The lesions are harmless, and no treatment is indicated beyond reassurance, unless the person requests it. The most common and simple treatment is construction of a specially made acrylic prosthesis that covers the biting surfaces of the teeth and protects the cheek, tongue and labial mucosa (an occlusal splint). This is either employed in the short term as a habit breaking intention, or more permanently (e.g. wearing the prosthesis each night during sleep). Psychological intervention is also reported, but does not appear to be beneficial.

Leukoedema is a harmless condition, and no treatment is indicated. People may be alarmed by the appearance and benefit from reassurance.

Surgical removal of the lesion is the first choice of treatment for many clinicians. However, the efficacy of this treatment modality cannot be assessed due to insufficient available evidence. This can be carried out by traditional surgical excision with a scalpel, with lasers, or with eletrocautery or cryotherapy. Often if biopsy demonstrates moderate or severe dysplasia then the decision to excise them is taken more readily. Sometimes white patches are too large to remove completely and instead they are monitored closely. Even if the lesion is completely removed, long term review is still usually indicated since leukoplakia can recur, especially if predisposing factors such as smoking are not stopped.

Many different topical and systemic medications have been studied, including anti-inflammatories, antimycotics (target Candida species), carotenoids (precursors to vitamin A, e.g. beta carotene), retinoids (drugs similar to vitamin A), and cytotoxics, but none have evidence that they prevent malignant transformation in an area of leukoplakia.Vitamins C and E have also been studied with regards a therapy for leukoplakia. Some of this research is carried out based upon the hypothesis that antioxidant nutrients, vitamins and cell growth suppressor proteins (e.g. p53) are antagonistic to oncogenesis. High doses of retinoids may cause toxic effects. Other treatments that have been studied include photodynamic therapy.

Apart from stopping the habit, no other treatment is indicated. Long term follow-up is usually carried out. Some recommend biopsy if the lesions persists more than 6 weeks after giving up smokeless tobacco use, or if the lesion undergoes a change in appearance (e.g. ulceration, thickening, color changes, especially to speckled white and red or entirely red). Surgical excision may be carried out if the lesion does not resolve.

Reassurance that the condition is benign, elimination of precipitating factors and improving oral hygiene are considered initial management for symptomatic OLP, and these measures are reported to be useful. Treatment usually involves topical corticosteroids (such as betamethasone, clobetasol, dexamethasone, and triamcinolone) and analgesics, or if these are ineffective and the condition is severe, the systemic corticosteroids may be used. Calcineurin inhibitors (such as pimecrolimus, tacrolimus or cyclosporin) are sometimes used.

Many different treatments have been reported for cutaneous lichen planus, however there is a general lack of evidence of efficacy for any treatment. Treatments tend to be prolonged, partially effective and disappointing. The mainstay of localized skin lesions is topical steroids. Additional treatments include retinoids, such as acitretin, or sulfasalazine. Narrow band UVB phototherapy or systemic PUVA therapy are known treatment modalities for generalized disease.

Many different medications have been used to treat bruxism, including benzodiazepines, anticonvulsants, beta blockers, dopamine agents, antidepressants, muscle relaxants, and others. However, there is little, if any, evidence for their respective and comparative efficacies with each other and when compared to a placebo. A systematic review is underway to investigate the evidence for drug treatments in sleep bruxism.

Specific drugs that have been studied in sleep bruxism are clonazepam, levodopa, amitriptyline, bromocriptine, pergolide, clonidine, propranolol, and l-tryptophan, with some showing no effect and others appear to have promising initial results; however, it has been suggested that further safety testing is required before any evidence-based clinical recommendations can be made. When bruxism is related to the use of selective serotonin reuptake inhibitors in depression, adding buspirone has been reported to resolve the side effect. Tricyclic antidepressants have also been suggested to be preferable to selective serotonin reuptake inhibitors in people with bruxism, and may help with the pain.

Botulinum toxin (Botox) is used as a treatment for bruxism, however there is only one randomized control trial which has reported that Botox reduces the myofascial pain symptoms. This scientific study was based on thirty people with bruxism who received Botox injections into the muscles of mastication and a control group of people with bruxism who received placebo injections. Normally multiple trials with larger cohorts are required to make any firm statement about the efficacy of a treatment. In 2013, a further randomized control trial investigating Botox in bruxism started. There is also little information available about the safety and long term followup of this treatment for bruxism.

