported an aching pain in her back and chest, and parasthesias in both legs.” Doctors then performed x-rays which showed “increased radiodensity” in her spine and abdomen area. Based on the patient’s age and lack of significant medical history, the doctors made “a working diagnosis of metastatic disease of unknown etiology.” After finding a “partial spinal block at the second and third thoracic levels,” the doctors initiated “radiation therapy” of the spine. The radiation therapy, however, failed to remove the spinal block, and a subsequent bone biopsy showed “no evidence of malignancy.” Based on the biopsy, which “was remarkable for increased osteoid and mineralized bone,” doctors diagnosed the woman as having “quiescent Paget’s disease or another non-neoplastic sclerotic disease.” Doctors thus ended the radiation therapy and conducted a “posterior decompressive laminectomy” to undo the spinal cord compression.

While performing the surgery, doctors noted that the woman’s vertebrae was “essentially fused,” with the bone “very soft and chalk-like in consistency.” It was only then that doctors made the diagnosis of fluorosis, which they confirmed by measuring the fluoride content in the woman’s bone (1,900 ppm) and urine (3.4 ppm). According to the doctors: “Our case report illustrates dramatically that fluorosis can lead to severe disability while closely mimicking a wide variety of other disorders… We believe increased awareness of this unusual disease is needed to enable physicians to make the proper diagnosis.”
SOURCE: Fisher RL, et al. (1989). Endemic fluorosis with spinal cord compression. A case report and review. Archives of Internal Medicine 149: 697-700Bruns BR, Tytle T. (1988). Skeletal fluorosis: a report of two cases. Orthopedics 11: 1083-1087.

Sandberg & Zichner (1985): A 64-year-old German woman, without any unusual exposures to fluoride, began suffering aching joints. “Her pain began in the right hip and then spread to the knee joints and finally to the spine.”  Doctors diagnosed her as having “rheumatism” and prescribed antirheumatic treatment. In addition to her joint pains, the woman suffered from “recurring gastritis and gastric ulcers,” “goiter with multiple calcified deposits,”  and allergies to “wood, soap, various medications, and cosmetics.” Despite the antirheumatic treatment, the woman’s condition “continued to deteriorate to such an extent that she was admitted to a hospital specializing in rheumatism.” Based on x-rays showing “a conspicuous fiber type and sclerosis of the pelvic area, femoral heads, and vertebrae,” the rheumatologists suspected the woman was suffering from “Paget’s disease.” She was then transferred to doctors specializing in Paget’s disease, who ruled out Paget’s disease as the cause. The Paget’s specialists then conducted a bone fluoride test which found that “the fluoride concentration was increased up to six times the normal level, to 2,640 ppm.” Based on this elevated level, as well as x-ray and histological findings, the doctors diagnosed her condition as skeletal fluorosis. They were struck, however, by the lack of significant fluoride exposure in the woman’s history (and absence of kidney disease), and concluded that some individuals may have a very high susceptibility to fluoride’s bone effects. “Because, despite painstaking research, none of the known causes of bone fluorosis could be found in our patient, a new pathomechanism is being offered for discussion, i.e., increased renal or intestinal absorption or an increase of fluoride deposited in the bone; i.e., an inborn or acquired error of fluoride metabolism.” Prior to publishing their study, the authors “observed a similar case” in a 68-year-old male patient.
SOURCE: Sandberg D, Zichner L. (1985). A case of bone fluorosis of undetermined origin. Arch Orthop Trauma Surg. 104:191-95.

