Acid erosion often coexists with abrasion and attrition. Abrasion is most often caused by brushing teeth too hard.

Any frothing or swishing acidic drinks around the mouth increases the risk of acid erosion.

There are many signs of dental erosion, including changes in appearance and sensitivity. One of the physical changes can be the color of teeth. There are two different colors teeth may turn if dental erosion is occurring, the first being a change of color that usually happens on the cutting edge of the central incisors. This causes the cutting edge of the tooth to become transparent. A second sign is if the tooth has a yellowish tint. This occurs because the white enamel has eroded away to reveal the yellowish dentin. A change in shape of the teeth is also a sign of dental erosion. Teeth will begin to appear with a broad rounded concavity, and the gaps between teeth will become larger. There can be evidence of wear on surfaces of teeth not expected to be in contact with one another. If dental erosion occurs in children, a loss of enamel surface characteristics can occur. Amalgam restorations in the mouth may be clean and non-tarnished. Fillings may also appear to be rising out of the tooth, the appearance being caused when the tooth is eroded away leaving only the filling. The teeth may form divots on the chewing surfaces when dental erosion is occurring. This mainly happens on the first, second, and third molars. One of the most severe signs of dental erosion is cracking, where teeth begin to crack off and become coarse. Other signs include pain when eating hot, cold, or sweet foods. This pain is due to the enamel having been eroded away, exposing the sensitive dentin.

Attrition occurs as a result of opposing tooth surfaces contacting. The contact can affect cuspal, incisal and proximal surface areas.

Indications of attrition can include:

- Loss of tooth anatomy: This results in loss of tooth characteristics including rounding or sharpening of incisal edges, loss of cusps and fracturing of teeth. Enamel of molar teeth may appear thin and flat. When in occlusion the teeth may appear the same height which is particularly apparent for anterior teeth.

- Sensitivity or pain: Attrition may be entirely asymptomatic, or there may be dentin hypersensitivity secondary to loss of the enamel layer, or tenderness of the periodontal ligament caused by occlusal trauma.

- Tooth discolouration: A yellow appearance of the tooth surface may be due to the enamel being worn away, exposing the darker yellower dentin layer underneath.

- Altered occlusion due to decreasing vertical height, or occlusal vertical dimension.

- Compromised periodontal support can result in tooth mobility and drifting of teeth

- Loss in posterior occlusal stability

- Mechanical failure of restorations

Clinical signs of TRs are often minimal since the discomfort can be minor. However, some authors have described discomfort while chewing, anorexia, dehydration, weight loss, and tooth fracture. The lower third premolar is the most commonly affected tooth.

Abrasion is a pathological, non-carious tooth loss that most commonly affects the premolars and canines. Abrasion frequently presents at the cemento-enamel junction and can be caused by many contributing factors, all with the ability to affect the tooth surface in varying degrees.

Sources of abrasion may arise from oral hygiene habits such as toothbrushes, toothpicks, floss, and dental appliance or may arise from other habits such as nail biting, chewing tobacco or another object. Abrasion can also occur from the type of dentifrice being utilized as some have more abrasive qualities such as whitening toothpastes.

The appearance may vary depending on the aetiology of abrasion, however most commonly presents in a V-shaped caused by excessive lateral pressure whilst tooth-brushing. The surface is shiny rather than carious, and sometimes the ridge is deep enough to see the pulp chamber within the tooth itself.

In order for successful treatment of abrasion to occur, the aetiology first needs to be identified and ceased, e.g. overzealous brushing. Once this has occurred subsequent treatment may involve the changes in oral hygiene or toothpaste, application of fluoride to reduce sensitivity or the placement of a restoration to aid in reducing the progression of further tooth loss.

Tooth wear (also termed non-carious tooth substance loss) refers to loss of tooth substance by means other than dental caries or dental trauma. Tooth wear is a very common condition that occurs in approximately 97% of the population. This is a normal physiological process occurring throughout life, but accelerated tooth wear can become a problem.