Botulinum toxin causes muscle paralysis/atrophy by inhibition of acetylcholine release at neuromuscular junctions. Botox injections are used in bruxism on the theory that a dilute solution of the toxin will partially paralyze the muscles and lessen their ability to forcefully clench and grind the jaw, while aiming to retain enough muscular function to enable normal activities such as talking and eating. This treatment typically involves five or six injections into the masseter and temporalis muscles, and less often into the lateral pterygoids (given the possible risk of decreasing the ability to swallow) taking a few minutes per side. The effects may be noticeable by the next day, and they may last for about three months. Occasionally, adverse effects may occur, such as bruising, but this is quite rare. The dose of toxin used depends upon the person, and a higher dose may be needed in people with stronger muscles of mastication. With the temporary and partial muscle paralysis, atrophy of disuse may occur, meaning that the future required dose may be smaller or the length of time the effects last may be increased.

Medication is the main method of managing pain in TMD, mostly because there is little if any evidence of the effectiveness of surgical or dental interventions. Many drugs have been used to treat TMD pain, such as analgesics (pain killers), benzodiazepines (e.g. clonazepam, prazepam, diazepam), anticonvulsants (e.g. gabapentin), muscle relaxants (e.g. cyclobenzaprine), and others. Analgesics that have been studied in TMD include non-steroidal anti-inflammatory drugs (e.g. piroxicam, diclofenac, naproxen) and cyclo-oxygenase-2 inhibitors (e.g. celecoxib). Topical methyl salicylate and topical capsaicin have also been used. Other drugs that have been described for use in TMD include glucosamine hydrochloride/chondroitin sulphate and propranolol. Despite many randomized control trials being conducted on these commonly used medications for TMD a systematic review carried out in 2010 concluded that there was insufficient evidence to support or not to support the use of these drugs in TMD. Low-doses of anti-muscarinic tricyclic antidepressants such as amitriptyline, or nortriptyline have also been described. In a subset of people with TMD who are not helped by either noninvasive and invasive treatments, long term use of opiate analgesics has been suggested, although these drugs carry a risk of drug dependence and other side effects. Examples include morphine, fentanyl, oxycodone, tramadol, hydrocodone, and methadone.

Botulinum toxin solution ("Botox") is sometimes used to treat TMD. Injection of botox into the lateral pterygoid muscle has been investigated in multiple randomized control trials, and there is evidence that it is of benefit in TMD. It is theorized that spasm of lateral pterygoid causes anterior disc displacement. Botulinum toxin causes temporary muscular paralysis by inhibiting acetylcholine release at the neuromuscular junction. The effects usually last for a period of months before they wear off. Complications include the creation of a "fixed" expression due to diffusion of the solution and subsequent involvement of the muscles of facial expression, which lasts until the effects of the botox wear off. Injections of local anesthetic, sometimes combined with steroids, into the muscles (e.g. the temoralis muscle or its tendon) are also sometimes used. Local anesthetics may provide temporary pain relief, and steroids inhibit pro-inflammatory cytokines. Steroids and other medications are sometimes injected directly into the joint (See Intra-articular injections).

Morsicatio buccarum (also termed chronic cheek biting and chronic cheek chewing) is a condition characterized by chronic irritation or injury to the buccal mucosa (the lining of the inside of the cheek within the mouth), caused by repetitive chewing, biting or nibbling.

Excoriation disorder, and trichotillomania have been treated with inositol and N-acetylcysteine.

TMD can be difficult to manage, and since the disorder transcends the boundaries between several health-care disciplines — in particular, dentistry and neurology, the treatment may often involve multiple approaches and be multidisciplinary. Most who are involved in treating and, researching TMD now agree that any treatment carried out should not permanently alter the jaw or teeth, and should be reversible. To avoid permanent change, over-the-counter or prescription pain medications may be prescribed.

Treatment can include behavior modification therapy, medication, and family therapy. The evidence base criteria for BFRBs is strict and methodical. Individual behavioral therapy has been shown as a "probably effective" evidence-based therapy to help with thumb sucking, and possibly nail biting. Cognitive behavioral therapy was cited as experimental evidence based therapy to treat trichotillomania and nail biting. Another form of treatment that focuses on mindfulness, stimuli and rewards has proven effective in some people. However, no treatment was deemed well-established to treat any form of BFRBs.

