The prognosis for impacted wisdom teeth depends on the depth of the impaction. When they lack a communication to the mouth, the main risk is the chance of cyst or neoplasm formation which is relatively uncommon.

Once communicating with the mouth, the onset of disease or symptoms cannot be predicted but the chance of it does increase with age. Less than 2% of wisdom teeth are free of either periodontal disease or caries by age 65. Further, several studies have found that between 30% – 60% of people with previously asymptomatic impacted wisdom teeth will have them extracted due to symptoms or disease, 4–12 years after initial examination.

Extraction of the wisdom teeth removes the disease on the wisdom tooth itself and also appears to improve the periodontal status of the second molar, although this benefit diminishes beyond the age of 25.

Prevention of early childhood caries begins before the baby is born; women are advised to maintain a well-balanced diet of high nutritional value, especially during the third trimester and within the infants first year of life. This is since enamel undergoes maturation; if the diet is not sufficient, a common condition that may occur is enamel hypoplasia.

Enamel hypoplasia is a developmental defect of enamel that occurs during tooth development, mainly pre-natally or during early childhood. Teeth affected by enamel hypoplasia are commonly at a higher risk of caries since there is an increased loss of minerals and therefore the tooth surface is able to breakdown more easily than in comparison to a non-hypoplastic tooth. It is therefore suggested to the mother to maintain a healthy diet since evidence suggests malnourishment during the perinatal period increases the risk of hypoplastic teeth in an infant.

Few studies have looked at the percentage of the time wisdom teeth are present or the rate of wisdom teeth eruption. The lack of up to five teeth (excluding third molars, i.e. wisdom teeth) is termed hypodontia. Missing third molars occur in 9-30% of studied populations.

One large scale study on a group of young adults in New Zealand showed 95.6% had at least 1 wisdom tooth with an eruption rate of 15% in the maxilla and 20% in the mandible. Another study on 5000 army recruits found 10,767 impacted wisdom teeth. The frequency of impacted lower third molars has been found to be 72% and the frequency of retained impacted wisdom teeth that are free of disease and symptoms is estimated at 11.6% to 29% which drops with age.

The incidence of wisdom tooth removal was estimated to be 4 per 1000 person years in England and Wales prior to the 2000 NICE guidelines.

Diet plays a key role in the process of dental caries. The type of foods along with the frequency at which they are consumed can determine the risk it puts for also developing carious lesions. With new products being put on supermarket shelves with irresistible prices, this can largely influence what people buy. It is common for infants and young children to frequently consume fermentable carbohydrates, in the form of liquids. The consumption of liquids containing fermentable carbohydrate, include drinks such as: juice, breast milk, formula, soda. These consumables all have the potential to increase the risk of dental caries due to prolonged contact between sugars in the liquid and cariogenic bacteria on the tooth surface.

Recent research has shown that breastfeeding does not increase caries risk up to 12 months of age. Poor feeding practices without appropriate preventive measures can lead to a distinctive pattern of caries in susceptible infants and toddlers commonly known as baby bottle tooth decay or ECC. Frequent and long duration bottle feeding, especially at night, is associated with ECC. This finding can be attributed to the fact that there is less salivary flow at night and hence less capacity for buffering and remineralisation. Each time a child drinks these liquids, acids attack for 20 minutes or longer. A parent's education and health awareness has a major influence on the caries experience of their child - feeding practices, dietary habits and food choices.

Research has shown that there are five million teeth knocked-out each year in the United States.

Up to 25% of school-aged children and military trainees and fighters experience some kind of dental trauma each year. The incidence of dental avulsion in school aged children ranges from 0.5 to 16% of all dental trauma. Many of these teeth are knocked-out during school activities or sporting events such as contact sports, football, basketball, and hockey.It is important for anyone whom is related, working, or witnessing sports that they be educated on this subject matter. Being educated could aid in minimizing injuries that could do further harm to the victim. Being informed and spreading awareness of dental avulsion in the state of knowledge, treatment, and prevention could make an impact.

