There are two main methods of detecting dental plaque in the oral cavity: through the application of a disclosing gel or tablet, and/or visually through observation. Plaque detection is usually detected clinically by plaque disclosing agents. Disclosing agents contain dye which turns bright red to indicate plaque build-up.

It is important for an individual to be aware of what to look for when doing a self-assessment for dental plaque. It is important to be aware that everyone has dental plaque, however, the severity of the build-up and the consequences of not removing the plaque can vary.

The presentation of caries is highly variable. However, the risk factors and stages of development are similar. Initially, it may appear as a small chalky area (smooth surface caries), which may eventually develop into a large cavitation. Sometimes caries may be directly visible. However other methods of detection such as X-rays are used for less visible areas of teeth and to judge the extent of destruction. Lasers for detecting caries allow detection without ionizing radiation and are now used for detection of interproximal decay (between the teeth). Disclosing solutions are also used during tooth restoration to minimize the chance of recurrence.

Primary diagnosis involves inspection of all visible tooth surfaces using a good light source, dental mirror and explorer. Dental radiographs (X-rays) may show dental caries before it is otherwise visible, in particular caries between the teeth. Large areas of dental caries are often apparent to the naked eye, but smaller lesions can be difficult to identify. Visual and tactile inspection along with radiographs are employed frequently among dentists, in particular to diagnose pit and fissure caries. Early, uncavitated caries is often diagnosed by blowing air across the suspect surface, which removes moisture and changes the optical properties of the unmineralized enamel.

Some dental researchers have cautioned against the use of dental explorers to find caries, in particular sharp ended explorers. In cases where a small area of tooth has begun demineralizing but has not yet cavitated, the pressure from the dental explorer could cause a cavity. Since the carious process is reversible before a cavity is present, it may be possible to arrest caries with fluoride and remineralize the tooth surface. When a cavity is present, a restoration will be needed to replace the lost tooth structure.

At times, pit and fissure caries may be difficult to detect. Bacteria can penetrate the enamel to reach dentin, but then the outer surface may remineralize, especially if fluoride is present. These caries, sometimes referred to as "hidden caries", will still be visible on X-ray radiographs, but visual examination of the tooth would show the enamel intact or minimally perforated.

The differential diagnosis for dental caries includes dental fluorosis and developmental defects of the tooth including hypomineralization of the tooth and hypoplasia of the tooth.

The early carious lesion is characterized by demineralization of the tooth surface, altering the tooth's optical properties. Technology utilizing laser speckle image (LSI) techniques may provide a diagnostic aid to detect early carious lesions.

Personal hygiene care consists of proper brushing and flossing daily. The purpose of oral hygiene is to minimize any etiologic agents of disease in the mouth. The primary focus of brushing and flossing is to remove and prevent the formation of plaque or dental biofilm. Plaque consists mostly of bacteria. As the amount of bacterial plaque increases, the tooth is more vulnerable to dental caries when carbohydrates in the food are left on teeth after every meal or snack. A toothbrush can be used to remove plaque on accessible surfaces, but not between teeth or inside pits and fissures on chewing surfaces. When used correctly, dental floss removes plaque from areas that could otherwise develop proximal caries but only if the depth of sulcus has not been compromised. Other adjunct oral hygiene aids include interdental brushes, water picks, and mouthwashes.

However oral hygiene is probably more effective at preventing gum disease (periodontal disease) than tooth decay. Food is forced inside pits and fissures under chewing pressure, leading to carbohydrate-fueled acid demineralisation where the brush, fluoride toothpaste, and saliva have no access to remove trapped food, neutralise acid, or remineralise demineralised tooth like on other more accessible tooth surfaces. (Occlusal caries accounts for between 80 and 90% of caries in children (Weintraub, 2001).) Higher concentrations of fluoride (>1,000 ppm) in toothpaste also helps prevents tooth decay, with the effect increasing with concentration. Chewing fibre like celery after eating forces saliva inside trapped food to dilute any carbohydrate like sugar, neutralise acid and remineralise demineralised tooth. The teeth at highest risk for carious lesions are the permanent first and second molars due to length of time in oral cavity and presence of complex surface anatomy.

