Periodontitis

Periodontal disease
Classification and external resources
This radiograph shows significant bone loss between the two roots of a tooth (black region). The spongy bone has receded due to infection under tooth, reducing the bony support for the tooth.
ICD-10	K05.4
DiseasesDB	29362
MedlinePlus	001059
MeSH	D010518

Periodontitis or pyorrhea is a set of inflammatory diseases affecting the periodontium, i.e., the tissues that surround and support the teeth. Periodontitis involves progressive loss of the alveolar bone around the teeth, and if left untreated, can lead to the loosening and subsequent loss of teeth. Periodontitis is caused by microorganisms that adhere to and grow on the tooth's surfaces, along with an overly aggressive immune response against these microorganisms. A diagnosis of periodontitis is established by inspecting the soft gum tissues around the teeth with a probe (i.e. a clinical exam) and by evaluating the patient's x-ray films (i.e. a radiographic exam), to determine the amount of bone loss around the teeth.^[1] Specialists in the treatment of periodontitis are periodontists; their field is known as "periodontology" or "periodontics".

The word "periodontitis" comes from peri ("around"), odont ("tooth") and -itis ("inflammation").

Contents 1 Classification 1.1 Extent 1.2 Severity 2 Signs and symptoms 2.1 Effects outside the mouth 3 Causes 4 Prevention 5 Management 5.1 Initial therapy 5.2 Reevaluation 5.3 Surgery 5.4 Maintenance 5.5 Alternative treatments 6 Prognosis 7 Epidemiology 8 In other animals 9 See also 10 Further reading 11 Footnotes 12 External links

Classification

The 1999 classification system for periodontal diseases and conditions listed seven major categories of periodontal diseases,^[2] of which the last six are termed destructive periodontal disease because they are essentially irreversible. The seven categories are as follows:

1. Gingivitis
2. Chronic periodontitis
3. Aggressive periodontitis
4. Periodontitis as a manifestation of systemic disease
5. Necrotizing ulcerative gingivitis/periodontitis
6. Abscesses of the periodontium
7. Combined periodontic-endodontic lesions

Moreover, terminology expressing both the extent and severity of periodontal diseases are appended to the terms above to denote the specific diagnosis of a particular patient or group of patients.

Extent

The extent of disease refers to the proportion of the dentition affected by the disease in terms of percentage of sites. Sites are defined as the positions at which probing measurements are taken around each tooth and, generally, six probing sites around each tooth are recorded, as follows:

1. mesiobuccal
2. mid-buccal
3. distobuccal
4. mesiolingual
5. mid-lingual
6. distolingual

If up to 30% of sites in the mouth are affected, the manifestation is classification as localized; for more than 30%, the term generalized is used.

Severity

The severity of disease refers to the amount of periodontal ligament fibers that have been lost, termed clinical attachment loss. According to the American Academy of Periodontology, the classification of severity is as follows:^[3]

• Mild: 1–2 mm of attachment loss
• Moderate: 3–4 mm of attachment loss
• Severe: ≥ 5 mm of attachment lo

Signs and symptoms

In the early stages, periodontitis has very few symptoms and in many individuals the disease has progressed significantly before they seek treatment. Symptoms may include the following:

• Redness or bleeding of gums while brushing teeth, using dental floss or biting into hard food (e.g. apples) (though this may occur even in gingivitis, where there is no attachment loss)
• Gum swelling that recurs
• spiting out blood after brushing teeth
• Halitosis, or bad breath, and a persistent metallic taste in the mouth
• Gingival recession, resulting in apparent lengthening of teeth. (This may also be caused by heavy handed brushing or with a stiff tooth brush.)
• Deep pockets between the teeth and the gums (pockets are sites where the attachment has been gradually destroyed by collagen-destroying enzymes, known as collagenases)
• Loose teeth, in the later stages (though this may occur for other reasons as well)

Patients should realize that the gingival inflammation and bone destruction are largely painless. Hence, people may wrongly assume that painless bleeding after teeth cleaning is insignificant, although this may be a symptom of progressing periodontitis in that patient.

