Diagnosis is usually clinical. Smear for fusospirochaetal bacteria and leukocytes; blood picture occasionally. The important differentiation is with acute leukaemia or herpetic stomatitis.

Treatment includes irrigation and debridement of necrotic areas (areas of dead and/or dying gum tissue), oral hygiene instruction and the uses of mouth rinses and pain medication. If there is systemic involvement, then oral antibiotics may be given, such as metronidazole. As these diseases are often associated with systemic medical issues, proper management of the systemic disorders is appropriate.

An examination by the dentist or dental hygienist should be sufficient to rule out the issues such as malnutrition and puberty. Additional corresponding diagnosis tests to certain potential disease may be required. This includes oral glucose tolerance test for diabetes mellitus, blood studies, human gonadotrophin levels for pregnancy, and X-rays for teeth and jaw bones.

In order to determine the periodontal health of a patient, the dentist or dental hygienist records the sulcular depths of the gingiva and observes any bleeding on probing. This is often accomplished with the use of a periodontal probe. Alternatively, dental floss may also be used to assess the Gingival bleeding index. It is used as an initial evaluation on patient's periodontal health especially to measure gingivitis. The number of bleeding sites is used to calculate the gingival bleeding score.

Peer-reviewed dental literature thoroughly establishes that bleeding on probing is a poor positive predictor of periodontal disease, but conversely lack of bleeding is a very strong negative predictor. The clinical interpretation of this research is that while BOP presence may not indicate periodontal disease, continued absence of BOP is a strong predictor (approximately 98%) of continued periodontal health.

Gingivitis is a category of periodontal disease in which there is no loss of bone but inflammation and bleeding are present.

Each tooth is divided into four gingival units (mesial, distal, buccal, and lingual) and given a score from 0-3 based on the gingival index. The four scores are then averaged to give each tooth a single score.

The diagnosis of the periodontal disease gingivitis is done by a dentist. The diagnosis is based on clinical assessment data acquired during a comprehensive periodontal exam. Either a registered dental hygienist or a dentist may perform the comprehensive periodontal exam but the data interpretation and diagnosis are done by the dentist. The comprehensive periodontal exam consists of a visual exam, a series of radiographs, probing of the gingiva, determining the extent of current or past damage to the periodontium and a comprehensive review of the medical and dental histories.

Current research shows that activity levels of the following enzymes in saliva samples are associated with periodontal destruction: aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma glutamyl transferase (GGT), alkaline phosphatase (ALP), and acid phosphatase (ACP). Therefore, these enzyme biomarkers may be used to aid in the diagnosis and treatment of gingivitis and periodontitis.

A dental hygienist or dentist will check for the symptoms of gingivitis, and may also examine the amount of plaque in the oral cavity. A dental hygienist or dentist will also look for signs of periodontitis using X-rays or periodontal probing as well as other methods.

If gingivitis is not responsive to treatment, referral to a periodontist (a specialist in diseases of the gingiva and bone around teeth and dental implants) for further treatment may be necessary.

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.

Gingivitis can be prevented through regular oral hygiene that includes daily brushing and flossing. Hydrogen peroxide, saline, alcohol or chlorhexidine mouth washes may also be employed. In a 2004 clinical study, the beneficial effect of hydrogen peroxide on gingivitis has been highlighted.

Rigorous plaque control programs along with periodontal scaling and curettage also have proved to be helpful, although according to the American Dental Association, periodontal scaling and root planing are considered as a treatment for periodontal disease, not as a preventive treatment for periodontal disease. In a 1997 review of effectiveness data, the U.S. Food and Drug Administration (FDA) found clear evidence showing that toothpaste containing triclosan was effective in preventing gingivitis.

Plasma cell gingivits is rare, and plasma cell cheilitis is very rare. Most people with plasma cell cheilitis have been elderly.

