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.

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.

Acute periapical periodontitis, also termed acute apical periodontitis, acute periradicular periodontitis, or symptomatic periapical periodontitis.

A person experiencing caries may not be aware of the disease. The earliest sign of a new carious lesion is the appearance of a chalky white spot on the surface of the tooth, indicating an area of demineralization of enamel. This is referred to as a white spot lesion, an incipient carious lesion or a "microcavity". As the lesion continues to demineralize, it can turn brown but will eventually turn into a cavitation ("cavity"). Before the cavity forms, the process is reversible, but once a cavity forms, the lost tooth structure cannot be regenerated.

A lesion that appears dark brown and shiny suggests dental caries were once present but the demineralization process has stopped, leaving a stain. Active decay is lighter in color and dull in appearance.

As the enamel and dentin are destroyed, the cavity becomes more noticeable. The affected areas of the tooth change color and become soft to the touch. Once the decay passes through enamel, the dentinal tubules, which have passages to the nerve of the tooth, become exposed, resulting in pain that can be transient, temporarily worsening with exposure to heat, cold, or sweet foods and drinks. A tooth weakened by extensive internal decay can sometimes suddenly fracture under normal chewing forces. When the decay has progressed enough to allow the bacteria to overwhelm the pulp tissue in the center of the tooth, a toothache can result and the pain will become more constant. Death of the pulp tissue and infection are common consequences. The tooth will no longer be sensitive to hot or cold, but can be very tender to pressure.

Dental caries can also cause bad breath and foul tastes. In highly progressed cases, an infection can spread from the tooth to the surrounding soft tissues. Complications such as cavernous sinus thrombosis and Ludwig angina can be life-threatening.

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.

There are two types of TR. "Type 1" lesions are focal defects often caused by local inflammation. "Type 2" lesions are characterized by a generalized loss of root radiopacity on a dental radiograph. The definitive cause of type 2 TRs is unknown, but histologically destruction of the cementum and other mineralized tissue of the tooth root by odontoclasts is seen. It occurs secondary to the loss of the protective covering of the root (the periodontal ligaments) and possibly to a stimulus such as periodontal disease and the release of cytokines, leading to odontoclast migration. However, FORLs can develop in the absence of inflammation. The natural inhibition to root resorption provided by the lining of the root may be altered by increased amounts of Vitamin D, in cats supplied by their diet.

Ankylosis of deciduous teeth ("submerged teeth") may rarely occur. The most commonly affected tooth is the mandibular (lower) second deciduous molar. Partial root resorption first occurs and then the tooth fuses to the bone. This prevents normal exfoliation of the deciduous tooth and typically causes impaction of the permanent successor tooth. As growth of the alveolar bone continues and the adjacent permanent teeth erupt, the ankylosed deciduous tooth appears to submerge into the bone, although in reality it has not changed position. Treatment is by extraction of the involved tooth, to prevent malocclusion, periodontal disturbance or dental caries.

The radiographic features of periapical inflammatory lesions vary depending on the time course of the lesion. Because very early lesions

may not show any radiographic changes, diagnosis of these lesions relies solely on the clinical symptoms . More chronic lesions may show lytic (radiolucent) or sclerotic (radiopaque) changes, or both.

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.

Increased sensitivity to stimuli, specifically hot and cold, is a common symptom of pulpitis. A prolonged throbbing pain may be associated with the disease. However, pulpitis can also occur without any pain.

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.

Pulpitis is inflammation of dental pulp tissue. The pulp contains the blood vessels the nerves and connective tissue inside a tooth and provides the tooth’s blood and nutrients. Pulpitis is mainly caused by bacteria infection which itself is a secondary development of caries (tooth decay). It manifests itself in the form of a toothache.

Early childhood caries (ECC), also known as "baby bottle caries," "baby bottle tooth decay" or "bottle rot," is a pattern of decay found in young children with their deciduous (baby) teeth. The teeth most likely affected are the maxillary anterior teeth, but all teeth can be affected. The name for this type of caries comes from the fact that the decay usually is a result of allowing children to fall asleep with sweetened liquids in their bottles or feeding children sweetened liquids multiple times during the day.

Another pattern of decay is "rampant caries", which signifies advanced or severe decay on multiple surfaces of many teeth. Rampant caries may be seen in individuals with xerostomia, poor oral hygiene, stimulant use (due to drug-induced dry mouth), and/or large sugar intake. If rampant caries is a result of previous radiation to the head and neck, it may be described as radiation-induced caries. Problems can also be caused by the self-destruction of roots and whole tooth resorption when new teeth erupt or later from unknown causes.

Children at 6–12 months are at increased risk of developing dental caries. For other kids aged 12–18 months, dental caries develop on primary teeth and approximately twice yearly for permanent teeth.

Repair with cementum or dentin occurs after partial root resorption, fusing the tooth with the bone. It may occur following dental trauma, especially occlusal trauma, or after periapical periodontitis caused by pulp necrosis. Ankylosis itself is not a reason to remove a permanent tooth, however teeth which must be removed for other reasons are made significantly more difficult to remove if they are ankylosed.

Opacities due to MIH can be quite visible especially on anterior teeth which could present as a problem aesthetically. Patients frequently claim aesthetic discomfort when anterior teeth are involved. The discoloured appearance of the anterior teeth could also have negative effects on a child’s psychological development and self-esteem.