Professional hygiene care consists of regular dental examinations and professional prophylaxis (cleaning). Sometimes, complete plaque removal is difficult, and a dentist or dental hygienist may be needed. Along with oral hygiene, radiographs may be taken at dental visits to detect possible dental caries development in high-risk areas of the mouth (e.g. "bitewing" X-rays which visualize the crowns of the back teeth).

The diagnosis of impaction can be made clinically if enough of the wisdom tooth is visible to determine its angulation, depth, and if the patient is old enough that further eruption or uprighting is unlikely. Wisdom teeth continue to move into adulthood (20–30 years old) due to eruption and then continue some later movement owing to periodontal disease.

If the tooth cannot be assessed with clinical exam alone, the diagnosis is made using either a panoramic radiograph or cone-beam CT. Where unerupted wisdom teeth still have eruption potential several predictors are used to determine the chance of the teeth becoming impacted. The ratio of space between the tooth crown length and the amount of space available, the angle of the teeth compared to the other teeth are the two most commonly used predictors, with the space ratio being the most accurate. Despite the capacity for movement into early adulthood, the likelihood that the tooth will become impacted can be predicted when the ratio of space available to the length of the crown of the tooth is under 1.

Plaque disclosing products, also known as disclosants, make plaque clinically visible. Clean surfaces of the teeth do not absorb the disclosant, only rough surfaces. Plaque disclosing gels can be either completed at home or in the dental clinic. Before using these at home or in the dental clinic check with your general practitioners for any allergies to iodine, food colouring or any other ingredients that may be present in these products. These gels provide a visual aid in assessing plaque biofilm presence and can also show the maturity of the dental plaque.

MIH examination should be carried out on clean, wet teeth. The ideal age for examination is when the child is 8 years old - the age where all permanent first molars and most of the incisors are erupted. The permanent first molar will also still be in a comparatively sound condition without excessive post-eruption breakdown. Judgements of each individual teeth should be recorded, aiding the correct diagnosis of the condition.

There is currently a lack of standardisation in the scoring system and severity indices used to record the diagnosis of MIH. Various systems commonly employed in studies include:

- Modified Defect of Dental Enamel (DDE) Index: This set of criteria allows for enamel defects to be detected, enabling a distinction between demarcated and diffused opacities.

- European Academy of Paediatric Dentistry (EAPD) judgement criteria: This set of criteria was developed in 2003 to standardise classifications for use in epidemiological studies. However, while it allows the categorisation of the enamel condition, it does not address the severity of the enamel condition.

- Molar Hypomineralisation Severity Index (MHSI): This set of criteria has been developed to address deficiencies in indices concerning the severity of hypomineralisation. It is based on both the clinical characteristics of hypomineralised defects and the EAPD judgement criteria.

There is no standard to screen for wisdom teeth. It has been suggested, absent evidence to support routinely retaining or removing wisdom teeth, that evaluation with panoramic radiograph, starting between the ages of 16 and 25 be completed every 3 years. Once there is the possibility of the teeth developing disease, then a discussion about the operative risks versus long-term risk of retention with an oral and maxillofacial surgeon or other clinician trained to evaluate wisdom teeth is recommended. These recommendations are based on expert opinion level evidence. Screening at a younger age may be required if the second molars (the "12-year molars") fail to erupt as ectopic positioning of the wisdom teeth can prevent their eruption. Radiographs can be avoided if the majority of the tooth is visible in the mouth.

To manage the condition, it is important to first diagnose it, describing the type of tooth surface loss, its severity and location. Early diagnosis is essential to ensure tooth wear has not progressed past the point of restoration. A thorough examination is required, because it might give explanation to the aetiology of the TSL.

