Clinical Aspects of Fluorosis in Horses

James L. Shupe, D.V.M., and Arland E. Olson, M.S.

From the Department of Veterinary Science, Utah State University, Logan, Utah 84321. Published with approval of the Utah State University Agricultural Experiment Station as journal paper No. 1055.

SUMMARY: Horses grazing in areas where cattle and sheep had developed severe fluorosis were examined clinically. Of those examined, 12 horses of different ages and with various degrees of fluorosis were selected for necropsy. Selected tissues were examined grossly, histologically, and radiographically. Major fluorotic lesions occurred in the permanent teeth and in the bones. Dental lesions occurred only when the horses ingested excessive amounts of fluorine during the period of tooth formation.

With the increase and expansion of certain industries into agricultural areas, fluorine toxicosis in livestock and wildlife has become an important toxicologic problem in many areas of the United States and some other countries. (1,2,4-7,12) Air pollution damage to agricultural production in the United States in 1967 was estimated at $500,000,000. (3) Fluoride damage to livestock and vegetation comprised a substantial part of this.

Fluorine is universally present in varying amounts in soils, water, the atmosphere, vegetation, and animal tissues. Because of its chemical reactivity, fluorine is found in nature in a combined (fluoride) state. It has beneficial effects when ingested in small amounts, but has adverse effects when ingested in excessive amounts.

Livestock normally ingest variable low level amounts of fluorides. Adverse effects have not been associated with this normal fluoride ingestion. (7,9)

Various sources may contribute to the total fluoride intake of animals. The most commonly encountered sources of excessive fluorides are: (1) forages subjected to airborne contamination in areas near certain industrial operations; (2) high-fluoride water from natural or industrial sources; (3) feed supplements and mineral mixtures containing excessive fluoride; (4) vegetation growing in soils high in fluoride; and (5) a combination of any or all of the preceding four. (8)

When excessive amounts of fluorine are ingested for prolonged periods chronic toxicosis or fluorosis may result. Fluorosis has been studied experimentally and under normal husbandry conditions in most species of domestic animals and in some wildlife, but its effects in horses have not been elucidated. (1,9,11)

Species tolerances to ingested fluoride vary widely. Clinically, fluorine toxicosis is usually detected in one of two typical forms, acute or chronic. Acute fluorine toxicosis most commonly results from accidental ingestion of high amounts of fluorine compounds, such as sodium floroacetate ("1080") and fluoroacetamide used as rodenticides, sodium fluorosilicate used as an insecticide, and sodium fluoride used as an ascaricide. Acute fluorine toxicosis in a horse was induced by feeding increasing doses of sodium fluoride up to 100 Gm. daily. (2)

Chronic fluorosis is the type of fluorine toxicosis most often detected in livestock. A 5-year-old horse that lived in the same region where darmous (fluorine poisoning in North Africa) in sheep was routinely detected had extensive abrasions of the incisor and cheek teeth. (12) A 1 1/2 -year-old horse and 2 colts had eaten for one entire summer fluorine-contaminated hay from pastures in the vicinity of an industry producing fluoric acid. Cows grazing the same pastures where the hay was harvested developed marked signs of fluorosis. One of the horses had exostosis on the limbs and thickening of the skull bones. (4)

Incidence and Prevalence

Fluorosis is not detected as often in horses as in cattle, sheep, or swine. Horses are considered to be more tolerant to fluorine than most species of domestic animals . (4,5,8,9)

Fluorosis in horses has resulted when airborne particulates and gaseous affluents high in fluorine have contaminated vegetation subsequently eaten by the horses. (4,12) Most waters containing excessive fluorine are from warm or hot springs, deep wells, or accidentally contaminated sources. Phosphorus supplements used for feeding livestock should be defluorinated and should contain not more than 0.2% (2,000 p.p.m.) of fluorine. Soils can normally contain relatively high amounts of fluorine without the translocation of excessive fluorine into the vegetation. However, animals grazing in such areas can ingest excessive fluorine from the soil, especially if the pastures are overgrazed and the animals are forced to eat the vegetation down close to the ground. Various degrees of fluorosis in horses have been diagnosed in some enzootic fluorosis areas where cattle and sheep had marked to severe fluorotic signs and lesions. (7,8)