Effects outside the mouth

Periodontitis has been linked to increased inflammation in the body such as indicated by raised levels of C-reactive protein and Interleukin-6.^[4][5][6][7] It is through this linked to increased risk of stroke,^[8][9] myocardial infarction,^[10] and atherosclerosis.^{[11][12][13][14][15][16][17]} It also linked in those over 60 years of age to impairments in delayed memory and calculation abilities.^[18][19] Individuals with impaired fasting glucose and diabetes mellitus have higher degree of periodontal inflammation, and often have difficulties with balancing their blood glucose level owing to the constant systemic inflammatory state, caused by the periodontal inflammation.^[20][21] Although no causative connection was proved yet, a recent study revealed an epidemiological association between chronic periodontitis and erectile dysfunction.^[22]

Causes

Periodontitis is an inflammation of the periodontium, i.e., the tissues that support the teeth. The periodontium consists of four tissues:

• gingiva, or gum tissue;
• cementum, or outer layer of the roots of teeth;
• alveolar bone, or the bony sockets into which the teeth are anchored;
• periodontal ligaments (PDLs), which are the connective tissue fibers that run between the cementum and the alveolar bone.

The primary etiology (cause) of gingivitis is poor oral hygiene which leads to the accumulation of a mycotic ^{[23][24][25][26]} and bacterial matrix at the gum line, called dental plaque. Other contributors are poor nutrition and underlying medical issues such as diabetes.^[27] New finger nick tests have been approved by the Food and Drug Administration in the US, and are being used in dental offices to identify and screen patients for possible contributory causes of gum disease such as diabetes.

In some people, gingivitis progresses to periodontitis –- with the destruction of the gingival fibers, the gum tissues separate from the tooth and deepened sulcus, called a periodontal pocket. Subgingival microorganism (those that exist under the gum line) colonize the periodontal pockets and cause further inflammation in the gum tissues and progressive bone loss. Examples of secondary etiology are those things that, by definition, cause microbic plaque accumulation, such as restoration overhangs and root proximity.

Smoking is another factor that increases the occurrence of periodontitis, directly or indirectly,^[28][29][30] and may interfere with or adversely affect its treatment.^[31][32][33]

Ehlers-Danlos Syndrome is a periodontitis risk factor.

If left undisturbed, microbic plaque calcifies to form calculus, which is commonly called tartar. Calculus above and below the gum line must be removed completely by the dental hygienist or dentist to treat gingivitis and periodontitis. Although the primary cause of both gingivitis and periodontitis is the microbic plaque that adheres to the tooth surface, there are many other modifying factors. A very strong risk factor is one's genetic susceptibility. Several conditions and diseases, including Down syndrome, diabetes, and other diseases that affect one's resistance to infection also increase susceptibility to periodontitis.

Another factor that makes periodontitis a difficult disease to study is that human host response can also affect the alveolar bone resorption. Host response to the bacterial-mycotic insult is mainly determined by genetics; however, immune development may play some role in susceptibility.

According to some researches periodontitis may be associated with higher stress.^[34]

Prevention

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 gum-line, to help disrupt the bacterial-mycotic growth and formation of subgingival plaque.
• Flossing daily and using interdental brushes (if there is a sufficiently large space between teeth), 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 a 'soft' tooth brush to prevent damage to tooth enamel and sensitive gums.
• 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.

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), microbic plaque tend to grow back to pre-cleaning levels after about 3–4 months. However, it is advocated that the interval between dental check-ups should be determined specifically for each patient between every 3 to 12 months.^[35][36]

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 of cancer.^[37]

Contributing causes may be high alcohol consumption or a diet low in antioxidants. ^[38]

Management

The cornerstone of successful periodontal treatment starts with establishing excellent oral hygiene. This includes twice daily brushing with daily flossing. Also the use of an interdental brush (called a Proxi-brush) is helpful if space between the teeth allows. For smaller spaces a product called "Soft Picks" are an excellent manual cleaning device. Persons with dexterity problems such as arthritis may find oral hygiene to be difficult and may require more frequent professional care and/or the use of a powered tooth brush. Persons with periodontitis must realize that it is a chronic inflammatory disease and a lifelong regimen of excellent hygiene and professional maintenance care with a dentist/hygienist or periodontist is required to maintain affected teeth.