Usually this lesion is reversible if the tobacco habit is stopped completely, even after many years of use. In one report, 98% of lesions disappeared within 2 weeks of stopping tobacco use. The risk of the lesion developing into oral cancer (generally squamous cell carcinoma and its variant verrucous carcinoma) is relatively low. Indeed, veruccous carcinoma is sometimes term snuff dipper's cancer. In most reported cases, malignant transformation has occurring in individuals with a very long history of chewing tobacco or who use dry snuff.

Smokeless tobacco use is also accompanied by increased risk of other oral conditions such as dental caries (tooth decay), periodontitis (gum disease), attrition (tooth wear) and staining.

Leukoedema (also spelled leucoedema) is a blue, grey or white appearance of mucosae, particularly the buccal mucosa (the inside of the cheeks); it may also occur on the mucosa of the larynx or vagina. It is a harmless and very common condition. Because it is so common, it has been argued that it may in fact represent a variation of the normal appearance rather than a disease, but empirical evidence suggests that leukoedema is an acquired condition caused by local irritation. It is found more commonly in black skinned people and tobacco users. The term is derived from the Greek words λευκός "leukós", "white" and οἴδημα "oídēma", "swelling".

Crenated tongue (also called scalloped tongue, pie crust tongue, lingua indentata, or crenulated tongue) is a descriptive term for the appearance of the tongue when there are indentations along the lateral borders (the sides), as the result of compression of the tongue against the adjacent teeth.

The oral mucosa in the area of crenation is usually of normal color, but there may be erythema (redness) if exposed to a high degree of friction or pressure. Crenated tongue is usually asymptomatic and harmless.

It is not a disease as such, but usually results from habits where the tongue is pressed against the lingual surfaces (the side facing the tongue) of the dental arches, or from any cause of macroglossia (enlarged tongue), which in itself has many causes such as Down syndrome.

Where crenation is caused by parafunctional habits, there may also be associated bruxism, linea alba, or morsicatio buccarum.

In traditional Chinese medicine, scalloping of the tongue is said to indicate qi vacuity. In some homeopathic sources, scalloping of the tongue is said to be indicative of high blood pressure.

Many conditions affect the human integumentary system—the organ system covering the entire surface of the body and composed of skin, hair, nails, and related muscle and glands. The major function of this system is as a barrier against the external environment. The skin weighs an average of four kilograms, covers an area of two square meters, and is made of three distinct layers: the epidermis, dermis, and subcutaneous tissue. The two main types of human skin are: glabrous skin, the hairless skin on the palms and soles (also referred to as the "palmoplantar" surfaces), and hair-bearing skin. Within the latter type, the hairs occur in structures called pilosebaceous units, each with hair follicle, sebaceous gland, and associated arrector pili muscle. In the embryo, the epidermis, hair, and glands form from the ectoderm, which is chemically influenced by the underlying mesoderm that forms the dermis and subcutaneous tissues.

The epidermis is the most superficial layer of skin, a squamous epithelium with several strata: the stratum corneum, stratum lucidum, stratum granulosum, stratum spinosum, and stratum basale. Nourishment is provided to these layers by diffusion from the dermis, since the epidermis is without direct blood supply. The epidermis contains four cell types: keratinocytes, melanocytes, Langerhans cells, and Merkel cells. Of these, keratinocytes are the major component, constituting roughly 95 percent of the epidermis. This stratified squamous epithelium is maintained by cell division within the stratum basale, in which differentiating cells slowly displace outwards through the stratum spinosum to the stratum corneum, where cells are continually shed from the surface. In normal skin, the rate of production equals the rate of loss; about two weeks are needed for a cell to migrate from the basal cell layer to the top of the granular cell layer, and an additional two weeks to cross the stratum corneum.

The dermis is the layer of skin between the epidermis and subcutaneous tissue, and comprises two sections, the papillary dermis and the reticular dermis. The superficial papillary dermis with the overlying rete ridges of the epidermis, between which the two layers interact through the basement membrane zone. Structural components of the dermis are collagen, elastic fibers, and ground substance. Within these components are the pilosebaceous units, arrector pili muscles, and the eccrine and apocrine glands. The dermis contains two vascular networks that run parallel to the skin surface—one superficial and one deep plexus—which are connected by vertical communicating vessels. The function of blood vessels within the dermis is fourfold: to supply nutrition, to regulate temperature, to modulate inflammation, and to participate in wound healing.

