DENTAL FLUOROSIS is a diffuse symmetric hypomineralization (irregular calcification) disorder of ameloblasts (enamel-forming cells). Fuorosis is irreversible and only occurs with exposure to fluoride when enamel is developing:

Instead of being a normal creamy-white translucent color, fluorosed enamel is porous (objectionable secondary staining often occurs) and opaque; teeth can resemble a ghastly-white chalk color (light refractivity is greatly reduced because the enamel’s prism structure is defective). Cloudy striated (lines of demarcation) enamel, white specks or blotches, "snow-capping", yellowish-brown spots, or brown pits on teeth are all characteristic of fluorosis. In its more severe form, fluorosed enamel is structurally weak (brittle) and prone to erosion and breakage, especially when drilled and filled. Even in the milder forms, there is increased enamel attrition. Fluorotic lesions are not just confined to enamel, but can be seen by microscope in dentin as well (dentin is the calcareous tissue beneath enamel). Because fluoride is a powerful bone and tooth seeking element, it also deposits bone or bone-like material externally on the roots of teeth, and internally in the tooth’s pulp chamber; the calcified material narrows the pulp chamber, and thereby interferes with tooth nutrition. The reigning paradigm in public health and dental circles has been to dismiss the significance of dental fluorosis by labelling it a cosmetic effect. However, fluorosis is a toxic manifestation of chronic (low-dose, long-term) fluoride intake. In other words, fluorosis means fluoride poisoning (see Webster's dictionary). Just as a blue-black line appearing on gums signifies chronic lead poisoning, fluorosis is the first visible sign that the whole body has been poisoned by too much fluoride. To prevent fluorosis from occurring in the ten or so most prominent and/or most susceptible teeth, the most critical time to avoid fluoride exposure is the first 3 to 6 years of a child’s life. See flteeth.htm for peer-reviewed abstracts.

HYPLOPASIA is "incomplete or underdeveloped organ or tissue, usually the result of a decrease in the number of cells." [Mosby's Medical Dictionary, 2nd ed]

OSTEOBLAST is "a cell that originates in the embryonic mesenchyme and, during the early development of the skeleten, differentiates from a fibroblast to function in the formation of bone tissue. Osteoblasts synthesize the collagen and glycoproteins to form the matric and, with growth, develop into osteocytes." [Mosby's Medical Dictionary]

OSTEOCLAST is "a large type of multinucleated bone cell that functions in the development and periods of growth or repair, as in the breakdown and resorption of osseous tissue." [Mosby's Medical Dictionary]

editor's note: in layman's terms, this means that osteoclasts eat away old bone, while osteoblasts lay down new bone at the site of the old bone.

OSTEOMA is a bone tumour.

OSTEOMALACIA is "an abnormal condition of the lamellar bone, characterized by a loss of calcification of the matrix resulting in softening of the bone, accompanied by weakness, fracture, pain, anorexia, and weight loss. The condition is the result of an inadequate amount of phosphorous and calcium available in the blood for mineralization of the bones. This deficiency may be caused by a diet lacking these minerals or vitamin D, or by a lack of exposure to sunlight, hence an inability to synthesize vitamin D, or by a metabolic disorder causing malabsorption. Osteomalacia results from and also complicates many diseases and conditions." [Mosby's Medical Dictionary]

[editor's note: osteomalacia is also produced with high fluoride intakes]

OSTEOPENIA is "a condition of subnormally mineralized bone, usually the result of a failure of the rate of bone matrix synthesis to compensate for the rate of bone lysis." [Mosby's Medical Dictionary]

OSTEOPOROSIS is a multi-factorial skeletal disorder which accelerates with menopause. It is predominantly characterised by a progressive atrophy (wasting away) of spongy bone, impaired mineralization, and fracture proclivity.