Initial therapy

Removal of microbic plaque and calculus is necessary to establish periodontal health. The first step in the treatment of periodontitis involves non-surgical cleaning below the gumline with a procedure called scaling and debridement. In the past, Root Planing was used (removal of cemental layer as well as calculus). This procedure involves use of specialized curettes to mechanically remove plaque and calculus from below the gumline, and may require multiple visits and local anesthesia to adequately complete. In addition to initial scaling and root planing, it may also be necessary to adjust the occlusion (bite) to prevent excessive force on teeth that have reduced bone support. Also it may be necessary to complete any other dental needs such as replacement of rough, plaque retentive restorations, closure of open contacts between teeth, and any other requirements diagnosed at the initial evaluation.

Reevaluation

Multiple clinical studies have shown that non-surgical scaling and root planing is usually successful if the periodontal pockets are shallower than 4–5 mm (See articles by Stambaugh RV, Int J Periodontics Rest Dent, 1981 or Waerhaug J, J Periodontol, 1978).^[39][40][41] It is necessary for the dentist or hygienist to perform a reevaluation 4–6 weeks after the initial scaling and root planing, to determine if the patient's oral hygiene has improved and inflammation has regressed. Probing should be avoided at 4–6 weeks, and an analysis by gingival index should determine the presence or absence of inflammation. Three monthly reevaluation of periodontal therapy should involve periodontal charting as a better indication of the success of treatment, and to see if other courses of treatment can be identified. Pocket depths of greater than 5-6mm which remain after initial therapy, with bleeding upon probing, indicate continued active disease and will very likely lead to further bone loss over time. This is especially true in molar tooth sites where furcations (areas between the roots) have been exposed.

Surgery

If non-surgical therapy is found to have been unsuccessful in managing signs of disease activity, periodontal surgery may be needed to stop progressive bone loss and regenerate lost bone where possible. There are many surgical approaches used in treatment of advanced periodontitis, including open flap debridement, osseous surgery, as well as guided tissue regeneration and bone grafting. The goal of periodontal surgery is access for definitive calculus removal and surgical management of bony irregularities which have resulted from the disease process to reduce pockets as much as possible. Long-term studies have shown that in moderate to advanced periodontitis, surgically treated cases often have less further breakdown over time and when coupled with a regular post-treatment maintenance regimen are successful in nearly halting tooth loss in nearly 85% of patients.^[42][43]

Maintenance

Once successful periodontal treatment has been completed, with or without surgery, an ongoing regimen of "periodontal maintenance" is required. This involves regular checkups and detailed cleanings every three months to prevent re-population of periodontitis-causing microorganism, and to closely monitor affected teeth so that early treatment can be rendered if disease recurs. Usually periodontal disease exists due to poor plaque control, therefore if the brushing techniques are not modified, a periodontal recurrence is probable.

Alternative treatments

Periodontitis has an inescapable relationship with subgingival calculus (tartar). The first step in any procedure is to eliminate calculus under the gum line, as it houses destructive anaerobic microorganisms that consume bone, gum and cementum (connective tissue) for food.

Most alternative “at-home” gum disease treatments involve injecting anti-microbial solutions, such as hydrogen peroxide, into periodontal pockets via slender applicators or oral irrigators. This process disrupts anaerobic microorganism colonies and is effective at reducing infections and inflammation when used daily. A number of potions and elixirs that are functionally equivalent to hydrogen peroxide are commercially available but at substantially higher cost. However, such treatments do not address calculus formations, and so are short-lived, as anaerobic microorganism colonies quickly regenerate in and around calculus.