Prevention of pericoronitis can be achieved by removing impacted third molars before they erupt into the mouth, or through preemptive operculectomy. A treatment controversy exists about the necessity and timing of the removal of asymptomatic, disease-free impacted wisdom teeth which prevents pericoronitis. Proponents of early extraction cite the cumulative risk for extraction over time, the high probability that wisdom teeth will eventually decay or develop gum disease and costs of monitoring to retained wisdom teeth. Advocates for retaining wisdom teeth cite the risk and costs of unnecessary operations and the ability to monitor the disease through clinical exam and radiographs.

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.

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.

If there is persistent continuation of inflammation and bleeding, a prescription of antiplaque rinse would be useful.

The diagnosis can typically be made from the clinical appearance alone, but not always. As candidiasis can be variable in appearance, and present with white, red or combined white and red lesions, the differential diagnosis can be extensive. In pseudomembraneous candidiasis, the membranous slough can be wiped away to reveal an erythematous surface underneath. This is helpful in distinguishing pseudomembraneous candidiasis from other white lesions in the mouth that cannot be wiped away, such as lichen planus, oral hairy leukoplakia. Erythematous candidiasis can mimic geographic tongue. Erythematous candidiasis usually has a diffuse border that helps distinguish it from erythroplakia, which normally has a sharply defined border.

Special investigations to detect the presence of candida species include oral swabs, oral rinse or oral smears. Smears are collected by gentle scraping of the lesion with a spatula or tongue blade and the resulting debris directly applied to a glass slide. Oral swabs are taken if culture is required. Some recommend that swabs be taken from 3 different oral sites. Oral rinse involves rinsing the mouth with phosphate-buffered saline for 1 minute and then spitting the solution into a vessel that examined in a pathology laboratory. Oral rinse technique can distinguish between commensal candidal carriage and candidiasis. If candidal leukoplakia is suspected, a biopsy may be indicated. Smears and biopsies are usually stained with periodic acid-Schiff, which stains carbohydrates in fungal cell walls in magenta. Gram staining is also used as Candida stains are strongly Gram positive.

Sometimes an underlying medical condition is sought, and this may include blood tests for full blood count and hematinics.

If a biopsy is taken, the histopathologic appearance can be variable depending upon the clinical type of candidiasis. Pseudomembranous candidiasis shows hyperplastic epithelium with a superficial parakeratotic desquamating (i.e., separating) layer. Hyphae penetrate to the depth of the stratum spinosum, and appear as weakly basophilic structures. Polymorphonuclear cells also infiltrate the epithelium, and chronic inflammatory cells infiltrate the lamina propria.

Atrophic candidiasis appears as thin, atrophic epithelium, which is non-keratinized. Hyphae are sparse, and inflammatory cell infiltration of the epithelium and the lamina propria. In essence, atrophic candidiasis appears like pseudomembranous candidiasis without the superficial desquamating layer.

Hyperplastic candidiasis is variable. Usually there is hyperplastic and acanthotic epithelium with parakeratosis. There is an inflammatory cell infiltrate and hyphae are visible. Unlike other forms of candidiasis, hyperplastic candidiasis may show dysplasia.

Histologically plasma cell gingivitis shows mainly plasma cells. The differential diagnosis is with acute leukemia and multiple myeloma. Hence, blood tests are often involved in ruling out other conditions. A biopsy is usually taken, and allergy testing may also be used. The histopathologic appearance is characterized by diffuse, sub-epithelial plasma cell inflammatory infiltration into the connective tissue. The epithelium shows spongiosis. Some consider that plasmoacanthoma (solitary plasma cell tumor) is part of the same spectrum of disease as plasma cell cheilitis.

Oral and maxillofacial pathology, previously termed oral pathology, is a speciality involved with the diagnosis and study of the causes and effects of diseases affecting the oral and maxillofacial regions (i.e. the mouth, the jaws and the face). It can be considered a speciality of dentistry and pathology. Oral pathology is a closely allied speciality with oral and maxillofacial surgery and oral medicine.

The clinical evaluation and diagnosis of oral mucosal diseases are in the scope of oral & maxillofacial pathology specialists and oral medicine practitioners, both disciplines of dentistry.

