Impacted wisdom teeth without a communication to the mouth, that have no pathology associated with the tooth and have not caused tooth resorption on the blocking tooth rarely have symptoms. In fact, only 12% of impacted wisdom teeth are associated with pathology.

When wisdom teeth communicate with the mouth, the most common symptom is localized pain, swelling and bleeding of the tissue overlying the tooth. This tissue is called the operculum and the disorder called pericoronitis which means inflammation around the crown of the tooth. Low grade chronic periodontitis commonly occurs on either the wisdom tooth or the second molar, causing less obvious symptoms such as bad breath and bleeding from the gums. The teeth can also remain asymptomatic (pain free), even with disease. As the teeth near the mouth during normal development, people sometimes report mild pressure of other symptoms similar to teething.

The term asymptomatic means that the person has no symptoms. The term asymptomatic should not be equated with absence of disease. Most diseases have no symptoms early in the disease process. A pain free or asymptomatic tooth can still be infected for many years before pain symptoms develop.

All teeth are classified as either developing, erupted (into the mouth), embedded (failure to erupt despite lack of blockage from another tooth) or impacted. An impacted tooth is one that fails to erupt due to blockage from another tooth.

Wisdom teeth develop between the ages of 14 and 25, with 50% of root formation completed by age 16 and 95% of all teeth erupted by the age of 25. However, tooth movement can continue beyond the age of 25.

Impacted wisdom teeth are classified by the direction and depth of impaction, the amount of available space for tooth eruption. and the amount of soft tissue or bone (or both) that covers them. The classification structure helps clinicians estimate the risks for impaction, infections and complications associated with wisdom teeth removal. Wisdom teeth are also classified by the presence (or absence) of symptoms and disease.

One review found that 11% of teeth will have evidence of disease and are symptomatic, 0.6% will be symptomatic but have no disease, 51% will be asymptomatic but have disease present and 37% will be asymptomatic and have no disease.

Impacted wisdom teeth are often described by the direction of their impaction (forward tilting, or mesioangular being the most common), the depth of impaction and the age of the patient as well as other factors such as pre-existing infection or the presence of pathology. Of these predictors, age correlates best with extraction difficulty and complications during wisdom teeth removal rather than the orientation of the impaction.

Another classification system often taught in U.S. dental schools is known as "Pell and Gregory Classification". This system includes a horizontal and vertical component to classify the location of third molars (predominately applicable to mandibular third molars): the third molar's relationship to the occlusal plane being the vertical or "x-component" and to the anterior border of the ramus being the horizontal or "y-component". Vertically, Class A impaction is one in which the occlusal surface of the impacted tooth is level or nearly level with the occlusal plane and the cervical line of the adjacent second molar.

This type of classification is based on the amount of impacted tooth that is covered with the mandibular ramus. It is known as the Pell and Gregory classification, classes 1, 2, and 3.

Most commonly used classification system with respect to treatment planning. Depending on the angulation the tooth might be classified as:

- Mesioangular

- Horizontal

- Vertical

- Distoangular

- Palatal

- Buccal

- Lingual

Gum recession is generally not an acute condition. In most cases, receding of gums is a progressive condition that occurs gradually over the years. This is one reason that it is common over the age of 40. Because the changes in the condition of the gums from one day to another are minimal, patients get used to the gums' appearance and tend not to notice the recession visually. Receding gums may remain unnoticed until the condition starts to cause symptoms.

The following signs and symptoms may indicate gum recession:

- Tooth mobility

- Dentin hypersensitivity (over-sensitive teeth) - short, sharp pain is triggered by hot, cold, sweet, sour, or spicy food and drink. If the cementum covering the root is not protected anymore by the gums, it is easily abraded exposing the dentin tubules to external stimuli.

- Teeth may also appear longer than normal (a larger part of the crown is visible if gums are receding)

- The roots of the tooth are exposed and visible

- The tooth feels notched at the gum line

- Change in the tooth’s color (due to the color difference between enamel and cementum)

- Spaces between teeth seem to grow (the space is the same, but it seems larger because the gums do not fill it any more)

- Cavities below the gum line

If the gum recession is caused by gingivitis, the following symptoms may also be present:

- Puffy, red, or swollen (inflamed) gums

- Gum bleeding while brushing or flossing

- Bad breath (halitosis)

In some cases, it is the treatment of gingivitis that reveals a gum recession problem, that was previously masked by the gums swelling.

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.

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

Supernumerary teeth can be classified by shape and by position. The shapes include the following:

- Supplemental (where the tooth has a normal shape for the teeth in that series);

- Tuberculate (also called "barrel shaped");

- Conical (also called "peg shaped");

- Compound odontoma (multiple small tooth-like forms);

- Complex odontoma (a disorganized mass of dental tissue)

When classified by position, a supernumerary tooth may be referred to as a "mesiodens", a "paramolar", or a "distomolar".

The most common supernumerary tooth is a mesiodens, which is a malformed, peg-like tooth that occurs between the maxillary central incisors.

Fourth and fifth molars that form behind the third molars are another kind of supernumerary teeth.

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.

For people, the relevance and functionality of teeth can be easily taken for granted, but a closer examination of their considerable significance will demonstrate how they are actually very important. Among other things, teeth serve to:

- support the lips and cheeks, providing for a fuller, more aesthetically pleasing appearance

- maintain an individual's vertical dimension of occlusion

- along with the tongue and lips, allow for the proper pronunciation of various sounds

- preserve and maintain the height of the alveolar ridge

- cut, grind, and otherwise chew food

There are many possible causes for gingival recession:

- By far the most common cause is gum disease (periodontal disease).