In a new field of study, calculus formations are addressed on a more fundamental level. At the heart of the formation of subgingival calculus, growing plaque formations starve out the lowest members of the community, which calcify into calcium phosphate salts of the same shape and size of the original, organic bacilli. Calcium phosphate salts (unlike calcium phosphate; the primary component in teeth) are ionic and adhere to tooth surfaces via electrostatic attraction. Smaller, free-floating calcium phosphate salt particles are equally attracted to the same areas, as are additional calcified microorganism, growing calculus formations as unorganized, yet strong, “brick and mortar” matrices. The microscopic voids in calculus formations house new anaerobic microorganism, as does the top “diseased layer”.

Because the root cause of subgingival calculus development is ionic attraction, it was hypothesized that the introduction of oppositely charged particles around the formations may chelate calcium phosphate salt components away from the matrix, thus reducing the size of subgingival calculus formations. To accomplish this, a sequestering agent solution consisting partly of sodium tripolyphosphate (STPP) and sodium fluoride (charge -1) was tested on a patient with burnished and new subgingival calculus at a depth of 6 mm. The patient delivered the solution using an oral irrigator, once a day, for 60 days. The results were the successful elimination of all calculus formations studied.^[44] This test was conducted using a subgingival endoscopic camera (perioscope) by an independent periodontist.

The promise of this new, alternative treatment is to keep subgingival calculus at bay, in concert with traditional periodontal treatments. In this way, periodontitis may be controlled by the patient, and complete restoration of dental health can be a collaborative effort between the patient and the dental professional.

Additionally, Periodontitis can be treated in a noninvasive manner by means of Periostat, an FDA-approved, orally-administered drug that has been shown to reduce bone loss. Its mechanism of action in part involves inhibition of Matrix metalloproteinases (such as collagenase), which degrade the extracellular matrix under inflammatory conditions. This ultimately can lead to reduction of aveolar bone-loss in patients with periodontal disease (as well as patients without periodontitis).

Prognosis

Dentists and dental hygienists measure periodontal disease using a device called a periodontal probe. This is a thin "measuring stick" that is gently placed into the space between the gums and the teeth, and slipped below the gum-line. If the probe can slip more than 3 millimeters below the gum-line, 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, it is generally accepted that pockets are self-cleansable (at home, by the patient, with a toothbrush) if they are 3 mm or less in depth. This is important because if there is a pocket which 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 6 and 7 mm in depth, the hand instruments and cavitrons used by the dental professionals may not reach deeply enough into the pocket to clean out the microbic plaque that cause 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 that 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 a patient has 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 patient remains 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 labourer 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). 80% will suffer from moderate loss (1–2 mm/year) and the remaining 10% will not suffer any loss.^[45][46]

Epidemiology

Periodontitis is very common, and is widely regarded as the second most common disease worldwide, after dental decay, and in the United States has a prevalence of 30–50% of the population, but only about 10% have severe forms.

Like other conditions that are intimately related to access to hygiene and basic medical monitoring and care, periodontitis tends to be more common in economically disadvantaged populations or regions. Its occurrence decreases with higher standard of living. In Israeli population, individuals of Yemenite, North-African, South Asian, or Mediterranean origin have higher prevalence of periodontal disease than individuals from European descent.^[48]

Presumably, individuals living in East Asia (e.g. Japan, South Korea and Taiwan) have the lowest incident of periodontal disease in the world.

In other animals

Periodontal disease is the most common disease found in dogs and affects more than 80% of dogs aged three years or older. The prevalence of periodontal disease in dogs increases with age but decreases with increasing body weight; i.e., toy and miniature breeds are more severely affected. Systemic disease may develop because the gums are very vascular (have a good blood supply). The blood stream carries these anaerobic microorganisms, and they are filtered out by the kidneys and liver, where they may colonize and create microabscesses. The microorganisms traveling through the blood may also attach to the heart valves, causing vegetative endocarditis (infected heart valves). Additional diseases that may result from periodontitis includes chronic bronchitis and pulmonary fibrosis.^[49]