When a microscopic evaluation is needed, a biopsy is taken, and microscopically observed by a pathologist. The American Dental Association uses the term oral and maxillofacial pathology, and describes it as "the specialty of dentistry and pathology which deals with the nature, identification, and management of diseases affecting the oral and maxillofacial regions. It is a science that investigates the causes, processes and effects of these diseases."

In some parts of the world, oral and maxillofacial pathologists take on responsibilities in forensic odontology.

Chronic ulcerative stomatitis is a recently discovered condition with specific immunopathologic features. It is characterized by erosions and ulcerations which relapse and remit. Lesions are located on the buccal mucosa (inside of the cheeks) or on the gingiva (gums). The condition resembles Oral lichen planus when biopsied.

The diagnosis is made with Immunofluorescence techniques, which shows circulating and tissue-bound autoantibodies (particulate stratified squamous-epithelium-specific antinuclear antibody) to DeltaNp63alpha protein, a normal component of the epithelium. Treatment is with hydroxychloroquine.

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.

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.

The presence of dental plaque or infection beneath an inflamed operculum without other obvious causes of pain will often lead to a pericoronitis diagnosis; therefore, elimination of other pain and inflammation causes is essential. For pericoronal infection to occur, the affected tooth must be exposed to the oral cavity, which can be difficult to detect if the exposure is hidden beneath thick tissue or behind an adjacent tooth. Severe swelling and restricted mouth opening may limit examination of the area. Radiographs can be used to rule out other causes of pain and to properly assess the prognosis for further eruption of the affected tooth.

Sometimes a "migratory abscess" of the buccal sulcus occurs with pericoronal infection, where pus from the lower third molar region tracks forwards in the submucosal plane, between the body of the mandible and the attachment of the buccinator muscle to the mandible. In this scenario, pus may spontaneously discharge via an intra-oral sinus located over the mandibular second or first molar, or even the second premolar.

Similar causes of pain, some which can occur in conjunction with pericoronitis may include:

- Dental caries (tooth decay) of the wisdom tooth and of the distal surface of the second molar is common. Tooth decay may cause pulpitis (toothache) to occur in the same region, and this may cause pulp necrosis and the formation of a periapical abscess associated with either tooth.

- Food can also become stuck between the wisdom tooth and the tooth in front, termed food packing, and cause acute inflammation in a periodontal pocket when the bacteria become trapped. A periodontal abscess may even form by this mechanism.

- Pain associated with temporomandibular joint disorder and myofascial pain also often occurs in the same region as pericoronitis. They are easily missed diagnoses in the presence of mild and chronic pericoronitis, and the latter may not be contributing greatly to the individual's pain (see table).

It is rare for pericoronitis to occur in association with both lower third molars at the same time, despite the fact that many young people will have both lower wisdom teeth partially erupted. Therefore, bilateral pain from the lower third molar region is unlikely to be caused by pericoronitis and more likely to be muscular in origin.

The diagnosis is usually made by tissue biopsy, however this cannot reliably distinguish between the granulomas of OFG and those of Crohn's disease or sarcoidosis. Other causes of granulomatous inflammation are ruled out, such as sarcoidosis,

Crohn's disease, allergic or foreign body reactions and mycobacterial infections.

Dry socket typically causes pain on the second to fourth day following a dental extraction. Other causes of post extraction pain usually occur immediately after the anesthesia/analgesia has worn off, (e.g., normal pain from surgical trauma or mandibular fracture) or has a more delayed onset (e.g., osteomyelitis, which typically causes pain several weeks following an extraction). Examination typically involves gentle irrigation with warm saline and probing of the socket to establish the diagnosis. Sometimes part of the root of the tooth or a piece of bone fractures off and is retained in the socket. This can be another cause of pain in a socket, and causes delayed healing. A dental radiograph (x-ray) may be indicated to demonstrate such a suspected fragment.