Clinical Description

Lesions of fluorosis develop in horses in much the same manner as they do in cattle, sheep, and other species of animals. Teeth and bones are the major sites of important lesions. (1,3,5,7,10)

Fluorotic dental lesions are induced during the period of tooth development and indicate the level of fluoride ingestion during the formation of enamel (amelogenesis) and dentine (dentinogenesis). Affected teeth erupt with characteristic fluorotic lesions such as mottling, staining, hypoplasia, hypocalcification, and excessive abrasion. Both enamel and dentine are adversely affected when increased amounts of fluorine are ingested during the formative stages of tooth development. Specific ameloblastic and dentinoblastic damage will vary in degree as influenced by the amount of fluoride intake.

Teeth can be used as an indicator of fluorosis in horses, if excessive fluoride was ingested during the time of tooth formation. We have seen cross-chalking of the enamel in a few deciduous incisor teeth of some colts. These lesions wen not typical of fluorotic mottling. When one considers the placental type and structure in horses, it is unlikely that enough fluorine passes the placental barrier from dam to offspring to induce similar changes. Even in cattle, a species that has a more intimate and permeable type of placenta, fluorine does not pass from dam to offspring in amounts sufficient to induce similar changes and adversely affect the offspring. (10) Experimental work with mares on long-term high level fluoride intake would have to be conducted to determine the precise amount of placental transfer. Such information has been developed for cattle and can can be extrapolated to horses. (8,10)

Dental fluorosis is usually diagnosed in animals by clinical examination of the incisor teeth. Cheek teeth are also important in evaluating the effects of fluorosis, but they are difficult to examine in the live animal because of problems in restraint, proper illumination of the teeth, the presence of unswallowed food, and discoloration caused by vegetative matter. The same criteria used in diagnosing and evaluating incisor fluorosis cannot be used in diagnosing and evaluating premelar and molar fluorosis. Premolar and molar fluorosis is estimated on the degree of abrasion only. In diagnosing and evaluating dental fluorosis, the cheek teeth must be examined, evaluated, and correlated with the incisor teeth effects.

Diagnosis

Individuals diagnosing and evaluating fluorosis in animals should have access to all available records, data, and findings that relate to the animals involved. The diagnostician should make detailed clinical examinations of all suspect animals. Each animal should be properly identified. Regardless of monitoring and sampling data relating to the source(s) of fluorine and analyses of fluorine values in the vegetation, each animal must be evaluated for its own expression of fluorosis.

It is advantageous to compare groups of animals with adjacent animals of approximately similar exposure and management practices, and with animals having different degrees of exposure and management practices. Important factors may be missed if one does not also observe animals in adjacent areas. Some abnormal findings thought to be attributed to fluorosis may not be, and some thought to be normal may be abnormal. The variability that can occur between individual animals within and between farms must also be considered.

Under field conditions the amounts of fluorine in the vegetation, the lengths of time during which they are ingested, and management practices are usually subject to wide variations. In some instances extremely high or low amounts of fluorine may be ingested intermittently. Management practices that can influence manifestations of fluorotic signs and lesions include preventive medical programs and housing facilities; type, quantity, and quality of feed; breeding program; and routine animal care.

The relationship of animal age to fluorine dosage and lesions is also important. Additional factors to be considered are the types of operations and purposes for which the horses are being raised. All findings must be considered carefully and interrelated before a definite and final evaluation of fluorine damage is made.