Tooth wear is majorly the result of three processes; attrition, abrasion and erosion. These forms of tooth wear can further lead to a condition known as abfraction, where by tooth tissue is 'fractured' due to stress lesions caused by extrinsic forces on the enamel. Tooth wear is a complex, multi-factorial problem and there is difficulty identifying a single causative factor. However, tooth wear is often a combination of the above processes. Many clinicians therefore make diagnoses such as "tooth wear with a major element of attrition", or "tooth wear with a major element of erosion" to reflect this. This makes the diagnosis and management difficult. Therefore, it is important to distinguish between these various types of tooth wear, provide an insight into diagnosis, risk factors, and causative factors, in order to implement appropriate interventions.

Multiple indices have been developed in order to assess and record the degree of tooth wear, the earliest was that by Paul Broca. In 1984, Smith and Knight developed the tooth wear index (TWI) where four visible surfaces (buccal, cervical, lingual, occlusal-incisal) of all teeth present are scored for wear, regardless of the cause.

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.

Dental trauma may result in discolorations. Following luxation injuries red discoloration may develop almost instantly. This is due to severance of the venous microcirculation to a tooth, while the arteries continue to supply blood to the pulp. The blood is then decomposed gradually and a blue-brown discoloration develops.

Teeth may turn grey following trauma-induced pulp necrosis (death of the pulp). This discoloration typically develops weeks or months after the injury and is caused by incorporation of pigments released during the breakdown of the pulpal tissue and blood into the dentin.

Yellow discoloration may occur following pulp canal obliteration, i.e., the sealing up of the pulp. Trauma to a developing adult tooth (e.g., intrusion of a baby tooth into the bone) may affect the enamel layer of the adult tooth. This becomes apparent when the adult tooth erupts into the mouth.

Internal resorption may sometimes follow dental trauma (although in other cases it appears unrelated). This is where the dentin is resorbed and replaced instead by hyperplastic, vascular pulp tissue. As this process starts to approach the external surface of the tooth, a pink hue of this replacement pulp tissue may become visible through the remaining overlying tooth substance. This appearance is sometimes termed "pink tooth of Mummery".

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.

Feline Tooth Resorption (TR) is a syndrome in cats characterized by resorption of the tooth by odontoclasts, cells similar to osteoclasts. TR has also been called "feline odontoclastic resorption lesion" (FORL), neck lesion, cervical neck lesion, cervical line erosion, feline subgingival resorptive lesion, feline caries, or feline cavity. It is one of the most common diseases of domestic cats, affecting up to two-thirds. TRs have been seen more recently in the history of feline medicine due to the advancing ages of cats, but 800-year-old cat skeletons have shown evidence of this disease. Purebred cats, especially Siamese and Persians, may be more susceptible.

TRs clinically appear as erosions of the surface of the tooth at the gingival border. They are often covered with calculus or gingival tissue. It is a progressive disease, usually starting with loss of cementum and dentin and leading to penetration of the pulp cavity. Resorption continues up the dentinal tubules into the tooth crown. The enamel is also resorbed or undermined to the point of tooth fracture. Resorbed cementum and dentin is replaced with bone-like tissue.

Dentin hypersensitivity (abbreviated to DH, or DHS, and also termed sensitive dentin, dentin sensitivity, cervical sensitivity, and cervical hypersensitivity) is dental pain which is sharp in character and of short duration, arising from exposed dentin surfaces in response to stimuli, typically thermal, evaporative, tactile, osmotic, chemical or electrical; and which cannot be ascribed to any other dental disease.

A degree of dentin sensitivity is normal, but pain is not usually experienced in everyday activities like drinking a cooled drink. Therefore, although the terms "dentin sensitivity" and "sensitive dentin" are used interchangeably to refer to dental hypersensitivity, the latter term is the most accurate.

