Acidic drinks and foods lower the pH level of the mouth so consuming them causes the teeth to demineralise. Drinks low in pH levels that cause dental erosion include fruit juices, sports drinks, wine, beer and carbonated drinks. Orange and apple juices are common culprits among fruit juices. Carbonated drinks such as colas, lemonades are also very acidic, as are fruit-flavoured drinks and dilutables. Frequency rather than total intake of acidic juices is seen as the greater factor in dental erosion; infants using feeding bottles containing fruit juices (especially when used as a comforter) are therefore at greater risk of acid erosion.

Saliva acts as a buffer, regulating the pH when acidic drinks are ingested. Drinks vary in their resistance to the buffering effect of saliva. Studies show that fruit juices are the most resistant to saliva's buffering effect, followed by, in order: fruit-based carbonated drinks and flavoured mineral waters, non-fruit-based carbonated drinks, sparkling mineral waters; Mineral water being the least resistant. Because of this, fruit juices in particular, may prolong the drop in pH levels.

A number of medications such as vitamin C, aspirin and some iron preparations are acidic and may contribute towards acid erosion.

Fluorosis is extremely common, with 41% of adolescents having definite fluorosis, and another 20% "questionably" having fluorosis according to the Centers for Disease Control.

The U.S. Centers for Disease Control found a 9 percentage point increase in the prevalence of confirmed dental fluorosis in a 1999-2002 study of American children and adolescents than was found in a similar survey from 1986-1987 (from 22.8% in 1986-1987 to 32% in 1999-2002). In addition, the survey provides further evidence that African Americans suffer from higher rates of fluorosis than Caucasian Americans.

The condition is more prevalent in rural areas where drinking water is derived from shallow wells or hand pumps. It is also more likely to occur in areas where the drinking water has a fluoride content greater than 1 ppm (part per million).

If the water supply is fluoridated at the level of 1 ppm, one must consume one litre of water in order to take in 1 mg of fluoride. It is thus improbable a person will receive more than the tolerable upper limit from consuming optimally fluoridated water alone.

Fluoride consumption can exceed the tolerable upper limit when someone drinks a lot of fluoride-containing water in combination with other fluoride sources, such as swallowing fluoridated toothpaste, consuming food with a high fluoride content, or consuming fluoride supplements. The use of fluoride supplements as a prevention for tooth decay is rare in areas with water fluoridation, but was recommended by many dentists in the UK until the early 1990s.

Dental fluorosis can be prevented by lowering the amount of fluoride intake to below the tolerable upper limit.

In November 2006 the American Dental Association published information stating that water fluoridation is safe, effective and healthy; that enamel fluorosis, usually mild and difficult for anyone except a dental health care professional to see, can result from ingesting more than optimal amounts of fluoride in early childhood; that it is safe to use fluoridated water to mix infant formula; and that the probability of babies developing fluorosis can be reduced by using ready-to-feed infant formula or using water that is either free of fluoride or low in fluoride to prepare powdered or liquid concentrate formula. They go on to say that the way to get the benefits of fluoride but minimize the risk of fluorosis for a child is to get the right amount of fluoride, not too much and not too little. "Your dentist, pediatrician or family physician can help you determine how to optimize your child’s fluoride intake."

The aetiology of dental abrasion can be due to a single stimuli or, as in most cases, multi-factorial. The most common cause of dental abrasion, is the combination of mechanical and chemical wear.

Tooth brushing is the most common cause of dental abrasion, which is found to develop along the gingival margin, due to vigorous brushing in this area. The type of toothbrush, the technique used and the force applied when brushing can influence the occurrence and severity of resulting abrasion. Further, brushing for extended periods of time (exceeding 2-3 min) in some cases, when combined with medium/hard bristled toothbrushes can cause abrasive lesions.

Different toothbrush types are more inclined to cause abrasion, such as those with medium or hard bristles. The bristles combined with forceful brushing techniques applied can roughen the tooth surface and cause abrasion as well as aggravating the gums. Repetitive irritation to the gingival margin can eventually cause recession of the gums. When the gums recede, the root surface is exposed which is more susceptible to abrasion.