Signs and visible or palpable clinical lesions sometimes are not definitive enough to warrant an unequivocal diagnosis of fluorosis. In such instances, or to substantiate a reasonably certain diagnosis, additional verification can be sought in several ways. When carefully interpreted, urinalysis is a useful diagnostic aid. Radiographs of bones can supply valuable information. Biopsies or necropsies can be used to obtain tissues for chemical analysis to determine tissue fluorine content and for gross and histologic examinations. Only small (less than 2.5 p.p.m.) amounts of fluorine are retained in soft tissues. Hair, skin, hoofs, and soft tissues do not evidence any significant pathognomonic: changes. Correlation of clinical findings with the ascertained fluorine contents of the water and forage sources often can help substantiate or disprove suspected instances of fluorosis.

Materials and Methods

Horses grazing in areas where cattle and sheep had developed severe fluorosis were examined clinically. Clinical classifications were made of all horses examined. The classification standards used were developed for horses by modifying the classification standards that had been successfully used in classifying 81,250 animals in enzootic fluorosis areas. (3, 10)

With modification, the widely used standards for classifying the degree of dental fluorosis in cattle and sheep are also applicable for horses. For the purpose of classifying and evaluating various degrees of dental fluorosis in horses, the following standards have been adapted and successfully used:

0) Normal: smooth, translucent, glossy-white enamel; tooth normal shape.

1) Questionable effect: some change, but absence of fluorotic lesions; may have off-colored flecks in the enamel or unilateral or bilateral cavities.

2) Slight effect: slight mottling of enamel; may have slight staining; tooth normal shape without wear due to fluorosis.

3) Mild effect: definite mottling (large patches of chalky enamel) and staining of enamel; tooth may have slightly more than normal abrasion.

4) Marked effect: pronounced mottling and staining; hypoplasia and hypocalcification; enamel may be pitted and off-colored; definite abrasion.

5) Excessive effect: more advanced or extensive changes than those described for marked effect.

8) Tooth erupting through the gum line - difficult to evaluate during this period.

9) Deciduous tooth.

Twelve horses of different ages and with various degrees of fluorosis were obtained for detailed necropsy studies. Tissues obtained at necropsy were placed in neutral 10% formalin for histologic examination. Metacarpus, metatarsus, mandible, ribs, and maxillary bones from all horses were measured, radiographed, and prepared for gross and microradiographic evaluation. The fluorine deposition in the bone and the degree of abnormal reactive bone changes were correlated both among the various bones of the body and with the degree of dental fluorosis, age of the animal, and amount of fluorine in the pasture vegetation.

Results

Horses with moderate to marked fluorosis appeared unthrifty even when they had ample amounts of good quality feed. Coats were rough and dry in appearance. and winter coats were slow to be shed in the spring (Fig. 1). The skin became taut and less pliable than normal. When tooth abrasion was excessive, feed utilization was poor and "slobbering" of poorly masticated food was common.

Horses with marked clinical fluorosis evidenced lameness and were unable to walk, run, and jump normally. They took shortened steps and then only reluctantly. They did not "warm-out" of this condition, in fact, the lameness frequently intensified with use, exercise,, or work. Even when the affected horses were not worked, there was apparent pain, for these animals often stood with their feet in unnatural positions (one forefoot placed in front of the other) and shifted the position of their feet frequently as if trying to relieve pain.

Many of the horses examined had severe dental fluorosis (Fig. 2) with excessive molar abrasion (Fig. 3). These dental lesions were typical and pathognomonic for fluorosis. (1,5-8,10,11). The premolar and molar tables were irregular and uneven. These irregularities resulted in poor mastication of food as well as occasional biting and trauma to the mucosal surface of the cheek and opposing gum surfaces.

The central portion of the 2nd lower premolar tooth in some horses broke down and allowed the food material to be forced through the hole into the pulp cavity. This material then formed an abscess within the mandibular bone. These infected areas were often 4 to 6 cm. in diameter and sometimes formed a fistulous tract that drained from the ventral aspect. These horses had a lumpy jaw appearance (Fig. 1).

The first clinically palpable bone lesions were found on the metatarsus, metacarpus, mandible, and ribs (Fig. 4). These hyperostotic lesions were usually bilateral in nature. Splint bones often became increased in diameter and fused to the metacarpal and metatarsal bones (Fig. 5).