Johnson, et al. (1979): A 69-year-old American man sought medical assistance for polyuria (excessive urge to urinate). Doctors gave the man sulfonamide which cleared a urinary infection, but the polyuria persisted. Within a year, the man developed signs of kidney disease followed by “bone pain, arthralgia of the knees and feet, and spontaneous ‘march fractures’ of both feet.” In the next 3 years, the man experienced 13 fractures. X-rays of the man’s skeleton showed “areas of increased bone density with a coarse trabecular pattern involving predominantly the axial skeleton and the calcification of interosseous ligaments, and new subperiosteal bone formation.” Based on these x-ray findings, and a b0ne biopsy showing “an increase of uncalcified osteoid tissue,” doctors prescribed the man “oral calcium supplements and vitamn D,” which helped reduce the bone pain. For the next four years, however, bone fractures continued to occur and the osteosclerosis continued to increase.  At that point, 8 years after the initial hospitalization, doctors tested the man’s blood and water supply for fluoride and found high levels. (226 ppb fluoride in blood; 2 ppm fluoride in water.) The patient was then “advised to stop drinking tap water and to use only fluoride-free spring water or distilled water for both drinking and cooking.” Upon doing so, “serum fluoride concentrations decreased [to 152 ppb], and for a period of approximately 8 years, the patient was relatively free of bone pain and did not experience further fractures.” Doctors thus diagnosed the man as suffering from “adult Fanconi’s syndrome wihth osteomalacia and superimposed fluorosis.”
SOURCE: Johnson W, et al. (1979). Fluoridation and bone disease in renal patients. In: E Johansen, DR Taves, TO Olsen, Eds. Continuing Evaluation of the Use of Fluorides. AAAS Selected Symposium. Westview Press, Boulder, Colorado. pp. 275-293. 

Waldbott & Lee (1978): A 57-year-old American man who had worked for ten years in the alkylation unit of a major oil company had been intermittently exposed to hydrogen fluoride fumes. Prior to working at the facility, the man had been in excellent health. Within 1 to 2 years of beginning the job, however, he began developing a variety of symptoms, including “rectal incontinence,” “severe headaches,” “weakness upon exertion,” and “pain in the lower back.” Over time, the back pains worsened  and spread to the legs, “especially to the left knee.” Eventually, after 8 years on the job, “his back and leg pains became so severe that he was obliged to seek medical advice.” A medical examination revealed an extruded disc in his spine which doctors removed. The surgery, however, did not improve his symptoms, which continued to worsen. Two years after the surgery, he was hospitalized after a fall and diagnosed  with “advanced osteoarthritis of the spine.” Ultimately, the “constant pain in the lower back and legs rendered him unable to work” and he “was placed on medical disability.” While on leave he “was examined by numerous physicians at several medical facilities” who diagnosed him as having “degenerative disease of cervical and lumbar spine,” “spondylosis, L-5,” “degenerative joint disease, left knee,” and “decreased gastrointestinal transit time.” Although doctors considered the possibility of fluoride toxicity, they dismissed it based on the lack of detectable bone changes. Three years later, he visited an expert on fluoride toxicity (George Waldbott) who diagnosed his condition as early stage skeletal fluorosis.
SOURCE: Waldbott GL, Lee JR. (1978). Toxicity from repeated low-grade exposure to hydrogen fluoride–Case report. Clinical Toxicology 13: 391-402.

Cook (1971): A 55-year old English woman, who consumed 3 to 4 pints of tea a day, “had been crippled by arthritis for about 25 years.” “X-rays from the local hospital showed spinal disc degeneration but no obvious signs of fluorosis; some discs showed possible signs of osteoarthritis, and there were some exostoses.” After visiting a doctor familiar with fluoride toxicity, urinary testing was conducted to determine how much fluoride she was ingesting through tea. It was determined that her average daily intake range from 6 to 9 milligrams of fluoride a day. Within 3 months of being instructed to stop consuming tea, “she reported that the pain had diminished to the point where she was almost able to do without analgesics, and that mobility had increased so that she had been able to take on a job as representative, involving a considerable amount of walking. The improvement continued, and after 6 months she reported that she was virtually free of pain, and considered she could do without drugs.” Based on these findings, which were published in The Lancet, the doctor cautioned that “some cases of pain diagnosed as rheumatism or arthritis may be due to subclinical fluorosis which is not radiologically demonstrable.”
SOURCE: Cook HA. (1971). Fluoride studies in a patient with arthritis. The Lancet 1: 817. [See study]