Comparatively, electric toothbrushes have less abrasive tendencies.

Types of toothpastes can also damage enamel and dentine due to the abrasive properties. Specific ingredients are used in toothpaste to target removal of the bio-film and extrinsic staining however in some cases can contribute to the pastes being abrasive.

Whitening toothpastes are found to be one of the most abrasive types of toothpastes, according to the RDA Scale, detailed below. In-home and clinical whitening have been proven to increase the likelihood of an individual experiencing dental abrasion. It is believed that dental abrasion due to the whitening process is caused by a combination of both mechanical and chemical irritants, for example, using whitening toothpaste and at home bleaching kits together. However, if an individual is regimented in their after-whitening care then they can avoid loss of dentine minerals and in turn abrasion can be avoided. (that contribute to developing abrasion).

Another factor that can contribute to abrasion is alteration of pH levels in the saliva. This can be sugary/ acidic foods and liquids. The reasoning behind this is that an increase in acidity of saliva can induce demineralization and therefore compromising the tooth structure to abrasive factors such as tooth brushing or normal wear from mastication. When the tooth structure is compromised, this is where the mineral content of the saliva can create shallow depressions in the enamel and thus, when brushed can cause irreparable damage on tooth surface. The dental abrasion process can be further stimulated and accelerated through the effects of dental Acid erosion.

Dental erosion can occur by non-extrinsic factors too. Intrinsic dental erosion is known as perimolysis, whereby gastric acid from the stomach comes into contact with the teeth. People with illnesses such as anorexia nervosa, bulimia, and gastroesophageal reflux disease (GERD) often suffer from this. GERD is quite common and an average of 7% of adults experience reflux daily. The main cause of GERD is increased acid production by the stomach. This is not exclusive to adults, as GERD and other gastrointestinal disorders may cause dental erosions in children. Rumination also may cause acid erosion.

Dentin hypersensitivity is a relatively common condition. Due to differences in populations studied and methods of detection, the reported incidence ranges from 4-74%. Dentists may under-report dentin hypersensitivity due to difficulty in diagnosing and managing the condition. When questionnaires are used, the reported incidence is usually higher than when clinical examination is used. Overall, it is estimated to affect about 15% of the general population to some degree.

It can affect people of any age, although those aged 20–50 years are more likely to be affected. Females are slightly more likely to develop dentin hypersensitivity compared to males. The condition is most commonly associated with the maxillary and mandibular canine and bicuspid teeth on the facial (buccal) aspect, especially in areas of periodontal attachment loss.

Dental attrition is tooth wear caused by tooth to tooth contact. Well-defined wear facets appear on tooth cusps or ridges. This can be caused by several factors, including parafunctional habits such as bruxism or clenching, developmental defects, hard or rough-textured diet, and absence of posterior teeth support. If the natural teeth oppose or occlude with porcelain restorations, then accelerated attrition of the natural teeth may result. Similarly, when an edge to edge class III incisal relationship is present dental attrition can occur. The underlying cause of attrition may be related to the temporomandibular joint as a disruption or dysfunction of the joint can result in compromised function and complications such as bruxism and clenching of the jaw may arise

The etiology of dental attrition is multifactorial one of the most common causes of attrition is bruxism, one of the major causes being the use of MDMA (ecstasy) and various other related entactogenic drugs. Bruxism is the para-functional movement of the mandible, occurring during the day or night. It can be associated with presence of audible sound when clenching or grinding the teeth. This is usually reported by parents or partners if the grinding occurs during sleep. In some cases, dental erosion is also associated with severe dental attrition. Dental erosion is tooth surface loss caused by extrinsic or intrinsic forms of acid. Extrinsic erosion is due to a highly acidic diet, while intrinsic erosion is caused by regurgitation of gastric acids. Erosion softens the dental hard tissues making them more susceptible to attrition. Thus, if erosion and bruxism both exist, surface loss due to attrition is faster. Severe attrition in young patients is usually associated with erosive factors in their diets. The different physiological processes of tooth wear (abrasion, attrition and erosion) usually occur simultaneously and rarely work individually. Therefore, it is important to understand these tooth wear processes and their interactions to determine causes of tooth surface loss. Demineralization of the tooth surface due to acids can cause occlusal erosion as well as attrition. Wedge-shaped cervical lesions are commonly found in association with occlusal erosion and attrition.