The 1st and 2nd phalanges also had abnormal periosteal hyperostosis, particularly at points of tendon insertion. The 3rd phalanx was often thickened with a layer of excessive rough-textured bone. This undoubtedly increased pressure within the hoof, causing pain, abnormal stances, restricted movement, and lameness.

Other bones were also responsive to prolonged, excessive fluoride ingestion. The mandibular bones were often thickened, even in the absence of abscesses. Diffuse hyperostosis often occurred on the nasal and maxillary bones, creating a characteristic "Roman nose" appearance. Bones also served as a record of periods of intermittent, excessive fluoride ingestion interspersed with periods of intake, as evidenced by layers of altered bone structure.

In severe chronic cases, all bones of the body were affected to some degree. Grossly, the fluorotic bones appear chalky white with a roughened irregular periosteal surface and were thicker than normal bones (Fig. 5). Grossly, articular cartilage appeared normal. In conditions such as osteoarthritis, the articular cartilage undergoes various changes and lesions, such as periarticular osteophytosis, that may be misinterpreted for fluoride-induced periosteal hyperostosis. Radiographic (Fig. 6) and microscopic bone lesions of fluorosis in horses were characteristic of the fluoride-induced bone lesions in other species.

Lameness and stiffness were inconclusive measures of fluoride toxicosis. The intermittent lameness and stiffness observed in horses with more advanced fluorosis appeared to be associated with the osteofluorotic lesions and mineralization of periarticular structures and tendon insertions. In turn, the intermittent lameness and stiffness deterred the affected animals from properly standing, eating, or grazing. The subsequently reduced feed intake fostered lower performance.

Discussion

Many factors influence biologic responses of livestock to ingested fluorides. The influencing factors are: (1) concentration of fluoride in substances ingested; (2) duration of ingestion; (3) chemical combination and, thus, solubility of fluoride in the ingesta; (4) species of animal affected; (5) age of animal at time of ingestion; (6) qualitative and quantitative nutritional adequacy of ration; (7) stress factors; (8) individual biologic response.

Fluorosis in horses can be diagnosed clinically by qualified individuals. If excessive fluorine ingestion takes place during the period of tooth formation, typical fluorotic dental lesions usually will be seen before other signs of chronic illness become apparent. After a tooth has fully formed and erupted, it does not have reconstructive ability to compensate for fluorotic enamel lesions. It is worthy of emphasis that fluorotic dental lesions will not be seen in animals brought into enzootic fluorosis areas after their permanent teeth have erupted.

Dental fluorosis can and should be correlated with other changes and lesions in evaluating fluorosis. The extent of osteofluorosis, amount of fluorine in the bones, amount of fluoride ingested, duration of ingestion, age of animal during the period of excessive fluoride ingestion, nutritional adequacy, and other reactive processes of the body should all be taken into account in evaluating the severity of fluorosis.

Fluorine has a remarkable affinity for bone. The amount of fluorine stored in the bone can increase within limits over a period, without inducing any demonstrable changes in structure and function. These changes first appear at sites of greatest metabolic activity and stress within a given bone and in bones that are under the greatest stress from weight bearing and locomotion. The osteofluorotic lesions may be porosis, sclerosis, hyperostosis, osteophytosis, and malacia, depending on the interacting factors influencing the degree of fluorosis.

The extent of fluorine-induced bone changes can be correlated among the various bones of the body and within certain anatomic and metabolic areas of specific bones. Thus, in taking bone samples for chemical analyses and other studies, it is very important to use bones for which standards have been established and take specimens from specific areas of given bones.

Roentgenographic findings will vary greatly depending on the effects of and interaction among the multiple factors that govern the degree of fluorosis. The onset of chronic fluorosis is insidious and may be confused with chronic debilitating diseases such as osteoarthritis.

Tolerances to ingested fluoride vary markedly among species (Table 1). Tolerances of horses for fluorine with other animals is given.