The most common fragility fracture sites are the proximal femur (hip), spine (generally non-traumatic, or asymptomatic), and the distal forearm. The lifetime risk of the three main fracture sites is: 40% in white women and 13% in white men from age 50 onwards (Chrischilles, et al., 1994). OP is a major public health concern both because of its morbidity and its mortality. Due to today’s ageing population, health care costs are likely to be substantial. Conservative estimates (because only the three main fracture sites were considered) have recently been completed in the U.S. "Among white U.S. women aged 45 or older, an estimated 5.2 million hip, spine, and forearm fractures; 2 million person-years of fracture-related functional impairment; and $45.2 billion total direct medical costs can be expected in the next 10 years". (Chrischilles, et al., 1994)

Sodium fluoride (NaF) treatment for OP was first introduced in the early 1960’s in the erroneous belief that by inducing subclinical skeletal fluorosis, fluoride might increase bone density, thereby strengthening the skeleton and reducing vertebral fractures. Despite global experimentation for over 25 years, it was not until 1988, that the NaF/OP theory was first tested in an adequately controlled prospective study (Mamelle, et al., 1988). Indeed a sad commentary on medical science!

NaF with concurrent calcium supplementation does have an anabolic effect on bone tissue [Kleerekoper, 1991]. However, as long as the cumulative effect of fluoride reaching bone is not taken into account, researchers who advocate fluoride "therapy" for osteoporosis are missing the boat -- boosting bone strength is much more complex than just increasing mass alone. Becuase the structure of trabecular bone is three-dimensional, if bone mass is increased solely by increasing the remaining trabeculae’s thickness after a large number are lost, the strength of these individual bone elements may be augmented somewhat, but the overall effect is limited. Connective structures contribute far more to the strength of bone than its mass alone. In a recent paper, Henry Bone summarized it succinctly:

"We are far from having sufficient understanding of what is required to cause trabecular formation, let alone enough to be able to control or purposefully stimulate this process. The reconstitution of bone is a long-term goal for which the tools are not yet at hand." (Bone, 1993)

While most researchers have abandoned fluoride as a treatment for osteoporosis, there are still some who advocate it even though both animal and humans studies have shown that new bone formed under long-term NaF therapy is abnormal, and that the induced abnormality can compromise the biomechanical competence of the skeleton.

Bone, Henry G, The Future of Osteoporosis Diagnosis and Therapy, Bone and Mineral, 22, 1993, S71-S79.
Chrischilles T, et al., Costs and Health Effects of Osteoporotic Fractures, Bone, 15:4, 1994 July/August, 377- 385.
Kleerekoper M, Balena R, Fluorides and Osteoporosis, Annu. Rev. Nutrition, 11, 1991, 309-324.
Mamelle N., et al., Risk-benefit ratio of sodium fluoride treatment in primary vertebral osteoporosis, Lancet, 2, 1988 August 13, 361-365.

Following is U.S. Food and Drug Administration material:
...[O]steoporosis is defined as a condition in which the bone mass per unit volume (density) of normally mineralized bone is reduced. However, reduced bone mineral density is not the only abnormality associated with reduced bone strength. The bone may no longer provide adequate mechanical support and there is a high risk of fracture without trauma or in response to minimal trauma.

Although osteoporosis may be associated with and secondary to a variety of systemic disorders such as Cushing's syndrome, hyperthyroidism, or immobilization, an associated disorder of etiological significance cannot be identified in most patients. There is an age related net loss of bone that usually begins during the fifth decade in most, if not all, people. Attempts have been made to divide involutional osteoporosis into two separate syndromes (Type I and Type II). This concept of two syndromes, though not universally accepted, may serve as a useful tool in selecting a treatment regimen. Type I osteoporosis affects women after menopause and results from an accelerated rate of bone loss (mainly trabecular) due to factors (mostly estrogen deficiency) related to menopause. Vertebral "crush" and distal radius fractures are common in Type I osteoporosis. Type II (age- related) osteoporosis involves both men and women over age 70 and is characterized by gradual (over several decades) loss of both trabecular and cortical bone mass due to factors related to aging process. In women with Type II osteoporosis, estrogen-deficiency also contributes to the overall bone loss. Both vertebral (multiple wedge type) and hip fractures are common in Type II osteoporosis.