The examination should include assessment of:

- Temporomandibular joint function and associated musculature

- Orthodontic examination

- Intra oral soft tissue analysis

- Hard tissue analysis

- Location and severity of tooth wear

- Social history, particularly diet

It is important to record severity of tooth wear for monitoring purposes, helping to differentiate between pathological and physiological tooth surface loss. It is essential to determine whether the tooth wear is ongoing or has stabilized. However where generalised, the underlying cause can be assumed to be bruxism. In fast-progressing cases, there is commonly a coexisting erosive diet contributing to tooth surface loss.

"Relative dentin abrasivity" ("RDA") is a standardised measurement of the abrasive effect that the components of the toothpaste have on a tooth.

The RDA scale was developed by the American Dental Association (ADA). The RDA scale compares toothpaste abrasivity to standard abrasive materials and measures the depth of cut at an average of 1 millimetre per 100,000 brush strokes onto dentine. This comparison generates abrasive values for the dentifrices that would be safe for daily use. In vitro dental studies showed a positive correlation between the highest RDAs and greater dentin wear.

Since 1998, the RDA value is set by the standards DIN EN ISO 11609. Currently, the claim on products such as toothpaste are not regulated by law, however a dentifrice is required to have a level lower than 250 to be considered safe and before being given the ADA seal of approval. The values obtained depend on the size, quantity and surface structure of abrasive used in toothpastes.

While the RDA score has been shown to have a statistically significant correlation to the presence of abrasion, it is not the only contributing factor to consider. Other factors such as the amount of pressure used whilst brushing, the type, thickness and dispersion of bristle in the toothbrush and the time spent brushing are other factors that contribute to dental abrasion.

It is recommended to parents and caregivers to take their children to a dental professional for examination as soon as the first few teeth start to erupt into the oral cavity

. The dental professional will assess all the present dentition for early carious demineralization and may provide recommendations to the parents or caregivers the best way to prevent ECC and what actions to take.

Studies suggest that children who have attended visits within the first few years of life (an early preventive dental visit) potentially experience less dental related issues and incur lower dental related costs throughout their lives.

Early childhood caries can be prevented through the combination of the following: adhering to a healthy nutritional diet, optimal plaque removal, use of fluoridation on the tooth surface once erupted, care taken by the mother during the pre-natal and peri-natal period and regular dental visits. The following are recommendations to help prevent ECC.

Daily oral hygiene measures to prevent periodontal disease include:

- Brushing properly on a regular basis (at least twice daily), with the patient attempting to direct the toothbrush bristles underneath the gumline, helps disrupt the bacterial-mycotic growth and formation of subgingival plaque.

- Flossing daily and using interdental brushes (if the space between teeth is large enough), as well as cleaning behind the last tooth, the third molar, in each quarter

- Using an antiseptic mouthwash: Chlorhexidine gluconate-based mouthwash in combination with careful oral hygiene may cure gingivitis, although they cannot reverse any attachment loss due to periodontitis.

- Using periodontal trays to maintain dentist-prescribed medications at the source of the disease: The use of trays allows the medication to stay in place long enough to penetrate the biofilms where the microorganism are found.

- Regular dental check-ups and professional teeth cleaning as required: Dental check-ups serve to monitor the person's oral hygiene methods and levels of attachment around teeth, identify any early signs of periodontitis, and monitor response to treatment.

- Microscopic evaluation of biofilm may serve as a guide to regaining commensal health flora.

Typically, dental hygienists (or dentists) use special instruments to clean (debride) teeth below the gumline and disrupt any plaque growing below the gumline. This is a standard treatment to prevent any further progress of established periodontitis. Studies show that after such a professional cleaning (periodontal debridement), microbial plaque tends to grow back to precleaning levels after about three to four months. Nonetheless, the continued stabilization of a patient's periodontal state depends largely, if not primarily, on the patient's oral hygiene at home, as well as on the go. Without daily oral hygiene, periodontal disease will not be overcome, especially if the patient has a history of extensive periodontal disease.

Periodontal disease and tooth loss are associated with an increased risk, in male patients, of cancer.

