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.

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."

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.

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.

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 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.

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.

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.

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

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

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.

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

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.

Extrinsic discolorations are common and have many different causes. The same range of factors are capable of staining the surface of restorations (e.g., composite fillings, porcelain crowns). Some extrinsic discolorations that are allowed to remain for a long time may become intrinsic.

- Dental plaque: Although usually virtually invisible on the tooth surface, plaque may become stained by chromogenic bacteria such as "Actinomyces" species.

- Calculus: Neglected plaque eventually calcifies, and leads to formation of a hard deposit on the teeth, especially around the gumline. The color of calculus varies, and may be grey, yellow, black or brown.

- Tobacco: Tar in smoke from tobacco products (and also smokeless tobacco products) tends to form a yellow-brown-black stain around the necks of the teeth above the gumline.

- Betel chewing.

- Certain foods and drinks. Foods, such as vegetables, that are rich with carotenoids or xanthonoids can stain teeth. Ingesting colored liquids like sports drinks, cola, coffee, tea and red wine can discolor teeth.

- Certain topical medications.

- Chlorhexidine (antiseptic mouthwash) binds to tannins, meaning that prolonged use in persons who consume coffee, tea or red wine is associated with extrinsic staining (i.e., removable staining) of teeth.

- Cetylpyridinium chloride, which is found in many antimicrobial mouthwashes, can result in staining due to dead bacterial residue.

- Metallic compounds. Exposure to such metallic compounds may be in the form of medication or other environmental exposure. Examples include iron (black stain), iodine (black), copper (green), nickel (green) and cadmium (yellow-brown).

- Antibiotics. Tetracycline and its derivatives are capable of intrinsic discoloration (discussed below). However other antibiotics may form insoluble complexes with calcium, iron and other elements that cause extrinsic staining.

Causes of intrinsic discoloration generally fall into those that occur during tooth development and those acquired later in life. The known causes of intrinsic staining are listed below, however some causes are unknown.

Most dental pain can be treated with routine dentistry. In rare cases, toothache can be a symptom representing a life-threatening condition, such as a deep neck infection (compression of the airway by a spreading odontogenic infection) or something more remote like a heart attack.

Dental caries, if left untreated, follows a predictable natural history as it nears the pulp of the tooth. First it causes reversible pulpitis, which transitions to irreversible pulpitis, then to necrosis, then to necrosis with periapical periodontitis and, finally, to necrosis with periapical abscess. Reversible pulpitis can be stopped by removal of the cavity and the placement of a sedative dressing of any part of the cavity that is near the pulp chamber. Irreversible pulpitis and pulp necrosis are treated with either root canal therapy or extraction. Infection of the periapical tissue will generally resolve with the treatment of the pulp, unless it has expanded to cellulitis or a radicular cyst. The success rate of restorative treatment and sedative dressings in reversible pulpitis, depends on the extent of the disease, as well as several technical factors, such as the sedative agent used and whether a rubber dam was used. The success rate of root canal treatment also depends on the degree of disease (root canal therapy for irreversible pulpitis has a generally higher success rate than necrosis with periapical abscess) and many other technical factors.

Teeth affected with MIH are at an increased risk of acquiring dental caries. This is because the properties of the enamel are altered by increased porosity and decreased hardness. Essentially, the balance between mineralisation and demineralisation shifts to favour demineralisation of enamel, giving the tooth less resilience in structure, thereby making it vulnerable to caries.

The poor structural properties of the enamel in teeth with MIH also increase the likelihood of cavitation of any lesions, thereby causing the lesion to progress at a faster rate. Progression of the carious lesion is also more rapid in teeth with MIH as patients may experience tooth sensitivity while carrying out oral hygiene, causing them to avoid doing so and consequentially accelerating the decay.

It is estimated that tooth loss results in worldwide productivity losses in the size of about US$63 billion yearly.

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.

Toothache may occur at any age, in any gender and in any geographic region. Diagnosing and relieving toothache is considered one of the main responsibilities of dentists. Irreversible pulpitis is thought to be the most common reason that people seek emergency dental treatment. Since dental caries associated with pulpitis is the most common cause, toothache is more common in populations that are at higher risk of dental caries. The prevalence of caries in a population is dependent upon factors such as diet (refined sugars), socioeconomic status, and exposure to fluoride (such as areas without water fluoridation). In the United States, an estimated 12% of the general population reported that they suffered from toothache at some point in the six months before questioning. Individuals aged 18–34 reported much higher experience of toothache than those aged 75 or over. In a survey of Australian schoolchildren, 12% had experienced toothache before the age of five, and 32% by the age of 12. Dental trauma is extremely common and tends to occur more often in children than adults.

Pericoronitis usually occurs in young adults, around the time when wisdom teeth are erupting into the mouth. If the individual has reached their twenties without any attack of pericoronitis, it becomes substantially less likely one will occur thereafter.

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.

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.

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.

Once the plaque stagnation area is removed either through further complete tooth eruption or tooth removal then pericoronitis will likely never return. A non-impacted tooth may continue to erupt, reaching a position which eliminates the operculum. A transient and mild pericoronal inflammation often continues while this tooth eruption completes. With adequate space for sustained improved oral hygiene methods, pericoronitis may never return. However, when relying on just oral hygiene for impacted and partially erupted teeth, chronic pericoronitis with occasional acute exacerbation can be expected.

Dental infections such as a pericoronal abscess can develop into septicemia and be life-threatening in persons who have neutropenia. Even in people with normal immune function, pericoronitis may cause a spreading infection into the potential spaces of the head and neck. Rarely, the spread of infection from pericoronitis may compress the airway and require hospital treatment (e.g. Ludwig's angina), although the majority of cases of pericoronitis are localized to the tooth. Other potential complications of a spreading pericoronal abscess include peritonsillar abscess formation or cellulitis.

Chronic pericoronitis may be the etiology for the development of paradental cyst, an inflammatory odontogenic cyst.