See also

• Actinomyces naeslundii, a kind of bacterium
• Calculus (dental), tartar
• Campylobacter, a kind of bacterium
• Candida albicans, a kind of micetum
• Chronic periodontitis
• Dental Implant
• Dental plaque, bacterial biofilm that clings to teeth
• Edentulism, condition of one or more missing teeth
• Epidemiology of periodontal diseases
• Gingivitis, inflammation of the gums
• Gum graft, a type of gum surgery, to replace lost gum tissue
• Halitosis, bad breath due to oral bacteria
• Head and neck anatomy, biological composition above the shoulders
• LANAP, Laser Assisted New Attachement Procedure
• Oral hygiene, how to promote good health of the mouth
• Oral microbiology, study of the microorganisms of the oral cavity
• Osteoimmunology, studies the immune system with respect to bones
• Periodontist
• Tooth loss

Further reading

Footnotes

External links

• Advanced stage of gum disease is periodontitis Gum disease causes and treatment
• Mayo Clinic
• OralDNA Labs, a Quest Diagnostics Company, providing DNA-PCR salivary diagnostics to advance wellness in dentistry
• Absolute Smile — Periodontal Disease in Profile
• Canadian Academy of Periodontology — What is periodontitis?
• Maladies parodontales - Etat général Le Courrier du Dentiste; Août 2011
• Healthy behaviors equal healthy gums — An article from ADA (American Dental Association)
• Gum disease in dogs treatment & symptoms — Dog health care sheet on spotting the symptoms of gum disease in dogs.
• Periodontal disease in dogs and cats — Blue Cross Animal Hospital's write up on peridontal disease.

Periodontology Tissues of the periodontium and their physiologic entities Alveolar bone · Biologic width · Bundle bone · Cementum · Free gingival margin · Gingiva · Gingival fibers · Gingival sulcus · Junctional epithelium · Mucogingival junction · Periodontal ligament · Sulcular epithelium · Stippling Diagnoses Chronic periodontitis · Localized aggressive periodontitis · Generalized aggressive periodontitis · Periodontitis as a manifestation of systemic disease · Necrotizing periodontal diseases · Abscesses of the periodontium · Combined periodontic-endodontic lesions Pathogenesis A. actinomycetemcomitans · Capnocytophaga sp. · F. nucleatum · P. gingivalis · P. intermedia · T. forsythia · T. denticola Pathologic entities Calculus · Clinical attachment loss · Edentulism · Fremitus · Furcation defect · Gingival enlargement · Gingival pocket · Gingivitis · Horizontal bony defect · Linear gingival erythema · Occlusal trauma · Periodontal pocket · Periodontal disease · Periodontitis · Plaque · Recession · Vertical bony defect Diagnosis, treatment planning, prevention and chemotherapeutic agents Brushing · Bleeding on probing · Chlorhexidine gluconate · Enamel matrix derivative · Flossing · Hydrogen peroxide · Mouthwash · Oral hygiene · Tetracycline · Triclosan Periodontal armamentarium Curette · Membrane · Probe · Scaler Conventional therapy Debridement · Scaling and root planing · Full mouth disinfection Surgical therapy and periodontal surgery Apically positioned flap · Bone graft · Coronally positioned flap · Crown lengthening · Open flap debridement · Free gingival graft · Gingivectomy · Guided bone regeneration · Guided tissue regeneration · Implant Placement · Lateral pedicle graft · Pocket reduction surgery · Sinus lift · Subepithelial connective tissue graft Important personalities Per-Ingvar Brånemark · Jan Lindhe · Preston D. Miller · Willoughby D. Miller · Carl E. Misch · John Mankey Riggs · Jørgen Slots · Dennis P. Tarnow · Hom-Lay Wang · James Leon Williams · W. J. Younger Other specialties Endodontology · Orthodontology · Prosthodontology M: MOU anat/devp noco/cofa(c)/cogi/tumr, sysi proc (peri), drug (A1)