Tooth wear is typically seen in the elderly and can be referred to as a natural aging process. Attrition, abrasion, erosion or a combination of these factors are the main reasons for tooth wear in elderly people who retain their natural teeth. This tooth wear can be pathological or physiological. The number of teeth with incisal or occlusal wear increases with age. Attrition occurs in 1 in 3 adolescents.

In addition to other occlusal factors, independent variables such as male gender, bruxism, and loss of molar occlusal contact, edge-to-edge relation of incisors, unilateral buccolingual cusp-to-cusp relation, and unemployment have been identified in affecting occlusal wear. Similarly, anterior cross-bite, unilateral posterior cross-bite, and anterior crowding have been found to be protective factors for high occlusal wear levels.

The most superficial concern in dental fluorosis is aesthetic changes in the permanent dentition (the adult teeth). The period when these teeth are at highest risk of developing fluorosis is between when the child is born up to 6 years old, though there has been some research which proposes that the most crucial course is during the first 2 years of the child's life. From roughly 7 years old thereafter, most children's permanent teeth would have undergone complete development (except their wisdom teeth), and therefore their susceptibility to fluorosis is greatly reduced, or even insignificant, despite the amount of intake of fluoride. The severity of dental fluorosis depends on the amount of fluoride exposure, the age of the child, individual response, weight, degree of physical activity, nutrition, and bone growth. Individual susceptibility to fluorosis is also influenced by genetic factors.

Many well-known sources of fluoride may contribute to overexposure including dentifrice/fluoridated mouthrinse (which young children may swallow), excessive ingestion of fluoride toothpaste, bottled waters which are not tested for their fluoride content, inappropriate use of fluoride supplements, ingestion of foods especially imported from other countries, and public water fluoridation. The last of these sources is directly or indirectly responsible for 40% of all fluorosis, but the resulting effect due to water fluoridation is largely and typically aesthetic. Severe cases can be caused by exposure to water that is naturally fluoridated to levels well above the recommended levels, or by exposure to other fluoride sources such as brick tea or pollution from high fluoride coal.

Dentin hypersensitivity may affect individuals' quality of life. Over time, the dentin-pulp complex may adapt to the decreased insulation by laying down tertiary dentin, thereby increasing the thickness between the pulp and the exposed dentin surface and lessening the symptoms of hypersensitivity. Similar process such as formation of a smear layer (e.g. from toothbrushing) and dentin sclerosis. These physiologic repair mechanisms are likely to occur with or without any form of treatment, but they take time.

"Relative dentin abrasivity" ("RDA") is a standardised measurement of the abrasive effect that the components of the toothpaste have on a tooth.

The RDA scale was developed by the American Dental Association (ADA). The RDA scale compares toothpaste abrasivity to standard abrasive materials and measures the depth of cut at an average of 1 millimetre per 100,000 brush strokes onto dentine. This comparison generates abrasive values for the dentifrices that would be safe for daily use. In vitro dental studies showed a positive correlation between the highest RDAs and greater dentin wear.

Since 1998, the RDA value is set by the standards DIN EN ISO 11609. Currently, the claim on products such as toothpaste are not regulated by law, however a dentifrice is required to have a level lower than 250 to be considered safe and before being given the ADA seal of approval. The values obtained depend on the size, quantity and surface structure of abrasive used in toothpastes.