Methamphetamine (meth), a psychologically addictive drug that produces a sharp increase in energy and possible euphoria, can have negative health effects that include serious dental problems. , it is the most discussed illegal drug in dental literature. The most notable effect of long-term use of methamphetamine on dental health is the development of caries (tooth decay); the teeth of some drug users appear to be dark and in the process of disintegrating. Caries often occur in the cervical regions of teeth, where the tooth surface narrows at the junction of the crown and the root. It is usually found on the buccal (cheek) side of the teeth and on tooth surfaces that are adjacent to incisors and canines; eventually, the coronal tooth area, near the crown, can be affected by the decay and erosion. The dental caries of meth mouth often progress slowly, perhaps because their advancement is hindered by intermittent hygienic practices. The decay can lead to tooth fractures and severe pain. In some cases, teeth are permanently damaged and must be removed. Along with malnutrition and weight loss, the dental effects of methamphetamine use contribute to the appearance of premature aging seen in some users. The effects of meth mouth are similar to those of Sjögren's syndrome, an autoimmune disease that causes a lack of saliva, which results in tooth decay.

Methamphetamine users sometimes experience soreness in the joint of the jaw and dental attrition (tooth wear), owing to bruxism (grinding of the teeth) caused by the drug. This bruxism can occur continuously. Chronic use of the drug might also cause trismus, the inability to open the jaw. Long-term users often experience xerostomia (dry mouth).

The pain is sharp and sudden, in response to an external stimulus. The most common trigger is cold, with 75% of people with hypersensitivity reporting pain upon application of a cold stimulus. Other types of stimuli may also trigger pain in dentin hypersensitivity, including:

- Thermal – hot and cold drinks and foods, cold air, coolant water jet from a dental instrument.

- Electrical – electric pulp testers.

- Mechanical–tactile – dental probe during dental examination, periodontal scaling and root planing, toothbrushing.

- Osmotic – hypertonic solutions such as sugars.

- Evaporation – air blast from a dental instrument.

- Chemical – acids, e.g. dietary, gastric, acid etch during dental treatments.

The frequency and severity with which the pain occurs are variable.

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.

Meth mouth is severe tooth decay and tooth loss, as well as tooth fracture, acid erosion, and other oral problems, potentially symptomatic of extended use of the drug methamphetamine. The condition is thought to be caused by a combination of side effects of the drug (clenching and grinding of teeth, dry mouth) and lifestyle factors (infrequent oral hygiene, frequent consumption of sugary drinks, as well as neglecting regular dental cleanings and preventative care), which may be present in long term users. However, the legitimacy of meth mouth as a unique condition has been questioned because of the similar effects of some other drugs on teeth. Images of diseased mouths are often used in anti-drug campaigns.

The condition is difficult to treat, and may involve fillings, fluoride to fight tooth decay and drugs that increase saliva for dry mouth, as well as oral hygiene instruction. It can be medically dangerous for active methamphetamine users because of the cardiac problems that can result from the interaction of local anesthetic with the drug.

True hyposalivation may give the following signs and symptoms:

- Dental caries (xerostomia related caries) – Without the anticariogenic actions of saliva, tooth decay is a common feature and may progress much more aggressively than it would otherwise ("rampant caries"). It may affect tooth surfaces that are normally spared, e.g., cervical caries and root surface caries. This is often seen in patients who have had radiotherapy involving the major salivary glands, termed radiation-induced caries.

- Acid erosion. Saliva acts as a buffer and helps to prevent demineralization of teeth.

- Oral candidiasis – A loss of the antimicrobial actions of saliva may also lead to opportunistic infection with "Candida" species.

- Ascending (suppurative) sialadenitis – an infection of the major salivary glands (usually the parotid gland) that may be recurrent. It is associated with hyposalivation, as bacteria are able to enter the ductal system against the diminished flow of saliva. There may be swollen salivary glands even without acute infection, possibly caused by autoimmune involvement.

- Dysgeusia – altered taste sensation (e.g., a metallic taste) and dysosmia, altered sense of smell.

- Intraoral halitosis – possibly due to increased activity of halitogenic biofilm on the posterior dorsal tongue (although dysgeusia may cause a complaint of nongenuine halitosis in the absence of hyposalivation).

- Oral dysesthesia – a burning or tingling sensation in the mouth.

- Saliva that appears thick or ropey.

- Mucosa that appears dry.

- A lack of saliva pooling in the floor of the mouth during examination.

- Dysphagia – difficulty swallowing and chewing, especially when eating dry foods. Food may stick to the tissues during eating.