Contributing causes may be high alcohol consumption or a diet low in antioxidants.

The diagnosis of DH may be challenging. It is a diagnosis of exclusion, reached once all other possible explanations for the pain have been ruled out. A thorough patient history and clinical examination are required. The examination includes a pain provocation test by blasting air from a dental instrument onto the sensitive area, or gentle scratching with a dental probe. If a negative result for the pain provocation test occurs, no treatment for dentinal hypersensitivity is indicated and another diagnosis should be sought, such as other causes of orofacial pain.

Inflammation of the dental pulp, termed pulpitis, produces true hypersensitivity of the nerves in the dental pulp. Pulpitis is classified as "irreversible" when pulpal inflammation will irreversibly progress to pulpal necrosis due to compression of the venous microcirculation and tissue ischemia, and "reversible" when the pulp is still capable of returning to a healthy, non-inflamed state, although usually dental treatment is required for this. Irreversible pulpitis is readily distinguishable from DH. There is poorly localized, severe pain which is aggravated by thermal stimuli, and which continues after the stimulus is removed. There also is typically spontaneous pain without any stimulus. Reversible pulpitis may not be so readily distinguishable from DH, however usually there will be some obvious sign such as a carious cavity, crack, etc. which indicates pulpitis. In contrast to pulpitis, the pain of DH is short and sharp.

The adequate diagnosis of fluorosis can be diagnosed by visual clinical examination. This requires inspection of dry and clean tooth surfaces under a good lighting. There are individual variations in clinical fluorosis manifestation which are highly dependent on the duration, timing, and dosage of fluoride exposure.There are different classifications to diagnose the severity based on the appearances. The clinical manifestation of mild dental fluorosis is mostly characterised a snow flaking appearance that lack a clear border, opaque, white spots, narrow white lines following the perikymata or patches as the opacities may coalesce with an intact, hard and smooth enamel surface on most of the teeth. With increasing severity, the subsurface enamel, all along the tooth becomes more porous. Enamel may appear yellow/ brown discolouration and/ or many and pitted white-brown lesions that look like cavities. They are often described as “mottled teeth”. Fluorosis does not cause discolouration to the enamel directly, as upon eruption into the mouth, affected permanent teeth are not discoloured yet. In dental enamel, fluorosis causes subsurface porosity or hypomineralizations, which extend toward the dentinal-enamel junction as severity increases. Hence, affected teeth are more susceptible to staining. Due to diffusion of exogenous ions (ex, iron and copper), the stains would develop into the abnormally porous enamel.

The differential diagnosis for this condition includes:

- Turner's hypoplasia (although this is usually more localized)

- Enamel defects caused by an undiagnosed and untreated celiac disease.

- Some mild forms of amelogenesis imperfecta

- Enamel defects caused by infection of a primary tooth predecessor

- Dental caries: Fluorosis-resembling enamel defects are often misdiagnosed as dental caries.

- Dental Trauma: Mechanical trauma to the primary tooth may cause disturbance to the maturation phase of enamel formation, which may result in enamel opacities on the permanent successors.

Dental fluorosis may or may not be of cosmetic concern. In some cases, there may be varying degrees of negative psychosocial effects. The treatment options are:

- Tooth bleaching

- Micro-abrasion

- Composite fillings

- Veneers

- Crowns

Generally, more conservative options such as bleaching are sufficient for mild cases.

Dentin hypersensitivity may affect individuals' quality of life. Over time, the dentin-pulp complex may adapt to the decreased insulation by laying down tertiary dentin, thereby increasing the thickness between the pulp and the exposed dentin surface and lessening the symptoms of hypersensitivity. Similar process such as formation of a smear layer (e.g. from toothbrushing) and dentin sclerosis. These physiologic repair mechanisms are likely to occur with or without any form of treatment, but they take time.