While the RDA score has been shown to have a statistically significant correlation to the presence of abrasion, it is not the only contributing factor to consider. Other factors such as the amount of pressure used whilst brushing, the type, thickness and dispersion of bristle in the toothbrush and the time spent brushing are other factors that contribute to dental abrasion.

Attrition is loss of tooth substance caused by physical tooth-to-tooth contact. The word attrition is derived from the Latin verb "attritium", which refers to the action of rubbing against something. Attrition mostly causes wear of the incisal and occlusal surfaces of the teeth. Attrition has been associated with masticatory force and parafunctional activity such as bruxism. A degree of attrition is normal, especially in elderly individuals.

Erosion is chemical dissolution of tooth substance caused by acids, unrelated to the acid produced by bacteria in dental plaque. Erosion may occur with excessive consumption of acidic foods and drinks, or medical conditions involving repeated regurgitation and reflux of gastric acid. derived from the Latin word "erosum", which describes the action ‘to corrode’. This is usually on the palatal (inside) surfaces of upper front teeth and the occluding (top) surfaces of the molar teeth.

- Gastroesophageal reflux disease (GERD)

- Vomiting, e.g. bulimia, alcoholism

- Rumination

- Eructation (burping)

- Dietary - liquids of low pH and high titratable acids.

Dental attrition is a type of tooth wear caused by tooth-to-tooth contact, resulting in loss of tooth tissue, usually starting at the incisal or occlusal surfaces. Tooth wear is a physiological process and is commonly seen as a normal part of aging. Advanced and excessive wear and tooth surface loss can be defined as pathological in nature, requiring intervention by a dental practitioner. The pathological wear of the tooth surface can be caused by bruxism, which is clenching and grinding of the teeth. If the attrition is severe, the enamel can be completely worn away leaving underlying dentin exposed, resulting in an increased risk of dental caries and dentin hypersensitivity. It is best to identify pathological attrition at an early stage to prevent unnecessary loss of tooth structure as enamel does not regenerate.

In dentistry, calculus or tartar is a form of hardened dental plaque. It is caused by precipitation of minerals from saliva and gingival crevicular fluid (GCF) in plaque on the teeth. This process of precipitation kills the bacterial cells within dental plaque, but the rough and hardened surface that is formed provides an ideal surface for further plaque formation. This leads to calculus buildup, which compromises the health of the gingiva (gums). Calculus can form both along the gumline, where it is referred to as supragingival ("above the gum"), and within the narrow sulcus that exists between the teeth and the gingiva, where it is referred to as subgingival ("below the gum").

Calculus formation is associated with a number of clinical manifestations, including bad breath, receding gums and chronically inflamed gingiva. Brushing and flossing can remove plaque from which calculus forms; however, once formed, it is too hard and firmly attached to be removed with a toothbrush. Calculus buildup can be removed with ultrasonic tools or dental hand instruments (such as a periodontal scaler).

Plaque accumulation causes the gingiva to become irritated and inflamed, and this is referred to as gingivitis. When the gingiva become so irritated that there is a loss of the connective tissue fibers that attach the gums to the teeth and bone that surrounds the tooth, this is known as periodontitis. Dental plaque is not the sole cause of periodontitis, however it is many times referred to as a primary aetiology. Plaque that remains in the oral cavity long enough will eventually calcify and become calculus. Calculus is detrimental to gingival health because it serves as a trap for increased plaque formation and retention; thus, calculus, along with other factors that cause a localized build-up of plaque, is referred to as a secondary aetiology of periodontitis.

When plaque is supragingival, the bacterial content contains a great proportion of aerobic bacteria and yeast, or those bacteria which utilize and can survive in an environment containing oxygen. Subgingival plaque contains a higher proportion of anaerobic bacteria, or those bacteria which cannot exist in an environment containing oxygen. Several anaerobic plaque bacteria, such as "Porphyromonas gingivalis", secrete antigenic proteins that trigger a strong inflammatory response in the periodontium, the specialized tissues that surround and support the teeth. Prolonged inflammation of the periodontium leads to bone loss and weakening of the gingival fibers that attach the teeth to the gums, two major hallmarks of periodontitis. Supragingival calculus formation is nearly ubiquitous in humans, but to differing degrees. Almost all individuals with periodontitis exhibit considerable subgingival calculus deposits. Dental plaque bacteria have been linked to cardiovascular disease and mothers giving birth to pre-term low weight infants, but there is no conclusive evidence yet that periodontitis is a significant risk factor for either of these two conditions.