- Overaggressive brushing is often assumed to cause gum recession, however a systematic review of the literature concludes that "The data to support or refute the association between tooth brushing and gingival recession are inconclusive." A subsequent study found horizontal tooth brushing technique (versus Bass technique or circular methods), medium-hardness toothbrush use and brushing only once daily were associated with gingival recession.

- Hereditary thin, fragile or insufficient gingival tissue predisposes to gingival recession.

- Dipping tobacco, which affects the mucous membrane lining in the mouth and will cause receding gums over time

- Self-inflicted trauma, such as habits like digging a fingernail or pencil into the gum. This type of recession more commonly associated with children and persons with psychiatric disorders.

- Scurvy (lack of dietary vitamin C)

- Acute necrotizing ulcerative gingivitis

- Abnormal tooth position, such as tooth crowding, giving inadequate cover of one or more teeth by the jaw bone.

- Piercings in the lip or tongue that wear away the gum by rubbing against it.

- Intentional gingival retraction. For example, the adult tooth may not grow out of the gum, and to remedy this, a procedure called an exposure is done. It involves the gum tissue being cut open to allow the adult tooth to grow out. This is a less common cause of gum recession.

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.

Loss of attachment:

- By far the most common cause is periodontal disease (gum disease). This is painless, slowly progressing loss of bony support around teeth. It is made worse by smoking and the treatment is by improving the oral hygiene above and below the gumline.

- Dental abscesses can cause resorption of bone and consequent loss of attachment. Depending on the type of abscess, this loss of attachment may be restored once the abscess is treated, or it may be permanent.

- Many other conditions can cause permanent or temporary loss of attachment and increased tooth mobility. Examples include: Langerhans cell histiocytosis.

Increased forces on the tooth:

- Bruxism (abnormal clenching and grinding of teeth) can aggravate attachment loss and tooth mobility if periodontal disease is already present. The tooth mobility is typically reversible and the tooth returns to normal level of mobility once the bruxism is controlled.

- Dental trauma. Luxations, and root fractures of teeth can cause sudden mobility after a blow. Dental trauma may be isolated or associated with other facial trauma.

- Increased biting force on one tooth can cause temporary increased mobility until corrected. A common scenario is a new filling or crown which is a fraction of a millimeter too prominent in the bite, which after a few days causes periodontal pain in that tooth and/or the opposing tooth.

Acute pericoronitis (i.e. sudden onset and short lived, but significant, symptoms) is defined as "varying degrees of inflammatory involvement of the pericoronal flap and adjacent structures, as well as by systemic complications." Systemic complications refers to signs and symptoms occurring outside of the mouth, such as fever, malaise or swollen lymph nodes in the neck.

Pericoronitis may also be chronic or recurrent, with repeated episodes of acute pericoronitis occurring periodically. Chronic pericoronitis may cause few if any symptoms, but some signs are usually visible when the mouth is examined.

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.

As stated, the position of maximal closure in the presence of teeth is referred to as maximum intercuspation, and the vertical jaw relationship in this position is referred to as the vertical dimension of occlusion. With the loss of teeth, there is a decrease in this vertical dimension, as the mouth is allowed to overclose when there are no teeth present to block further upward movement of the mandible towards the maxilla. This may contribute, as explained above, to a sunken-in appearance of the cheeks, because there is now "too much" cheek than is needed to extend from the maxilla to the mandible when in an overclosed position. If this situation is left untreated for many years, the muscles and tendons of the mandible and the TMJ may manifest with altered tone and elasticity.

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.

Clinically, there is a number of physiological results that serve as evidence of occlusal trauma:,

- Tooth mobility

- Fremitus

- Tooth migration

- Pain

- Thermal sensitivity

- Pain on chewing or percussion

- Wear facets

The term primary failure of eruption was named by Dr. William Proffit and Dr. Katherine Vig in 1981. This type of failure of eruption has a genetic or familial background precursor as a cause. The prevalence is of PFE is about 0.06% in population. In this type of failure, teeth that are non-ankylosed fail to erupt in the mouth. These teeth do not have a precursor tooth that is blocking their path. These teeth tend to erupt partially but then fail to erupt as the time goes on. Profitt stated that only the posterior teeth are the ones to be affected and all the teeth which are distal to the affected tooth are also affected. Both permanent and primary teeth may equally be affected. This often results in posterior open bite in patients mouth who have primary failure of eruption. This phenomenon can occur in any quadrant of the mouth.

There are two types of primary failure of eruption. Type I involves failure of eruption of teeth distal to the most mesial affected tooth to be all same. Type II involves a greater eruption pattern, not complete, among the teeth distal to the most mesial affected tooth. It is difficult to diagnose between these two types of failure of eruption because 2nd molar does not erupt until a patient is 15 years of age. Plenty of times, patient's receive orthodontic care much before they turn 15 years old. Therefore, to properly diagnose between two types, a patient needs to be over 15 and a definitive proof of uneruption of 2nd molar is required.

This type of failure of eruption takes place when the affected tooth is ankylosed to the bone around it. This is different than primary failure of eruption where the affected tooth/teeth were not ankylosed. In mechanical failure of eruption, affected tooth has partial or complete loss of PDL in a panoramic radiograph and teeth distal to affected tooth do not have this condition. On a percussion test, a tooth with mechanical failure of eruption will have a dull metallic sound.

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.

Microscopically, there will be a number of features that accompany occlusal trauma:

- Hemorrhage

- Necrosis

- Widening of the periodontal ligament, or PDL (also serves as a very common radiographic feature)

- Bone resorption

- Cementum loss and tears

It was concluded that widening of the periodontal ligament was a "functional adaptation to changes in functional requirements".

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.

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