Webb-Peploe & Bradley (1966): A tea-drinking English man began developing “progressive stiffness of both legs” with “pain in the calves after walking for an hour” over a three month period at the age of 52.  Medical examination showed, among other things, “limitation of movement of the right hip, reduction in power of all muscles,” and “pathologically brisk knee and ankle jerks.” No diagnosis was made at the time. Nine months later, the man went to an orthopedic surgeon “because of pain in the lower lumbar region radiating to the groins and the inner aspects of both thighs.” Examination showed “limited and painful movements of the lumbar spine,” while x-rays “revealed marked sclerosis of the pelvis and lumbar vertebral bodies.” The sclerosis was attributed to Paget’s disease while the pain was attributed to osteoarthritis. Although he was given a “surgical corset” to manage the back pain, the pain did not cease and, four years later, the man once again sought medical consultation where doctors discovered spinal cord compression with neurological symptoms. Based on x-rays showing axial osteosclerosis and “prominent bone spurs at the site of tendon insertions,” as well as a bone biopsy showing histological evidence of fluorosis and elevated bone fluoride (2,530 ppm), doctors diagnosed the man as having skeletal fluorosis.
SOURCE: Webb-Peploe MM, Bradley WG. (1966). Endemic fluorosis with neurological complications in a Hampshire man. Journal of Neurology, Neurosurgery and Psychiatry 29:577-583.

Gilbaugh & Thompson (1966): A 73-year old South Dakota man, who lived in an area with a known high high-fluoride content, visited his doctor complaining of urinary incontinence and nocturia. A physical examination revealed “moderate limitation in his right hip due to long-standing osteoarthritis.” X-rays revealed “widespread, increased density” of the ribs and “increased density” and calcification of the skull. An x-ray of the abdomen showed “widespread bony involvement of the lumbar spinal column and the pelvis,” with the bone displaying a “ground-glass appearance,” the lumbar spine showing “hypertrophic changes,” and the pelvis showing “bilateral calcification of the sacrospinous ligament.”  Since the man also had an enlarged prostrate, doctors suspected “widespread bony metastasis.” The doctors then re-inspected x-rays they had taken of the patient 13 years previously, which “revealed a moderate increase in bone density confined to the lumbar spinal column and the pelvis.” Suspecting cancer, the authors tested tissue from the man’s prostrate, but it came back negative. The authors then concluded that “because of the long-standing bony changes and the history of excessive lifelong intake of water of high fluoride content,” the man had been suffering from skeletal fluorosis. Left unmentioned was the fact that the doctors failed to diagnose the condition for over 13 years–despite having x-ray evidence of increased bone density in the same pelvic area where the man suffered from “osteoarthritis.”
SOURCE: Gilbaugh JH, Thompson GJ. (1966). Fluoride osteosclerosis simulating carcinoma of the prostate with widespread bony metastasis: a case report. Journal of Urology 96: 944-946.

Sauerbrunn, et al (1965): A 64-year-old Texan man who had lived most of his life in an area with 2.2 to 3.5 ppm fluoride in the water, repeatedly sought medical help in the past 14 years of his life to address his bone pain and urinary tract problems. In his first visit, the man — who at the time had “moderate kyphosis” (pokerback) — “complained of pain and cramping in the left leg and of weakness and stiffness of all limbs for several years.” He described polyuria (excessive urination) and polydipsia (excessive thirst) of 20 years duration. X-rays revealed “increased size and density” of his long bones and spine, and spinal cord compression from “calcification of the paravertebral ligaments and calcification of sacrospinous ligaments.” The doctors, who unsuccessfully attempted to undo the cord compression, diagnosed the man as having “amyotrophic lateral sclerosis.” Four years later, the man was readmitted to the hospital due to epididymitis and urinary problems. Upon examination, the doctors found that “the neurological signs of spastic quadraparesis had increased,” that the man’s muscles were wasting, and that his bone density was continuing to increase. The doctors were unable to determine the basis for the bone changes, nor were they able to do so during three additional readmissions over the next 7 years. By the time of the man’s sixth and final admission, he had become a “complete invalid” and was “critically ill with pneumonia and shock.” He died shortly after admission. After his death, a bone biopsy revealed a high fluoride content (6,100 ppm). Thus, after six hospitalizations spanning fourteen years, the doctors finally diagnosed the (then deceased) man’s disease as crippling skeletal fluorosis.