There is a wide variation in reported epidemiologic data for bruxism, and this is largely due to differences in the definition, diagnosis and research methodologies of these studies. E.g. several studies use self-reported bruxism as a measure of bruxism, and since many people with bruxism are not aware of their habit, self-reported tooth grinding and clenching habits may be a poor measure of the true prevalence.

The ICSD-R states that 85–90% of the general population grind their teeth to a degree at some point during their life, although only 5% will develop a clinical condition. Some studies have reported that awake bruxism affects females more commonly than males, while in sleep bruxism, males are as equally affected as females.

Children are reported to brux as commonly as adults. It is possible for sleep bruxism to occur as early as the first year of life – after the first teeth (deciduous incisors) erupt into the mouth, and the overall prevalence in children is about 14–20%. The ICSD-R states that sleep bruxism may occur in over 50% of normal infants. Often sleep bruxism develops during adolescence, and the prevalence in 18- to 29-year-olds is about 13%. The overall prevalence in adults is reported to be 8%, and people over the age of 60 are less likely to be affected, with the prevalence dropping to about 3% in this group.

A 2013 systematic review of the epidemiologic reports of bruxism concluded a prevalence of about 22.1–31% for awake bruxism, 9.7–15.9% for sleep bruxism, and an overall prevalence of about 8–31.4% of bruxism generally. The review also concluded that overall, bruxism affects males and females equally, and affects elderly people less commonly.

Bruxism is excessive teeth grinding or jaw clenching. It is an oral parafunctional activity; i.e., it is unrelated to normal function such as eating or talking. Bruxism is a common behavior; reports of prevalence range from 8–31% in the general population. Several symptoms are commonly associated with bruxism, including hypersensitive teeth, aching jaw muscles, headaches, tooth wear, and damage to dental restorations (e.g. crowns and fillings) to teeth. But symptoms may be minimal, without patient awareness of the condition.

There are two main types of bruxism: one occurs during sleep (sleep bruxism) and one during wakefulness (awake bruxism). Dental damage may be similar in both types, but the symptoms of sleep bruxism tend to be worse on waking and improve during the course of the day, and the symptoms of awake bruxism may not be present at all on waking, and then worsen over the day. The causes of bruxism are not completely understood, but probably involve multiple factors. Awake bruxism is thought to have different causes from sleep bruxism, and is more common in females, whereas males and females are affected in equal proportions by sleep bruxism. Several treatments are in use, although there is little evidence of robust efficacy for any particular treatment.

Dental calculus (tartar) is a hard substance formed on the teeth from the mineralization of plaque. Dental tartar primarily comes from wet food which get stuck to the teeth for extended periods of time. Tartar can be avoided by ferrets eating raw meat, bones and preferably whole prey. The biomechanics of consuming meat and bones will keep the teeth clean. Left to itself, tartar may lead to gingivitis which in turn can lead to a dental abscess, bone loss, infections which may spread bacteria through the bloodstream to internal organs and lead to death if not treated. Tartar can be removed either mechanical or by ultrasound at a veterinarian (this usually involves anesthesia), a small toothbrush can also be used as a preventive measure if one is unable to feed the animal with raw meat. Tartar can be prevented by feeding raw food or giving specially made gelatin treats for ferrets.

