Fluoride affects the bone growth and bone-resorbing cells, the developing growth plate, and cartilage, all of which can contribute to arthritic changes. More than
99% of fluoride in human bodies is found in bone. The functions of fluoride are as follows:
The stomach and small intestine assimilate fluoride. It quickly reaches mineralized tissue after entering the blood circulation. Fluoride does not accumulate in soft tissue at normal consumption levels.
Calcium and phosphate crystals, known as hydroxyapatite crystals, are the most common mineral constituents in bone.
Fluoride’s strong chemical reaction and modest radius enable it to shift the greater hydroxyl (-OH) ion in the hydroxyapatite crystal, generating fluorapatite. This fluorapatite hardens tooth enamel and helps maintain bone mineral stability.
The effects of fluoride on bones include the following:
Fluoride reacts with calcium phosphate present in the bones and improves the structural integrity of bones.
The enhancement of osteoblast growth is fluoride’s effect on the bones. Through clinical researches, scientists found an improvement in vertebral bone mineral density as a result of proliferation.
Fluoride’s impacts on osteoclast or bone resorption are not so well understood. However, according to few studies, fluoride reduces osteoclast genesis and osteoclast interaction during in vitro systems.
There have been various conflicts on the effects of fluoride on bones. Some studies have also found that fluoride can increase the risk of bone cancer in males. However, other studies found no relation between them.
Use of fluoride in treating osteoporosis
Osteoporosis is defined by a reduced bone mineral density (BMD), bone weakness, and fracture risk. Generally, lower BMD is linked to a higher risk of fracture.
If very high prescribed fluoride doses are used for treating osteoporosis, the conventional link involving BMD and fracture risk may reduce significantly. The majority of osteoporosis treatments reduce bone loss (resorption), resulting in minor gains in BMD.
Substantial gains in the BMD of the lumbar spine can be achieved with pharmacologic dosages of fluoride. Despite large improvements in lumbar spine BMD, treatment evaluations of fluoride in patients with osteoporosis have not consistently revealed significant reductions in the frequency of vertebral fractures.
In cases of lack of calcium and vitamin D, early trials utilizing high doses of fluoride may have triggered fast bone mineralization, culminating in denser but not functionally stronger bones.
Reduced vertebral and non-vertebral fractures and enhanced lumbar spine bone density have been observed in randomized controlled trials employing reduced fluoride levels, periodic dosage regimens, or gradual formulations.
Even though fluoride therapy improves bone density, it is unlikely to minimize bone resorption and restore a connection in individuals with severe bone loss. Hence, fluoride treatment is less helpful in osteoporotic patients who have already lost a significant amount of trabecular connections.
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