The subcutaneous tissue is a layer of fat between the dermis and underlying fascia. This tissue may be further divided into two components, the actual fatty layer, or panniculus adiposus, and a deeper vestigial layer of muscle, the panniculus carnosus. The main cellular component of this tissue is the adipocyte, or fat cell. The structure of this tissue is composed of septal (i.e. linear strands) and lobular compartments, which differ in microscopic appearance. Functionally, the subcutaneous fat insulates the body, absorbs trauma, and serves as a reserve energy source.

Conditions of the human integumentary system constitute a broad spectrum of diseases, also known as dermatoses, as well as many nonpathologic states (like, in certain circumstances, melanonychia and racquet nails). While only a small number of skin diseases account for most visits to the physician, thousands of skin conditions have been described. Classification of these conditions often presents many nosological challenges, since underlying etiologies and pathogenetics are often not known. Therefore, most current textbooks present a classification based on location (for example, conditions of the mucous membrane), morphology (chronic blistering conditions), etiology (skin conditions resulting from physical factors), and so on. Clinically, the diagnosis of any particular skin condition is made by gathering pertinent information regarding the presenting skin lesion(s), including the location (such as arms, head, legs), symptoms (pruritus, pain), duration (acute or chronic), arrangement (solitary, generalized, annular, linear), morphology (macules, papules, vesicles), and color (red, blue, brown, black, white, yellow). Diagnosis of many conditions often also requires a skin biopsy which yields histologic information that can be correlated with the clinical presentation and any laboratory data.

Contact dermatitis is caused by certain substances coming in contact with the skin.

- Abietic acid dermatitis

- Acid-induced

- Acrylic monomer dermatitis

- Adhesive dermatitis

- African blackwood dermatitis

- Airbag dermatitis (airbag burn)

- Alkali-induced

- Allergic

- Antifungal agent-induced

- Antimicrobial agent-induced

- Arsenic dermatitis

- Artificial nail-induced

- Axillary antiperspirant-induced

- Axillary deodorant-induced

- Baboon syndrome

- Black dermatographism

- Bleaching cream-induced

- Capsaisin-induced

- Chemical burn

- Chloracne

- Chrome dermatitis

- Clothing-induced

- Cobalt dermatitis

- Contact stomatitis (contact lichenoid reaction, lichenoid amalgam reaction, oral mucosal cinnamon reaction)

- Contact urticaria

- Corticosteroid-induced

- Cosmetic dermatitis

- Cosmetic intolerance syndrome

- Dentifrice-induced

- Dermatitis from metals and metal salts

- Dust-induced

- Epoxy resin dermatitis

- Ethylenediamine-induced

- Eye makeup-induced

- Fiberglass dermatitis

- Flower-induced

- Formaldehyde-induced

- Formaldehyde-releasing agent-induced

- Fragrance-induced

- Gold dermatitis

- Hair bleach-induced

- Hair dye-induced

- Hair lotion-induced

- Hair spray-induced

- Hair straightener-induced

- Hair tonic-induced

- Houseplant-induced

- Hydrocarbon-induced

- Irritant folliculitis

- Lacquer dermatitis (lacquer sensitivity)

- Lanolin-induced

- Lipstick-induced

- Local anesthetic-induced

- Makassar ebony dermatitis

- Marine plant-induced

- Mechanical irritant dermatitis

- Mercury dermatitis

- Mouthwash-induced

- Nail lacquer-induced

- Nail polish remover-induced

- Nickel dermatitis

- Occupation-induced

- p-Chloro-meta-xylenol-induced

- Paraben-induced

- Paraphenylenediamine dermatitis

- Permanent wave preparation-induced

- Phenothiazine drug-induced

- Photoallergic

- Photoirritant

- Plant derivative-induced

- Pollen-induced

- Polyester resin dermatitis

- Propylene glycol-induced

- Protein contact dermatitis

- Quaternium-15 hypersensitivity

- Reed dermatitis

- Rosewood dermatitis

- Rosin dermatitis

- Rubber dermatitis

- Seed-induced

- Shoe dermatitis

- Solvent-induced

- Sorbic acid-induced

- Subjective irritant contact dermatitis (sensory irritant contact dermatitis)

- Sunscreen-induced

- Systemic contact dermatitis

- Tear gas dermatitis

- Textile dermatitis

- Traumatic irritant contact dermatitis

- Tree-associated plant-induced

- Tree-induced

- Tulip fingers

- Urshiol-induced

- Vegetable-induced