Dental caries is an infectious disease caused primarily by "Streptococcus mutans", characterized by acid demineralization of the enamel, which can progress to further breakdown of the more organic, inner dental tissue (dentin). Everybody is susceptible to caries but the probability of development depends on the patient’s individual disease indicators, risk factors and preventive factors. Factors that are considered high-risk for developing carious lesions on the teeth include:

- Low fluoride exposure

- Time, length, and frequency of sugar consumption

- Quality of tooth cleaning

- Fluctuations in salivary flow rates and composition

- Behavior of the individual

- Socioeconomic status of the individual

- Quality and composition of biofilms

Organic acids released from dental plaque lead to demineralization of the adjacent tooth surface, and consequently to dental caries. Saliva is also unable to penetrate the build-up of plaque and thus cannot act to neutralize the acid produced by the bacteria and remineralize the tooth surface.

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.

Although the etiology is unclear and it is speculated to be multifactorial. Contributing factors may include the following:

1. children born preterm and those with poor general health or systemic conditions in their first 3 years may develop MIH.

2. environmental changes

3. exposure to dioxine by prolonged breast-feeding could lead to an increase in the risk of MIH

4. respiratory diseases and oxygen shortage of the ameloblasts

5. oxygen shortage combined with low birth weight

Before root canal treatment or extraction are carried out, the clinician should have thorough knowledge about the root canal morphology to avoid complications.

Reduced salivary flow rate is associated with increased caries since the buffering capability of saliva is not present to counterbalance the acidic environment created by certain foods. As a result, medical conditions that reduce the amount of saliva produced by salivary glands, in particular the submandibular gland and parotid gland, are likely to lead to dry mouth and thus to widespread tooth decay. Examples include Sjögren's syndrome, diabetes mellitus, diabetes insipidus, and sarcoidosis. Medications, such as antihistamines and antidepressants, can also impair salivary flow. Stimulants, most notoriously methylamphetamine, also occlude the flow of saliva to an extreme degree. This is known as meth mouth. Tetrahydrocannabinol (THC), the active chemical substance in cannabis, also causes a nearly complete occlusion of salivation, known in colloquial terms as "cotton mouth". Moreover, 63% of the most commonly prescribed medications in the United States list dry mouth as a known side-effect. Radiation therapy of the head and neck may also damage the cells in salivary glands, somewhat increasing the likelihood of caries formation.

Susceptibility to caries can be related to altered metabolism in the tooth, in particular to fluid flow in the dentin. Experiments on rats have shown that a high-sucrose, cariogenic diet "significantly suppresses the rate of fluid motion" in dentin.

The use of tobacco may also increase the risk for caries formation. Some brands of smokeless tobacco contain high sugar content, increasing susceptibility to caries. Tobacco use is a significant risk factor for periodontal disease, which can cause the gingiva to recede. As the gingiva loses attachment to the teeth due to gingival recession, the root surface becomes more visible in the mouth. If this occurs, root caries is a concern since the cementum covering the roots of teeth is more easily demineralized by acids than enamel. Currently, there is not enough evidence to support a causal relationship between smoking and coronal caries, but evidence does suggest a relationship between smoking and root-surface caries.

Exposure of children to secondhand tobacco smoke is associated with tooth decay.

Intrauterine and neonatal lead exposure promote tooth decay. Besides lead, all atoms with electrical charge and ionic radius similar to bivalent calcium,

such as cadmium, mimic the calcium ion and therefore exposure to them may promote tooth decay.

Poverty is also a significant social determinant for oral health. Dental caries have been linked with lower socio-economic status and can be considered a disease of poverty.

Forms are available for risk assessment for caries when treating dental cases; this system using the evidence-based Caries Management by Risk Assessment (CAMBRA). It is still unknown if the identification of high-risk individuals can lead to more effective long-term patient management that prevents caries initiation and arrests or reverses the progression of lesions.

Saliva also contains iodine and EGF. EGF results effective in cellular proliferation, differentiation and survival. Salivary EGF, which seems also regulated by dietary inorganic iodine, plays an important physiological role in the maintenance of oral (and gastro-oesophageal) tissue integrity, and, on the other hand, iodine is effective in prevention of dental caries and oral health.

Aetiology of CTS is multifactorial, the causative factors include:

- previous restorative procedures.

- occlusal factors

- developmental conditions/anatomical considerations.

- trauma

- others, e.g, aging dentition or presence of lingual tongue studs.

Most commonly involved teeth are mandibular molars followed by maxillary premolars, maxillary molars and maxillary premolars. in a recent audit, mandibular first molar thought to be most affected by CTS possibly due to the wedging effect of opposing pointy, protruding maxillary mesio-palatal cusp onto the mandibular molar central fissure.