In addition to making the diagnosis of fluorosis, the doctors reviewed the medical records of the man’s brother, who was still living.  The brother — who had consumed the same water supply as the the deceased man — had severe dental fluorosis, as evident by his “discolored, pitted, ridged, and worn” teeth, as well as “osteoarthritis” of the spine. However, because there was no evidence of osteosclerosis in the brother’s spine, the doctors reasoned that he must not have skeletal fluorosis.
SOURCE: Sauerbrunn BJ, et al. (1965). Chronic fluoride intoxication with fluorotic radiculomyelopathy. Annals of Internal Medicine 63: 1074-1078.

The fluorosis/misdiagnosis problem: Conclusions from scientific reviews:

“As other causes of osteosclerosis, osteopenia, and calcification of ligaments and tendons are common in end-stage kidney disease, fluorosis may be overlooked until it reaches a late stage.”
SOURCE: Applbaum YK. (2010). Imaging of the skeleton and the joints in CKD. p. 208. In: The Spectrum of Mineral and Bone Disorders in Chronic Kidney Disease. (Olgaard K, Salusky IB, Silver J, eds.) Oxford University Press.

“Although skeletal fluorosis has been studied intensely in other countries for more than 40 years, virtually no research has been done in the U.S. to determine how many people are afflicted with the earlier stages of the disease, particularly the preclinical stages. Because some of the clinical symptoms mimic arthritis, the first two clinical phases of skeletal fluorosis could be easily misdiagnosed [as arthritis]… Even if a doctor is aware of the disease, the early stages are difficult to diagnose. ”
SOURCE: Hileman B. (1988). Fluoridation of water.Questions about health risks and benefits remain after more than 40 years. Chemical and Engineering News August 1, 1988, 26-42.

“It should also be noted that chronic fluorosis is not easily diagnosed, and that few physicians have ever seen a case. Three of the cases reported in the U.S. literature were not diagnosed until post-mortem examination revealed excessive fluoride content in the bone. It is possible that the disease may be occurring to some extent without having been recognized.”
SOURCE: Groth, E. (1973), Two Issues of Science and Public Policy: Air Pollution Control in the San Francisco Bay Area, and Fluoridation of Community Water Supplies. Ph.D. Dissertation, Department of Biological Sciences, Stanford University, May 1973.

“It is quite possible that many cases of (skeletal fluorosis) have gone misdiagnosed and unreported over the years… The state of knowledge among practicing physicians, even those in high-fluoride areas, concerning the diagnosis of skeletal fluorosis seems to be deficient and should be more carefully assessed.”
SOURCE: Prival MJ. (1972). Fluorides and human health. Center for Science in the Public Interest, Washington D.C.

“Symptoms of fluoride poisoning are actually common in this country. The question is not at all whether they occur, but when and how often they are produced by fluoride… It is true that reports (of skeletal fluorosis in the U.S.) are few. This is both the cause and the effect of the fact that physicians, by and large, are unaware that such a thing exists. It is hardly mentioned in the textbooks or in the medical literature. ”
SOURCE: Exner FB. (1957). Fallacies of the fluoridation thesis. In: J Rorty, ed. (1957). The American Fluoridation Experiment. Delvin-Adair Co, New York. pp. 29-153.

“One common feature of the three manifestations of chronic fluorine intoxication is that isolated cases may be difficult to diagnose.”
SOURCE: Roholm K. (1937). Fluoride intoxication: a clinical-hygienic study with a review of the literature and some experimental investigations. London: H.K. Lewis Ltd.