Dental abrasion or tooth wear is common in ferrets, and is caused by mechanical wear of the teeth. Eating manufactured dry food (kibble) will erode (due to the hard and extremely dry kibble) the carnassial teeth of the ferret, the wear from the eating kibble can become significant with old age (after three to five years). If teeth are overly ground down, a ferret cannot use them as scissors to eat raw meat. Tooth erosion eventually affects a ferret's ability to eat solid food. Dental abrasion can also be caused by excessive chewing on fabrics or toys, and cage biting. If the ferret engages in these activities a lot, it might be a sign of boredom, and more stimulating activities (such as play) should rectify the situation.

Hairballs can occur in ferrets, but are not readily expelled by vomiting like the way cats deal with them. One or more hairballs in a ferret may lead to loss of appetite and subsequent weight loss. A hairball may enter the intestine and cause a life-threatening obstruction. Ferrets typically replace their coats twice a year, and at that time require brushing to remove loose hairs before they can be ingested, and possibly administration of a hairball remedy as a preventive. Artificial lighting or administration of certain medications may alter the normal spring and fall seasonal coat changes in the ferret.

Fiddler’s neck does not usually form unless the musician is practicing or playing for more than a few hours each day, and only seems to develop after a few years of serious playing. Thus, when not infected or otherwise problematic, fiddler’s neck may be known as a benign practice mark and may be worn proudly as an indication of long hours of practice. Blum & Ritter (1990) found that 62% of 523 professional violinists and violists in West Germany experienced fiddler’s neck, with the percentage among violists being higher (67%) than among violinists (59%). Viola players are believed to be more predisposed to developing fiddler’s neck than violinists because the viola is larger and heavier, but this has not been empirically confirmed.

The development of fiddler’s neck does not depend on preexisting skin problems, and Blum & Ritter find that only 23% of men and 14% of women in their study reported cutaneous disorders in other parts of the face (mainly acne and eczema) that were independent of playing the violin or viola. Fiddler’s neck may exacerbate existing acne, but acne may also be limited solely to the lesion and not appear elsewhere. Nonetheless, musicians with underlying dermatologic diseases like acne and eczema are more endangered by fiddler’s neck than others. Males may develop folliculitis or boils due to involvement of beard hair.

The proximal causes of fiddler’s neck are friction and pressure, but both repetitive shearing stress and occlusion with consequent trapping of sweat give rise to progressive damage. This damage along with poor hygiene predisposes the area to local infection, and such infection can progress to scarring and other long-term effects. Hot weather is reported to exacerbate fiddler’s neck, as are tiredness, playing emotional music, and playing in smaller groups where individual stress is higher. Type I hypersensitivity reactions may also be involved, particularly to rosewood and ebony in the chinrest and tailpiece, as well as to varnish of the instrument body when chinrests are not used and to rosin deposits on the instrument and on chin cloths. Nickel or other metal allergies are common causes if the chin rest has a metal clip that comes into constant contact with the skin. Rosin exposure in particular may lead to abietic acid dermatitis.

People with diabetes face special skin challenges. Because diabetes affects the capillaries, the small blood vessels which feed the skin, thickening of the skin with callus increases the difficulty of supplying nutrients to the skin. Callus formation is seen in high numbers of patients with diabetes, and together with absent foot pulses and formation of hammer toe, this may be an early sign of individuals at an increased risk for foot ulcers.

The stiffness of a callus or corn, coupled with the shear and pressure that caused it, may tear the capillaries or adjoining tissue, causing bleeding within the callus or corn. Often, bleeding within a callus is an early sign of diabetes, even before elevated blood sugars may be noticed. Although the bleeding can be small, sometimes small pools of blood or hematoma are formed. The blood itself is an irritant, a foreign body within the callus that makes the area burn or itch. If the pool of blood is exposed to the outside, infection may follow. Infection may also lead to ulceration. Fortunately, this process can be prevented at several places. Diabetic foot infections are the leading cause of diabetic limb amputation.

Calluses and corns may go away by themselves eventually, once the irritation is consistently avoided. They may also be dissolved with keratolytic agents containing salicylic acid, sanded down with a pumice stone or silicon carbide sandpaper or filed down with a callus shaver, or pared down by a professional such as a podiatrist or a foot health practitioner.