- The tongue may stick to the palate, causing a clicking noise during speech, or the lips may stick together.

- Gloves or a dental mirror may stick to the tissues.

- Fissured tongue with atrophy of the filiform papillae and a lobulated, erythematous appearance of the tongue.

- Saliva cannot be "milked" (expressed) from the parotid duct.

- Difficulty wearing dentures, e.g., when swallowing or speaking. There may be generalized mucosal soreness and ulceration of the areas covered by the denture.

- Mouth soreness and oral mucositis.

- Lipstick or food may stick to the teeth.

- A need to sip drinks frequently while talking or eating.

- Dry, sore, and cracked lips and angles of mouth.

- Thirst.

However, sometimes the clinical findings do not correlate with the symptoms experienced. E.g., a person with signs of hyposalivation may not complain of xerostomia. Conversely a person who reports experiencing xerostomia may not show signs of reduced salivary secretions (subjective xerostomia). In the latter scenario, there are often other oral symptoms suggestive of oral dysesthesia ("burning mouth syndrome"). Some symptoms outside the mouth may occur together with xerostomia.

These include:

- Xerophthalmia (dry eyes).

- Inability to cry.

- Blurred vision.

- Photophobia (light intolerance).

- Dryness of other mucosae, e.g., nasal, laryngeal, and/or genital.

- Burning sensation.

- Itching or grittiness.

- Dysphonia (voice changes).

There may also be other systemic signs and symptoms if there is an underlying cause such as Sjögren's syndrome, for example, joint pain due to associated rheumatoid arthritis.

Bleeding on probing which is also known as bleeding gums or gingival bleeding is a term used by dentists and dental hygienists when referring to bleeding that is induced by gentle manipulation of the tissue at the depth of the gingival sulcus, or interface between the gingiva and a tooth. Bleeding on probing, often abbreviated BOP, is a sign of inflammation and indicates some sort of destruction and erosion to the lining of the sulcus or the ulceration of sulcular epithelium. The blood comes from lamina propria after the ulceration of the lining.

An examination by the dentist or dental hygienist should be sufficient to rule out the issues such as malnutrition and puberty. Additional corresponding diagnosis tests to certain potential disease may be required. This includes oral glucose tolerance test for diabetes mellitus, blood studies, human gonadotrophin levels for pregnancy, and X-rays for teeth and jaw bones.

In order to determine the periodontal health of a patient, the dentist or dental hygienist records the sulcular depths of the gingiva and observes any bleeding on probing. This is often accomplished with the use of a periodontal probe. Alternatively, dental floss may also be used to assess the Gingival bleeding index. It is used as an initial evaluation on patient's periodontal health especially to measure gingivitis. The number of bleeding sites is used to calculate the gingival bleeding score.

Peer-reviewed dental literature thoroughly establishes that bleeding on probing is a poor positive predictor of periodontal disease, but conversely lack of bleeding is a very strong negative predictor. The clinical interpretation of this research is that while BOP presence may not indicate periodontal disease, continued absence of BOP is a strong predictor (approximately 98%) of continued periodontal health.

The differential of hyposalivation significantly overlaps with that of xerostomia. A reduction in saliva production to about 50% of the normal unstimulated level will usually result in the sensation of dry mouth. Altered saliva composition may also be responsible for xerostomia.

HLLE begins as small pits of receding epithelium (skin) around the fish’s head and/or lateral line, and sometimes onto the unpaired fins. Rarely fatal, it does cause disfigurement, making the fish less suitable for public aquarium display. At least 20 families of fish have been identified as having developed HLLE in captivity. Not all species of fish show the same symptoms, and do not always develop lesions to the same degree.

AC almost always affects the lower lip and only rarely the upper lip, probably because the lower lip is more exposed to the sun. In the unusual cases reported where it affects the upper lip, this may be due to upper lip prominence. The commissures (corners of the mouth) are not usually involved.

Affected individuals may experience symptoms such as a dry sensation and cracking of the lips.

It is usually painless and persistent.