The reported symptoms are very variable, and frequently have been present for many months before the condition is diagnosed. Reported symptoms may include some of the following:

- Sharp pain when biting on a certain tooth, which may get worse if the applied biting force is increased. Sometimes the pain on biting occurs when the food being chewed is soft with harder elements, e.g. seeded bread.

- "Rebound pain" i.e. sharp, fleeting pain occurring when the biting force is released from the tooth, which may occur when eating fibrous foods.

- Pain when grinding the teeth backward and forward and side to side.

- Sharp pain when drinking cold beverages or eating cold foods, lack of pain with heat stimuli.

- Pain when eating or drinking sugary substances.

- Sometimes the pain is well localized, and the individual is able to determine the exact tooth from which the symptoms are originating, but not always.

If the crack propagates into the pulp, irreversible pulpitis, pulpal necrosis and periapical periodontitis may develop, with the respective associated symptoms.

The lesions that appear in teeth affected with MIH can present as opacities that vary from white to yellow-brown. They are usually asymmetrical in appearance, with a sharp demarcation that distinguishes between normal and affected enamel. The lesions usually do not involve the cervical third of affected teeth.

Acid erosion, also known as dental erosion, is a type of tooth wear. It is defined as the irreversible loss of tooth structure due to chemical dissolution by acids not of bacterial origin. Dental erosion is the most common chronic disease of children ages 5–17, although it is only relatively recently that it has been recognised as a dental health problem. There is generally widespread ignorance of the damaging effects of acid erosion; this is particularly the case with erosion due to fruit juices, because they tend to be seen as healthy. Erosion is found initially in the enamel and, if unchecked, may proceed to the underlying dentin.

The most common cause of erosion is by acidic foods and drinks. In general, foods and drinks with a pH below 5.0–5.7 have been known to trigger dental erosion effects. Numerous clinical and laboratory reports link erosion to excessive consumption of drinks. Those thought to pose a risk are soft drinks, some alcohol and fruit drinks, fruit juices such as orange juice (which contain citric acid) and carbonated drinks such as colas (in which the carbonic acid is not the cause of erosion, but citric and phosphoric acid). Additionally, wine has been shown to erode teeth, with the pH of wine as low as 3.0–3.8. Other possible sources of erosive acids are from exposure to chlorinated swimming pool water, and regurgitation of gastric acids.

Apical abscesses can spread to involve periodontal pockets around a tooth, and periodontal pockets cause eventual pulp necrosis via accessory canals or the apical foramen at the bottom of the tooth. Such lesions are termed periodontic-endodontic lesions, and they may be acutely painful, sharing similar signs and symptoms with a periodontal abscess, or they may cause mild pain or no pain at all if they are chronic and free-draining. Successful root canal therapy is required before periodonal treatment is attempted. Generally, the long-term prognosis of perio-endo lesions is poor.

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.

Cracked tooth syndrome refers to a highly variable set of pain-sensitivity symptoms that may accompany a tooth fracture, usually sporadic, sharp pain that occurs during biting or with release of biting pressure, or relieved by releasing pressure on the tooth. The term is falling into disfavor and has given way to the more generalized description of fractures and cracks of the tooth, which allows for the wide variations in signs, symptoms, and prognosis for traumatized teeth. A fracture of a tooth can involve the enamel, dentin, and/or pulp, and can be orientated horizontally or vertically. Fractured or cracked teeth can cause pain via several mechanisms, including dentin hypersensitivity, pulpitis (reversible or irreversible), or periodontal pain. Accordingly, there is no single test or combination of symptoms that accurately diagnose a fracture or crack, although when pain can be stimulated by causing separation of the cusps of the tooth, it's highly suggestive of the disorder. Vertical fractures can be very difficult to identify because the crack can rarely be probed or seen on radiographs, as the fracture runs in the plane of conventional films (similar to how the split between two adjacent panes of glass is invisible when facing them).

When toothache results from dental trauma (regardless of the exact pulpal or periodontal diagnosis), the treatment and prognosis is dependent on the extent of damage to the tooth, the stage of development of the tooth, the degree of displacement or, when the tooth is avulsed, the time out of the socket and the starting health of the tooth and bone. Because of the high variation in treatment and prognosis, dentists often use trauma guides to help determine prognosis and direct treatment decisions.

The prognosis for a cracked tooth varies with the extent of the fracture. Those cracks that are irritating the pulp but do not extend through the pulp chamber can be amenable to stabilizing dental restorations such as a crown or composite resin. Should the fracture extend though the pulp chamber and into the root, the prognosis of the tooth is hopeless.

Teeth die mainly as a result of extensive tooth decay, however this may also occur following dental trauma or heavy drilling down of the tooth during tooth preparation prior to restoration.

The main types of dental abscess are:

- Periapical abscess: The result of a chronic, localized infection located at the tip, or apex, of the root of a tooth.

- Periodontal abscess: begins in a periodontal pocket (see: periodontal abscess)

- Gingival abscess: involving only the gum tissue, without affecting either the tooth or the periodontal ligament (see: periodontal abscess)

- Pericoronal abscess: involving the soft tissues surrounding the crown of a tooth (see: Pericoronitis)

- Combined periodontic-endodontic abscess: a situation in which a periapical abscess and a periodontal abscess have combined (see: Combined periodontic-endodontic lesions).

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.