A saddle sore in humans is a skin ailment on the buttocks due to, or exacerbated by, horse riding or cycling on a bicycle saddle. It often develops in three stages: skin abrasion, folliculitis (which looks like a small, reddish acne), and finally abscess.

Because it most commonly starts with skin abrasion, it is desirable to reduce the factors which lead to skin abrasion. Some of these factors include:

- Reducing the friction. In equestrian activities, friction is reduced with a proper riding position and using properly fitting clothing and equipment. In cycling, friction from bobbing or swinging motion while pedaling is reduced by setting the appropriate saddle height. Angle and fore/aft position can also play a role, and different cyclists have different needs and preferences in relation to this.

- Selecting an appropriate size and design of horse riding saddle or bicycle saddle.

- Wearing proper clothing. In bicycling, this includes cycling shorts, with chamois padding. For equestrian activity, long, closely fitted pants such as equestrian breeches or jodhpurs minimize chafing. For western riding, closely fitted jeans with no heavy inner seam, sometimes combined with chaps, are preferred. Padded cycling shorts worn under riding pants helps some equestrians, and extra padding, particularly sheepskin, on the seat of the saddle may help in more difficult situations such as long-distance endurance riding.

- Using petroleum jelly, chamois cream or lubricating gel to further reduce friction.

If left untreated over an extended period of time, saddle sores may need to be drained by a physician.

In animals such as horses and other working animals, saddle sores often form on either side of the withers, which is the area where the front of a saddle rests, and also in the girth area behind the animal's elbow, where they are known as a girth gall. Saddle sores can occur over the loin, and occasionally in other locations. These sores are usually caused by ill-fitting gear, dirty gear, lack of proper padding, or unbalanced loads. Reducing friction is also of great help in preventing equine saddle sores. Where there is swelling but not yet open sores, the incidence of sore backs may be reduced by loosening the girth, but not immediately removing the saddle after a long ride, thus allowing normal circulation to return slowly.

In August 2010, DePuy recalled its hip replacement systems ASR XL Acetabular Hip Replacement System and ASR Hip Resurfacing System due to failure rates and side effects including metallosis. The recalls triggered a large number of lawsuits against DePuy and its parent company Johnson & Johnson upon claims that the companies knew about the dangers of the implants before they went on the market in the United States.

Metallosis is the putative medical condition involving deposition and build-up of metal debris in the soft tissues of the body.

Metallosis has been hypothesized to occur when metallic components in medical implants, specifically joint replacements, abrade against one another.

Metallosis has also been observed in some patients either sensitive to the implant or for unknown reasons even in the absence of malpositioned prosthesis. Though rare, metallosis has been observed at an estimated incidence of 5% of metal joint implant patients over the last 40 years. Women may be at slightly higher risk than men. If metallosis occurs, it may involve the hip and knee joints, the shoulder, wrist, or elbow joints.

The abrasion of metal components may cause metal ions to be solubilized. The hypothesis that the immune system identifies the metal ions as foreign bodies and inflames the area around the debris may be incorrect because of the small size of metal ions may prevent them from becoming haptens. Poisoning from metallosis is rare, but cobaltism is an established health concern. The involvement of the immune system in this putative condition has also been theorized but has never been proven.

Purported symptoms of metallosis generally include pain around the site of the implant, pseudotumors (a mass of inflamed cells that resembles a tumor but is actually collected fluids), and a noticeable rash that indicates necrosis. The damaged and inflamed tissue can also contribute to loosening the implant or medical device. Metallosis can cause dislocation of non-cemented implants as the healthy tissue that would normally hold the implant in place is weakened or destroyed. Metallosis has been demonstrated to cause osteolysis.

Women, those who are small in stature, and the obese are at greater risk for metallosis because their body structure causes more tension on the implant, quickening the abrasion of the metal components and the subsequent build-up of metallic debris.