Therapy

There are no substances known that completely prevent the toxic effects of increased amounts of ingested fluorides. Some products, however, can counteract and lessen the potential damage that ingested fluorides can cause. Aluminum sulfate, aluminum chloride, calcium aluminate, calcium carbonate, and defluorinated phosphate can reduce the toxicity of fluorine in animals. Heifers ingesting aluminum sulfate as a fluorosis inhibitor deposited 30 to 42% less fluorine in their ribs than did heifers ingesting comparable diets without aluminum sulfate. (7,9,11)

In areas where fluorosis is a problem because of contaminated pastures, the following procedures may be used:

(1) Grow grain on part of the land formerly used for hay and pasture.

(2) Increase the grain allowance in the diets where indicated.

(3) Mix hay low in fluorine content with hay high in fluorine content to make a ration with less than 60 p.p.m. of fluorine. If feasible, use high-fluoride hay only for less valuable, mature animals and those not being kept for breeding purposes.

(4) Avoid field grazing during late fall and winter periods when vegetative growth is slow and inversion-type weather persists.

(5) If animals' teeth are severely damaged from fluorine, it may be desirable to chop the hay. Warm the drinking water if necessary and practical.

These suggested management procedures will not eliminate a fluorosis problem. They can, however, often reduce the severity of effects and aid in the management of animals that have been adversely affected until they can be disposed of.

References

1. Anon.: The Fluorosis Problem in Livestock Production. Report of the Committee on Animal Nutrition Agricultural Board, Nat Acad. Sci., Nat. Res. Council, Washington D.C., 824, (1960): 1-29.

2. Damman, C., and O. Manegold: Vergiftungen durch fluorhaltigen phosphorsauren Futterkalk. Deutsche tieriirztl. Wchnschr., l2 (1904): 129-131; 141-143.

3. Greenwood, D. A., Shupe, J. L., Stoddard, G. E. Harris, Lorin E., Nielsen, Harold M. and Ulson, L. Elmer: Fluorosis in Cattle, Special Report 17. Agricultural Experimental Station, Utah State University, Logan, Utah, 1964,

4. Hupka, E., and Yuy, P.: Gehauftes Auftreten von Osteornalacie unter Weiderindern, verursacht durch Fluorwasserstoffsdure enthaltenden Fabrikraucb. Arch. wissensch. u. prakt. Tierheilk., 60, (1929): 21-39.

5. Roholm, K.: Fluorose der Schafe auf Island nach Vulkanausbriiehen? Arch. wissensch. U. prakt. Tierheilk., 67, (1934): 420-435.

6. Shupe, James L.: Diagnosis of Fluorois in Cattle. Publikation der IV. Internationalen Tagung der Weltgesellschaft fur Buiatrik, Zurich, Switzerland (Aug. 4-9, 1966): 1-18.

7. Shupe, J. L., and Alther, E. W.: The Effects of Fluorides on Livestock with Particular Reference to Cattle. Handbuch der experimentellen Pharmakologie. Vol. XX/1. SpringerVerlag, New York, N.Y. (1966): 307-354,

8. Shupe, James L.: Fluorosis in Livestock. Air Quality Monographs, No. 69-4, Americoan Petroleum Institute, New York, N.Y. (Feb.. 1969): 1-29.

9. Shupe, James L.: Levels of Toxicity to Animals Provide Sound Basis for Fluorine Standards. Environmental Sci. & Tech., 3 (Aug., 1969): 721-726.

10. Shupe, James L., Miner, M. L Greenwood, D. A., Harris, L. E., and Stoddard, G. E.: The Effect of Fluorine on Dairy Cattle. II Clinical and Pathologic Effects. Am. J. Vet Res., 24, (Sept., 1963): 964-979.

11. Shupe, James L.: Fluorine, Toxicosis and Industry. Am. indust. Hyg. A. J., 31, (March-April, 1970): 240-247.

12. Velu, H.: Relations due darmous et la nappe phreatique des zones phosphatees. Bull. Acad. vet. France, 4, (n.s.), (1931): 392-394.

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