The cause of germination is still unknown. However, there are a few possible factors contributing to germination:

- Vitamin deficiency

- Hormonal irregularities

- Infection or inflammation of areas near to the developing tooth bud

- Drug induced

- Genetic predisposition

- Radiotherapy that caused damage to the developing tooth germ

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 etiology, or cause of edentulism, can be multifaceted. While the extraction of non-restorable or non-strategic teeth by a dentist does contribute to edentulism, the predominant cause of tooth loss in developed countries is periodontal disease. While the teeth may remain completely decay-free, the bone surrounding and providing support to the teeth may reabsorb and disappear, giving rise to tooth mobility and eventual tooth loss. In the radiograph at the beginning of the article, tooth #21 (the lower left first premolar, to the right of #22, the lower left canine) exhibits 50% bone loss, presenting with a distal horizontal defect and a mesial vertical defect. Tooth #22 exhibits roughly 30% bone loss.

Periodontitis is an infection of the gums which leads to bone destruction around the teeth in the jaw. Periodontitis occurs after gingivitis has been established, but not all individuals who have gingivitis will get periodontitis. Plaque accumulation is vital in the progression of periodontitis as the bacteria in plaque release enzymes which attack the bone and cause it to break down, and at the same time osteoclasts in the bone break down the bone as a way to prevent further infection. This can be treated with strict oral hygiene such as tooth brushing and cleaning in between the teeth as well as surgical debridement completed by a dental professional.

The Kennedy classification quantifies partial edentulism. An outline is covered at the removable partial denture article.

Regular use of a mouthguard during sports and other high-risk activities (such as military training) is the most effective prevention for dental trauma. Custom made mouthguard is preferable as it fits well, provides comfort and adequate protection. However, studies in various high-risk populations for dental injuries have repeatedly reported low compliance of individuals for the regular using of mouthguard during activities. Moreover, even with regular use, effectiveness of prevention of dental injuries is not complete, and injuries can still occur even when mouthguards are used as users are not always aware of the best makes or size, which inevitably result in a poor fit.

One of the most important measures is to impart knowledge and awareness about dental injury to those who are involved in sports environments like boxing and in school children in which they are at high risk of suffering dental trauma through an extensive educational campaign including lectures,leaflets,Posters which should be presented in an easy understandable way.

Secondary occlusal trauma occurs when "normal or excessive occlusal forces" are placed on teeth with "compromised periodontal attachment", thus contributing harm to an already damaged system. As stated, secondary occlusal trauma occurs when there is a compromised periodontal attachment and, thus, a "pre-existing periodontal condition".

There are certain diseases and disorders affecting teeth that may leave an individual at a greater risk for cavities.

Molar incisor hypomineralization, which seems to be increasingly common. While the cause is unknown it is thought to be a combination of genetic and environmental factors. Possible contributing factors that have been investigated include systemic factors such as high levels of dioxins or polychlorinated biphenyl (PCB) in the mother’s milk, premature birth and oxygen deprivation at birth, and certain disorders during the child’s first 3 years such as such as mumps, diphtheria, scarlet fever, measles, hypoparathyroidism, malnutrition, malabsorption, hypovitaminosis D, chronic respiratory diseases, or undiagnosed and untreated coeliac disease, which usually presents with mild or absent gastrointestinal symptoms.

Amelogenesis imperfecta, which occurs in between 1 in 718 and 1 in 14,000 individuals, is a disease in which the enamel does not fully form or forms in insufficient amounts and can fall off a tooth. In both cases, teeth may be left more vulnerable to decay because the enamel is not able to protect the tooth.

In most people, disorders or diseases affecting teeth are not the primary cause of dental caries. Approximately 96% of tooth enamel is composed of minerals. These minerals, especially hydroxyapatite, will become soluble when exposed to acidic environments. Enamel begins to demineralize at a pH of 5.5. Dentin and cementum are more susceptible to caries than enamel because they have lower mineral content. Thus, when root surfaces of teeth are exposed from gingival recession or periodontal disease, caries can develop more readily. Even in a healthy oral environment, however, the tooth is susceptible to dental caries.

The evidence for linking malocclusion and/or crowding to dental caries is weak; however, the anatomy of teeth may affect the likelihood of caries formation. Where the deep developmental grooves of teeth are more numerous and exaggerated, pit and fissure caries is more likely to develop (see next section). Also, caries is more likely to develop when food is trapped between teeth.