When a diagnosis of bruxism has been confirmed, it is recommended that the patient buy a full-coverage acrylic occlusal splint, such as a Michigan Splint or Tanner appliance, to prevent further bruxism. Patients must be monitored closely, with clinical photographs 6–12 monthly to evaluate if the tooth surface loss is being prevented.

Pulp sensibility tests are routinely used in the diagnosis of dental disease. There are 2 general types:

- Thermal-- most commonly, ethyl chloride sprayed onto a small ball of cotton wool, which produces intense cold. Alternatively gutta percha can be heated to produce heat.

- Electrical pulp test-- electric pulp testing (EPT) has been available for over a century and used by dentists worldwide. It is used to determine the health of the pulp and pulp-related pain. It does not provide information on vascular supply to the pulp. EPT produces electrical stimuli that cause an ionic change across the neural membrane, inducing an action potential in myelinated nerves. The threshold of pain level will be determined by increasing the voltage. The requirements of an EPT are appropriate application method, careful interpretation of the results, and an appropriate stimulus. The tests must be done with tooth isolation and conduction media. EPT is not recommended for patients with orthodontic bands or crowned teeth. Key factors in testing are the enamel and dentine thickness and the number of nerve fibers underlying the pulp. Pulp nerve fibers respond to lower current intensities and a small number of pulpal afferents, creating neural responses when electrical stimulation is applied. EPTs may be unreliable and lead to false-positive and false-negative results. False-positive responses in teeth may be attributed to pulpal necrosis. Also, since pulpal and periodontal nerve thresholds may overlap, the periodontal nerves may give a false indication in tooth sensibility.

Possible explanations for false-positives include:

- Response caused by conduction of the current because of periodontal or gingival issues

- Breakdown products associated with pulp necrosis may be able to conduct electric current next to infected and hypersensitive pulp tissue

- Inflamed pulp tissue may still be present

- Metallic restorations or orthodontic gear are still present

Studies have indicated that there is little correlation between histopathological status of the pulp and clinical information. A negative EPT response showed localized necrosis in 25.7% of cases and 72% of cases. Thus, 97.7% of cases with a negative response to EPT indicated that a root canal treatment should be carried out.

Prevention is of prior importance at an early developmental age as the defective tooth is more likely to have caries and post-eruptive breakdown due to its increased porosity. Appropriate dietary advice and toothpaste with a fluoride level of at least 1,000 ppm F should be recommended. For treating spontaneous hypersensitivity professional applications of fluoride varnish (e.g. Duraphat 22,600ppm F) or 0.4% stannous fluoride gel may be helpful.

Casein Phosphopepetide-Amorphus Calcium Phosphate (CPP-ACP) provides a supersaturated environment of calcium and phosphate on the enamel surface to enhance remineralisation in the form of toothpaste or sugar free chewing gum. Its clinical effectiveness is still debatable but may benefit those patients who complain of mild pain to external stimuli.

Dentists and dental hygienists measure periodontal disease using a device called a periodontal probe. This thin "measuring stick" is gently placed into the space between the gums and the teeth, and slipped below the gumline. If the probe can slip more than below the gumline, the patient is said to have a gingival pocket if no migration of the epithelial attachment has occurred or a periodontal pocket if apical migration has occurred. This is somewhat of a misnomer, as any depth is, in essence, a pocket, which in turn is defined by its depth, i.e., a 2-mm pocket or a 6-mm pocket. However, pockets are generally accepted as self-cleansable (at home, by the patient, with a toothbrush) if they are 3 mm or less in depth. This is important because if a pocket is deeper than 3 mm around the tooth, at-home care will not be sufficient to cleanse the pocket, and professional care should be sought. When the pocket depths reach in depth, the hand instruments and cavitrons used by the dental professionals may not reach deeply enough into the pocket to clean out the microbial plaque that causes gingival inflammation. In such a situation, the bone or the gums around that tooth should be surgically altered or it will always have inflammation which will likely result in more bone loss around that tooth. An additional way to stop the inflammation would be for the patient to receive subgingival antibiotics (such as minocycline) or undergo some form of gingival surgery to access the depths of the pockets and perhaps even change the pocket depths so they become 3 mm or less in depth and can once again be properly cleaned by the patient at home with his or her toothbrush.

