Effects of Fluoride widely distributed in nature and since its effectiveness in the prevention of dental caries was postulated in the late 40 ‘, its use has been widely accepted and practiced. To that end it is used in local forms applied directly to the teeth and systemic forms which are swallowed. Both methods are described equally effective in preventing dental caries.
Effects Of Fluoride
Fluoridation programs drinking water at a concentration of 1 ppm (1 mg / l), have been considered as important public health benefit since their use began, it was recognized that a clear understanding of their behavior in organism and probable toxic effects associated with systemic use, is critical in the implementation and evaluation of mass fluoridation of drinking water.
Given a fluoride intake, approximately 80% is absorbed in the stomach and small intestine and the rest mainly eliminated through bowel movements.
The fluorine absorbed passes to the blood plasma and is then distributed to various tissues, which is kept in set proportions about plasma concentration. This dynamic equilibrium is possible because the fluorine is not bound to proteins in plasma and its diffusion through membranes of different gradients are pH dependent and requires no carriers.
The above does not determine saturation concentrations in the different compartments organic, as originally seen, since the human body has no mechanism of homeostatic regulation of fluorine.
The fluoride concentration in breast milk is constant (0.008 ppm) and independent of the plasma concentration of fluoride in the mother, which can be considered as the only mechanism of homeostatic regulation present in humans.
The concentration of fluoride in different tissues following absorption depends on the intake and plasma clearance. This latter is done in equal proportions through uptake by calcified tissues and renal excretion.
The affinity of calcified tissue fluoride is important for determining its persistent and cumulative retention in bone, being higher in growing organisms. In the newborn, about 90% of absorbed fluoride is retained in bone. This affinity decreases with age and is stabilized at about 50% of fluoride absorbed on completion skeletal development, with the remaining 50% excreted through the kidney.
Renal excretion depends on the functionality of the kidney and urinary pH. A higher acidity, tubular reabsorption of fluoride are increasing from the interstitium and then to the capillaries, increasing the plasma pool.
ACUTE TOXICITY FLUOR.
A concentration of 1 ppm fluoride intake is devoid of major deleterious effects, except for patients undergoing chronic renal dialysis, in whom deaths have been reported in verticular fibrillation cardiac arrest secondary to excessive concentrations of fluoride in the dialysis solution and hyperkalemia important. This situation results from the inability of deionization equipment commonly used to ensure adequate clearance of fluoride in the dialysis solution and significantly corrected using procedures in reverse osmosis deionization.
Another acute situation can also lead to death, is given by voluntary or involuntary intake of preparations with high concentrations of fluoride.
In the gastric lumen, the fluorine is present as hydrofluoric acid (HF). This non-ionized molecule readily crosses the membrane of epithelial cells, penetrating into the cells where it is dissociated into ions and hydrogen fluoride, which injure alter cellular functions and structures by rupture of the gastric mucosal barrier.
Single dose and high concentration of fluoride for topical application to the oral cavity level with swallowing of fluoride, gastric mucosal damage, resulting in alteration of the structure. The injury is enhanced by using a fluoride gel at concentrations of fluorine in a range from 5,000 to 12,300 ppm and higher product viscosity.
Involuntary intake of these products generates gastric irritation manifested in epigastric pain, nausea, vomiting. The accidental or deliberate ingestion of high concentrations may cause coma, acidosis, convulsions, respiratory paralysis or death from arrhythmia followed by cardiac failure.
Studies in humans and experimental application of fluoride gel at concentrations of 1.23% (12,300 ppm), have shown in some instances, epigastric symptoms appeared, changes in cAMP levels in plasma and tissue metabolism in gIucosa and secretion of salivary amylase. The standardization of the methods of application of the gel decreases the amount of fluoride ingested.
In 1989, Col Spak and in a sample of twelve adult volunteers ordinary endoscopic gastric mucosa, are gastric mucosal damage after intake of twenty mg single dose. sodium fluoride (NAF). After two hours, the twelve subjects had petechiae and erosions in the gastric body to endoscopy and gastric biopsy.
Half of them also showed changes in the gastric antrum. In four of these volunteers was found bleeding on a large area of the gastric mucosa. Both the epithelium and superficial stroma as gastric acini were affected; epithelial cells were smaller than normal. The epithelium was observed more severely damaged or completely lost disintegrated. In acini appeared irregular dilatation and widening of epithelial cells. The loss of ammunition was very noticeable.
In 1990 and again Spak Col performed oral application of a fluoride gel of lower concentration (0.42%) in ten adults with previously healthy gastric mucosa. The amount of fluorine retained after the application was 40% of the amount of F applied. In seven subjects were presented petechiae and erosions. Histological examination showed gastric epithelial abnormalities in nine of the volunteers. Experiences in rats show that gastric lesions are fast and steady recovery to suspend the application of fluoride.
FLUOR chronic toxicity.
Persistent accumulation of fluoride in osteoblast activity favors bone, which at some point was regarded as beneficial in the treatment of osteoporosis.
The newly formed bone tissue structure does not maintain normal bone tissue, bone being one but less elastic denser, making it more susceptible to fracture.
The accumulation of fluoride in tooth produces similar changes in the appearance of enamel fluorosis, a defect in tooth enamel mineralization secondary to excessive fluoride during its formation. The fluorosis initially evidenced in a mottled appearance of the tooth colored substance reservoir feeding a porous tooth until significant deformation and destruction of the teeth.
Fluorosis prevalence studies in elementary school children in different areas of our country, have documented high rates of fluorosis (61.4%) in Iquique, with high natural levels of fluoride in drinking water, Fifth Region (56.0%) with programs fluoridation of drinking water 10 years ago in Santiago medium (18.6%) prior to the start of programs fluoridation of drinking water and low in Temuco (4.2%). The collective index of fluorosis in Iquique has exceeded the value of 0.6 on the different pathologies which is considered a public health problem.
Evidence of manifestations of excessive exposure to areas without fluoridation programs are made water supply, indicates the existence of other potential sources of fluoride that should be studied.
At the level of the gastrointestinal tract, chronic administration of fluorine may be associated with the presence of dyspeptic symptoms.
Waldbott various gastrointestinal symptoms reported with chronic use of F at concentrations of 1 ppm, represented by nausea, vomiting, abdominal pain, intermittent diarrhea and constipation.
The metabolism ingested determines the feasibility prolonged biological deleterious systemic effects occur, dependent on different intra-and inter metabolic variases. The local administration fluorinated products pose no risk to human health, except for accidental ingestion in large quantities.