Dental trauma is most common in younger people, accounting for 17% of injuries to the body in those aged 0–6 years compared to an average of 5% across all ages. It is more frequently observed in males compared to females. Traumatic dental injuries are more common in permanent teeth compared to deciduous teeth and usually involve the front teeth of the upper jaw.

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.

Teeth are constantly subject to both horizontal and vertical occlusal forces. With the center of rotation of the tooth acting as a fulcrum, the surface of bone adjacent to the pressured side of the tooth will undergo resorption and disappear, while the surface of bone adjacent to the tensioned side of the tooth will undergo apposition and increase in volume.

In both primary and secondary occlusal trauma, tooth mobility might develop over time, with it occurring earlier and being more prevalent in secondary occlusal trauma. To treat mobility due to primary occlusal trauma, the cause of the trauma must be eliminated. Likewise for teeth subject to secondary occlusal trauma, though these teeth may also require splinting together to the adjacent teeth so as to eliminate their mobility.

In primary occlusal trauma, the cause of the mobility was the excessive force being applied to a tooth with a normal attachment apparatus, otherwise known as a "periodontally-uninvolved tooth". The approach should be to eliminate the cause of the pain and mobility by determining the causes and removing them; the mobile tooth or teeth will soon cease exhibiting mobility. This could involve removing a high spot on a recently restored tooth, or even a high spot on a non-recently restored tooth that perhaps moved into hyperocclusion. It could also involve altering one's parafunctional habits, such as refraining from chewing on pens or biting one's fingernails. For a bruxer, treatment of the patient's primary occlusal trauma could involve selective grinding of certain interarch tooth contacts or perhaps employing a nightguard to protect the teeth from the greater than normal occlusal forces of the patient's parafunctional habit. For someone who is missing enough teeth in non-strategic positions so that the remaining teeth are forced to endure a greater "per square inch" occlusal force, treatment might include restoration with either a removable prosthesis or implant-supported crown or bridge.

In secondary occlusal trauma, simply removing the "high spots" or selective grinding of the teeth will not eliminate the problem, because the teeth are already periodontally involved. After splinting the teeth to eliminate the mobility, the cause of the mobility (in other words, the loss of clinical attachment and bone) must be managed; this is achieved through surgical periodontal procedures such as soft tissue and bone grafts, as well as restoration of edentulous areas. As with primary occlusal trauma, treatment may include either a removable prosthesis or implant-supported crown or bridge.

The long-term prognosis of replanted knocked out teeth is very variable. The treatment for knocked-out teeth has progressed from a success rate of 10% to over 90%.

However, this success rate can only be achieved with the institution of optimum care within fifteen minutes to an hour of the accident. In the case of knocked-out teeth, being prepared and knowing what to do can mean the difference between a person retaining or losing replanted knocked-out teeth for life. Teeth that have been knocked out when they are fully matured, that is, when the root has completely formed, have a much better prognosis than those teeth that are immature and not fully formed. This is due to the fragility of the root. When teeth have not fully formed, the walls of the root are thinner and thus more fragile. Another complication for the prognosis is the length of time that the tooth has been out of its socket. Teeth that are replanted within fifteen minutes of the accident have an excellent prognosis. Teeth that have been extra-oral and dry stored for more than one hour have a poor prognosis. Teeth that have been placed in an optimal storage medium within one hour of the accident also have an excellent prognosis. All teeth that have been knocked out should be replanted but watched carefully for the development of root resorption. Teeth that do not have root canal treatment within two weeks of replantation also have a poor prognosis.

Periapical periodontitis of some form is a very common condition. The prevalence of periapical periodontitis is generally reported to vary according to age group, e.g. 33% in those aged 20–30, 40% in 30- to 40-year-olds, 48% in 40- to 50-year-olds, 57% in 50- to 60-year-olds and 62% in those over the age of 60. Most epidemiologic data has been generated in European countries, especially Scandinavia. Millions of root canal treatments are carried out in the United States each year, although the total number of root canal treatments is an imperfect indicator of the prevalence of periapical periodontitis, since not always is it performed due to the presence of periapacial periodontitis, and not all cases of asymptomatic periodontitis will be treated in this manner, either due to lack of patient attendance or watchful waiting.