If patients have 7-mm or deeper pockets around their teeth, then they would likely risk eventual tooth loss over the years. If this periodontal condition is not identified and the patients remain unaware of the progressive nature of the disease, then years later, they may be surprised that some teeth will gradually become loose and may need to be extracted, sometimes due to a severe infection or even pain.

According to the Sri Lankan tea laborer study, in the absence of any oral hygiene activity, approximately 10% will suffer from severe periodontal disease with rapid loss of attachment (>2 mm/year). About 80% will suffer from moderate loss (1–2 mm/year) and the remaining 10% will not suffer any loss.

Any tooth that is identified, in either the history of pain or base clinical exam, as a source for toothache may undergo further testing for vitality of the dental pulp, infection, fractures, or periodontitis. These tests may include:

- Pulp sensitivity tests, usually carried out with a cotton wool sprayed with ethyl chloride to serve as a cold stimulus, or with an electric pulp tester. The air spray from a three-in-one syringe may also be used to demonstrate areas of dentin hypersensitivity. Heat tests can also be applied with hot Gutta-percha. A healthy tooth will feel the cold but the pain will be mild and disappear once the stimulus is removed. The accuracy of these tests has been reported as 86% for cold testing, 81% for electric pulp testing, and 71% for heat testing. Because of the lack of test sensitivity, a second symptom should be present or a positive test before making a diagnosis.

- Radiographs utilized to find dental caries and bone loss laterally or at the apex.

- Assessment of biting on individual teeth (which sometimes helps to localize the problem) or the separate cusps (may help to detect cracked cusp syndrome).

Less commonly used tests might include trans-illumination (to detect congestion of the maxillary sinus or to highlight a crack in a tooth), dyes (to help visualize a crack), a test cavity, selective anaesthesia and laser doppler flowmetry.

In order for successful treatment of abrasion to occur, the aetiology first needs to be identified. The most accurate way of doing so is completing a thorough medical, dental, social and diet history. All aspects needs to be investigated as in many cases the cause of abrasion can be multi-factorial. Once a definitive diagnosis is completed the appropriate treatment can commence.

Treatment for abrasion can present in varying difficulties depending on the current degree or progress caused by the abrasion. Abrasion often presents in conjunction with other dental conditions such as attrition, decay and erosion however the below treatment is for abrasion alone. Successful treatment focuses on the prevention and progression on the condition and modifies the current habit/s instigating the condition.

Discoloration of the front teeth is one of the most common reasons people seek dental care. However, many people with teeth of normal shade ask for them to be whitened. Management of tooth discoloration depends on the cause. Most discoloration is harmless and may or may not be of cosmetic concern to the individual. In other cases it may indicate underlying pathology such as pulp necrosis or rarely a systemic disorder.

Most extrinsic discoloration is readily removed by cleaning the teeth, whether with "whitening" (i.e., abrasive) toothpaste at home, or as treatment carried out by a professional (e.g., scaling and/or polishing). To prevent future buildup of extrinsic stains, identification of the cause (e.g., smoking) is required.

Intrinsic discoloration generally requires one of the many types of tooth bleaching. Alternatively the appearance of the tooth can be hidden with dental restorations (e.g., composite fillings, veneers, crowns).

Recent advances have seen the introduction of platelet derived growth factor (PDGF) infused bone graft material. This material is usually combined with the cellular matrix to form a soft bone paste that is then covered by the allograft. The development of this type of bone and tissue cellular matrix (also known as ortho filler) results in greater osseointegration with the patient's healthy bone and soft tissue.

Healing from such procedures requires 2–4 weeks. After a few months the results can be evaluated and in some cases the new tissue needs to be reshaped in a very minor procedure to get an optimal result. In cases where recession is not accompanied by periodontal bone loss, complete or near complete coverage of the recession area is achievable.

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.