Loss of bone mass in osteoporotic patients (Type I) generally involves the entire skeleton including cortical and trabecular portions of both axial and appendicular bones. Rate of bone loss may vary, and bone loss may be more advanced in some skeletal locations than in others. During the first five to ten years after menopause, bone loss occurs at an accelerated rate. Thereafter, bone loss continue at a slower rate for up to 20 years.

Many patients with osteoporosis are asymptomatic. Episodic back pain may be coincident with vertebral fracture, but such fractures frequently are not associated with pain. Chronic pain generally is attributed to muscle spasm, nerve root irritation, and/or degenerative arthritis secondary to previous fracture and bone deformity. A significant vertebral deformation is generally needed to cause marked back pain and immobilization.

The most important morbid event in osteoporosis is fracture. The common fracture sites include proximal femur (hip), vertebrae, distal radius, proximal humerus shaft, and ankle. In epidemiologic studies, bone mineral density (BMD) has predicted the risk of vertebral fracture. However, a treatment related increase in BMD cannot be assumed to result in reduced risk of fracture. For example, the relationship between BMD and fracture risk has been validated only for patients receiving estrogens, and does not apply to patients receiving fluoride.
SOURCE: Guidelines for preclinical and clinical evaluation of agents used in the prevention or treatment of postmenopausal osteoporosis, DRAFT, Division of Metabolism and Endocrine Drug Products, Food and Drug Administration, April 1994.

OSTEOSARCOMA is a rare bone cancer which mostly originates in the growing end of bones. It is more prevalent among young males 10-19 years of age and seems to occur 1.4 times more often in males than in females. Girls are at risk at an earlier age because their adolescent growth spurt occurs before that of boys

OSTEOSCLEROSIS "an abnormal increase in the density of bone tissue. The condition occurs in a variety of disease states, is commonly associated with ischemia [decreased blood supply to an organ or body part], chronic infection, and tumor formation, and may be caused by faulty bone resorption as a result of some abnormality involving osteoclasts."

(Mosby's Medical Dictionary). It is also caused by prolonged chronic fluoride ingestion.

SKELETAL FLUOROSIS is an abnormal increase in bone density.

"Endemic skeletal fluorosis is a chronic metabolic bone and joint disease caused by ingesting large amounts of fluoride either through water or rarely from foods of endemic areas. Fluoride is a cumulative toxin which can alter accretion and resorption of bone tissue. It also affects the homeostasis of bone mineral metabolism. The total quantity of ingested fluoride is the single most important factor which determines the clinical course of the disease which is characterized by immobilization of joints of the axial skeleton and of the major joints of the extremities. A combination of osteosclerosis, osteomalacia and osteoporosis of varying degrees as well as exostosis formation characterizes the bone lesions. In a proportion of cases secondary hyperparathyroidism is observed with associated characteristic bone changes. Contrary to earlier thinking, severe crippling forms of skeletal fluorosis are seen in paediatric age group too. Increased metabolic turnover of the bone, impaired bone collagen synthesis and increased avidity for calcium are features in fluoride toxicity. Osteosclerotic picture is evident when small doses of fluoride are ingested over a long period of time during which calcium intakes are apparently normal while osteoporotic forms are common in paediatric age group and with higher body load of the element. Alterations in hormones concerned with bone mineral metabolism are seen in fluorosis. Kidney is the primary organ of excretion for fluorides. Age, sex, calcium intake in the diet, dose and duration of fluoride intake and renal efficiency in fluoride handling are the factors which influence the outcome. Serum parameters rarely help in the diagnosis. Elevated urinary fluoride and increased bone fluoride content are indicators of fluoride toxicity. Fluorosis is a preventable crippling disease. No effective therapeutic agent is available which can cure fluorosis. Industrial fluorosis is on the increase on a global basis. Bone density measurement is a tool for early diagnosis."
Source: Krishnamachari KA, Skeletal fluorosis in humans: a review of recent progress in the understanding of the disease, Prog Food Nutr Sci, 1986, 10 (3-4): 279-314

Please also see skeletal.htm

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