The severity of oral candidiasis is subject to great variability from one person to another and in the same person from one occasion to the next. The prognosis of such infection is usually excellent after the application of topical or systemic treatments. However, oral candidiasis can be recurrent. Individuals continue to be at risk of the condition if underlying factors such as reduced salivary flow rate or immunosuppression are not rectifiable.

Candidiasis can be a marker for underlying disease, so the overall prognosis may also be dependent upon this. For example, a transient erythematous candidiasis that developed after antiobiotic therapy usually resolves after antibiotics are stopped (but not always immediately), and therefore carries an excellent prognosis—but candidiasis may occasionally be a herald of a more sinister undiagnosed pathology, such as HIV/AIDS or leukemia.

It is possible for candidiasis to spread to/from the mouth, from sites such as the pharynx, esophagus, lungs, liver, anogenital region, skin or the nails. The spread of oral candidiasis to other sites usually occurs in debilitated individuals. It is also possible that candidiasis is spread by sexual contact. Rarely, a superficial candidal infection such as oral candidiasis can cause invasive candidiasis, and even prove fatal. The observation that Candida species are normally harmless commensals on the one hand, but are also occasionally capable of causing fatal invasive candidiases has led to the description "Dr Jekyll and Mr Hyde".

The role of thrush in the hospital and ventilated patients is not entirely clear however there is a theoretical risk of positive interaction of candida with topical bacteria that could increase the risk for Ventilator Associated Pneumonia and other diseases.

Dental plaque accumulates at the surfaces when proper cleaning and maintaining is not done. There is inflammation due to the bacteria released from the toxins. calculus forms and if not removed, causes this disease.

A systematic review reported that there is some evidence that rinsing with chlorhexidine (0.12% or 0.2%) or placing chlorhexidine gel (0.2%) in the sockets of extracted teeth reduces the frequency of dry socket. Another systematic review concluded that there is evidence that prophylactic antibiotics reduce the risk of dry socket (and infection and pain) following third molar extractions of wisdom teeth, however their use is associated with an increase in mild and transient adverse effects. The authors questioned whether treating 12 patients with antibiotics to prevent one infection would do more harm overall than good, in view of the potential side effects and also of antibiotic resistance. Nevertheless, there is evidence that in individuals who are at clear risk may benefit from antibiotics. There is also evidence that antifibrinolytic agents applied to the socket after the extraction may reduce the risk of dry socket.

Some dentists and oral surgeons routinely debride the bony walls of the socket to encourage hemorrhage (bleeding) in the belief that this reduces the incidence of dry socket, but there is no evidence to support this practice. It has been suggested that dental extractions in females taking oral contraceptives be scheduled on days without estrogen supplementation (typically days 23–28 of the menstrual cycle). It has also been suggested that teeth to be extracted be scaled prior to the procedure.

Prevention of alveolar osteitis can be exacted by following post-operative instructions, including:

1. Taking any recommended medications

2. Avoiding intake of hot fluids for one to two days. Hot fluids raise the local blood flow and thus interfere with organization of the clot. Therefore, cold fluids and foods are encouraged, which facilitate clot formation and prevent its disintegration.

3. Avoiding smoking. It reduces the blood supply, leading to tissue ischemia, reduced tissue perfusion and eventually higher incidence of painful socket.

4. Avoiding drinking through a straw or spitting forcefully as this creates a negative pressure within the oral cavity leading to an increased chance of blood clot instability.

Since most toothache is the result of plaque-related diseases, such as tooth decay and periodontal disease, the majority of cases could be prevented by avoidance of a cariogenic diet and maintenance of good oral hygiene. That is, reduction in the number times that refined sugars are consumed per day and brushing the teeth twice a day with fluoride toothpaste and flossing. Regular visits to a dentist also increases the likelihood that problems are detected early and averted before toothache occurs. Dental trauma could also be significantly reduced by routine use of mouthguards in contact sports.

Anti-tumour necrosis factor α antagonists (e.g. infliximab)

Dietary restriction of a particular suspected or proven antigen may be involved in the management of OFG, such as cinnamon or benzoate-free diets.