The appearance is variable. White lesions indicate hyperkeratosis. Red, erosiive or ulcerative lesions indicate atrophy, loss of epithelium and inflammation. Early, acute lesions may be erythematous (red) and edematous (swollen). With months and years of sun exposure, the lesion becomes chronic and may be grey-white in color and appear dry, scaly and wrinkled.

There is thickening whitish discoloration of the lip at the border of the lip and skin. There is also a loss of the usually sharp border between the red of the lip and the normal skin, known as the vermillion border. The lip may become scaly and indurated as AC progresses.

When palpated, the lip may have a texture similar to rubbing the gloved finger along sandpaper.

AC may occur with skin lesions of actinic keratosis or skin cancer elsewhere, particularly on the head and neck since these are the most sun exposed areas. Rarely it may represent a genetic susceptibility to light damage (e.g. xeroderma pigmentosum or actinic prurigo).

As a result of radiotherapy to the mouth, radiation-induced stomatitis may develop, which can be associated with mucosal erosions and ulceration. If the salivary glands are irradiated, there may also be xerostomia (dry mouth), making the oral mucosa more vulnerable to frictional damage as the lubricating function of saliva is lost, and mucosal atrophy (thinning), which makes a breach of the epithelium more likely. Radiation to the bones of the jaws causes damage to osteocytes and impairs the blood supply. The affected hard tissues become hypovascular (reduced number of blood vessels), hypocellular (reduced number of cells), and hypoxic (low levels of oxygen). Osteoradionecrosis is the term for when such an area of irradiated bone does not heal from this damage. This usually occurs in the mandible, and causes chronic pain and surface ulceration, sometimes resulting in non-healing bone being exposed through a soft tissue defect. Prevention of osteradionecrosis is part of the reason why all teeth of questionable prognosis are removed before the start of a course of radiotherapy.

"Hole in the head can be reversed by removing all activated carbon and conducting large percentage water changes. Greater than 90% water changes may need to be done to reduce the effects of activated carbon. More commonly, cures are made by moving the fish to a new aquarium that has never had fish develop HLLE in it.

Aphthous stomatitis (also termed recurrent aphthous stomatits, RAS, and commonly called "canker sores") is a very common cause of oral ulceration. 10–25% of the general population suffer from this non-contagious condition. The appearance of aphthous stomatitis varies as there are 3 types, namely minor aphthous ulceration, major aphthous ulceration and herpetiform ulceration. Minor aphthous ulceration is the most common type, presenting with 1–6 small (2-4mm diameter), round/oval ulcers with a yellow-grey color and an erythematous (red) "halo". These ulcers heal with no permanent scarring in about 7–10 days. Ulcers recur at intervals of about 1–4 months. Major aphthous ulceration is less common than the minor type, but produces more severe lesions and symptoms. Major aphthous ulceration presents with larger (>1 cm diameter) ulcers that take much longer to heal (10–40 days) and may leave scarring. The minor and major subtypes of aphthous stomatitis usually produce lesions on the non-keratinized oral mucosa (i.e. the inside of the cheeks, lips, underneath the tongue and the floor of mouth), but less commonly major aphthous ulcers may occur in other parts of the mouth on keratinized mucosal surfaces. The least common type is herpetiform ulceration, so named because the condition resembles primary herpetic gingivostomatitis. Herpetiform ulcers begin as small blisters (vesicles) which break down into 2-3mm sized ulcers. Herpetiform ulcers appear in "crops" sometimes hundreds in number, which can coalesce to form larger areas of ulceration. This subtype may cause extreme pain, heals with scarring and may recur frequently.

The exact cause of aphthous stomatitis is unknown, but there may be a genetic predisposition in some people. Other possible causes include hematinic deficiency (folate, vitamin B, iron), stopping smoking, stress, menstruation, trauma, food allergies or hypersensitivity to sodium lauryl sulphate (found in many brands of toothpaste). Aphthous stomatitis has no clinically detectable signs or symptoms outside the mouth, but the recurrent ulceration can cause much discomfort to sufferers. Treatment is aimed at reducing the pain and swelling and speeding healing, and may involve systemic or topical steroids, analgesics (pain killers), antiseptics, anti-inflammatories or barrier pastes to protect the raw area(s).