Acquired tooth disease (K02–K05, 521–525) Hard tissues Caries (tooth decay) · Attrition · Abrasion · Erosion · Hypercementosis · tooth resorption (External resorption, Internal resorption, Root resorption) Pulp/periapical (Endodontal) Pulpal External resorption · Internal resorption · Irreversible pulpitis · Reversible pulpitis · Necrotic pulp · Pink tooth of Mummery Periapical Acute apical periodontitis · Chronic apical periodontitis · Combined periodontic-endodontic lesions · Fistula · Periapical abscess · Phoenix abscess · Vertical root fracture Ungrouped Pulpitis · Radicular cyst · Periapical abscess Gingiva/periodontal (Periodontal) Gingivitis · Periodontitis (Chronic periodontitis) · Periodontal disease Bone cyst Dentigerous cyst · Calcifying odontogenic cyst · Glandular odontogenic cyst Other Toothache · Cracked tooth syndrome To be grouped from periodontology Diagnoses Chronic periodontitis · Localized aggressive periodontitis · Generalized aggressive periodontitis · Periodontitis as a manifestation of systemic disease · Necrotizing periodontal diseases · Abscesses of the periodontium · Combined periodontic-endodontic lesions Pathogenesis A. actinomycetemcomitans · Capnocytophaga sp. · F. nucleatum · P. gingivalis · P. intermedia · T. forsythia · T. denticola Pathologic entities Calculus · Edentulism · Fremitus · Furcation defect · Gingival enlargement · Gingival pocket · Gingivitis · Horizontal bony defect · Linear gingival erythema · Occlusal trauma · Periodontal pocket · Periodontal disease · Periodontitis · Plaque · Recession · Vertical bony defect M: TTH anat/devp/phys noco/cong/jaws/tumr, epon, injr dent, proc (endo, orth, pros)

Oral pathology: Stomatognathic disease (K06, K11–K14, 523, 527–529) Vestibule of mouth Lip Cheilitis (Angular, Actinic) · Herpes labialis · Plasma cell cheilitis · Cheilitis granulomatosa · Chapped lips Cheilitis exfoliativa · Cheilitis glandularis · Allergic contact cheilitis Drug-induced ulcer of the lip · Epidermization of the lip Cheek Morsicatio buccarum Oral cavity proper Hard, soft, and periapical tissues gingival disease: Gingivitis (Desquamative gingivitis), Pericoronitis, Necrotizing ulcerative gingivitis, Noma, Epulis · Acute necrotizing ulcerative gingivitis Periodontitis  · Ulcer Salivary glands Sialadenitis (Parotitis) · Benign lymphoepithelial lesion · Necrotizing sialometaplasia · Ranula · Sialolithiasis · Mucocele of salivary gland saliva: Drooling/sialorrhea · Xerostomia Tongue Glossitis (Geographic tongue) · Fissured tongue · Glossodynia · Black hairy tongue · Strawberry tongue · Caviar tongue · Median rhomboid glossitis · Osseous choristoma of the tongue · Smooth tongue General Stomatitis: Aphthous ulcer (Major aphthous ulcer) · Herpetic stomatitis Velopharyngeal inadequacy oral mucosa: Erythroplakia · Leukoplakia (Hairy leukoplakia) · White sponge nevus To be grouped from derm Acquired dyskeratotic leukoplakia · Angina bullosa haemorrhagica · Behçet syndrome · Cutaneous sinus of dental origin · Cyclic neutropenia · Epulis fissuratum · Eruptive lingual papillitis · Melanocytic oral lesion · Melkersson–Rosenthal syndrome · Mucosal lichen planus · Oral Crohn's disease · Oral florid papillomatosis · Oral melanosis · Plasmoacanthoma · Proliferative verrucous leukoplakia · Pyogenic granuloma · Pyostomatitis vegetans · Recurrent intraoral herpes simplex infection · Stomatitis nicotina · Trumpeter's wart · Vestibular papillomatosis M: MOU anat/devp noco/cofa(c)/cogi/tumr, sysi proc (peri), drug (A1)