Healing is prolonged, and usually takes 6–10 weeks. The ulcer heals by secondary intention.

Currently, there is no direct treatment for AEN. Only treatment is for the underlying main diseases or conditions. Appropriate hydration is set. Antacids are also added for further recovery support. Common support drugs of antacids are either H receptor antagonists, and/or a proton pump inhibitor. Sucralfate was used as an option. Parenteral nutrition greatly increased chance of recovery. An esophagectomy can be issued if the disorder is severe enough.

Treatments involve antibiotics that cover for "Pseudomonas aeruginosa". Antipseudomonal penicillins, aminoglycosides, fluoroquinolones, third generation cephalosporins or aztreonam can be given. Usually, the antibiotics are changed according to the culture and sensitivity result. In patients with very low white blood cell counts, Granulocyte-macrophage colony-stimulating factor may be given. Depending on the causal agents, antivirals or antifungals can be added.

Surgery will be needed if there is extensive necrosis not responding to medical treatments.

Treatment is not necessary since the lesion is benign, however the person may have esthetic concerns about the appearance. The condition often resolves rapidly with high dose acyclovir or desiclovir but recurs once this therapy is stopped, or as the underlying immunocompromise worsens. Topical use of podophyllum resin or retinoids has also been reported to produce temporary remission. Antiretroviral drugs such as zidovudine may be effective in producing a significant regression of OHL. Recurrence of the lesion may also signify that highly active antiretroviral therapy (HAART) is becoming ineffective.

Fournier gangrene is a urological emergency requiring intravenous antibiotics and debridement (surgical removal) of necrotic (dead) tissue. In addition to surgery and antibiotics, hyperbaric oxygen therapy (HBOT) may be useful and acts to inhibit the growth of and kill the anaerobic bacteria.

Treatment is cause-related, but also symptomatic if the underlying cause is unknown or not correctable. It is also important to note that most ulcers will heal completely without any intervention. Treatment can range from simply smoothing or removing a local cause of trauma, to addressing underlying factors such as dry mouth or substituting a problem medication. Maintaining good oral hygiene and use of an antiseptic mouthwash or spray (e.g. chlorhexidine) can prevent secondary infection and therefore hasten healing. A topical analgesic (e.g. benzydamine mouthwash) may reduce pain. Topical (gels, creams or inhalers) or systemic steroids may be used to reduce inflammation. An antifungal drug may be used to prevent oral candidiasis developing in those who use prolonged steroids. People with mouth ulcers may prefer to avoid hot or spicy foods, which can increase the pain. Self-inflicted ulceration can be difficult to manage, and psychiatric input may be required in some people.

Treatment should be directed towards the specific underlying cause of the vasculitis. If no underlying cause is found and the vasculitis is truly limited to the skin then treatment is primarily supportive. Such treatment involves measures such as leg elevation, stockings, and topical steroids to relieve itching/burning. If the vasculitis does not self-resolve within 3–4 weeks, more aggressive treatment may be warranted. Oral colchicine or dapsone are often used for this purpose. If rapid control of symptoms is needed, a short course of high-dose oral steroids may be given. Immunosuppressive agents such as methotrexate and azathioprine may be used in truly refractory cases not responsive to colchicine or dapsone.

The main organism associated with ecthyma gangrenosum is "Pseudomonas aeruginosa". However, multi-bacterial cases are reported as well. Prevention measures include practicing proper hygiene, educating the immunocompromised patients for awareness to avoid possible conditions and seek timely medical treatment.

Treatment is usually symptomatic, (i.e., analgesic medications) and also the removal of debris from the socket by irrigation with saline or local anesthetic. Medicated dressings are also commonly placed in the socket; although these will act as a foreign body and prolong healing, they are usually needed due to the severe pain. Hence, the dressings are usually stopped once the pain is lessened. Examples of medicated dressings include antibacterials, topical anesthetics and obtundants, or combinations of all three, e.g., zinc oxide and eugenol impregnated cotton pellets, alvogyl (eugenol, iodoform and butamen), dentalone, bismuth subnitrate and iodoform paste (BIPP) on ribbon gauze and metronidazole and lidocaine ointment. A systematic review of the efficacy of treatments for dry socket concluded that there was not enough evidence to discern the effectiveness of any treatments. People who develop a dry socket typically seek medical/dental advice several times after the dental extraction, where the old dressing is removed, the socket irrigated and a new dressing placed. Curettage of the socket increases the pain and has been discouraged by some.

Surgical debridement (cutting away affected tissue) is the mainstay of treatment for necrotizing fasciitis. Early medical treatment is often presumptive; thus, antibiotics should be started as soon as this condition is suspected. Given the dangerous nature of the disease, a high index of suspicion is needed. Initial treatment often includes a combination of intravenous antibiotics including piperacillin/tazobactam, vancomycin, and clindamycin. Cultures are taken to determine appropriate antibiotic coverage, and antibiotics may be changed when culture results are obtained.

Treatment for necrotizing fasciitis may involve an interdisciplinary care team. For example, in the case of a necrotizing fasciitis involving the head and neck, the team could include otolaryngologists, speech pathologists, intensivists, infectious disease specialists, and plastic surgeons or oral and maxillofacial surgeons. Maintaining strict asepsis during any surgical procedure and regional anaesthesia techniques is vital in preventing the occurrence of the disease.

Antifungals are used for treatment with the specific type and dose depending on the patient's age, immune status, and specifics of the infection. For most adults, the initial treatment is an echinocandin class antifungal (caspofungin, micafungin, or anidulafungin) given intravenously. Fluconazole, amphotericin B, and other antifungals may also be used. Treatment normally continues for two weeks after resolution of signs and symptoms and "Candida" yeasts can no longer can be cultured from blood samples. Some forms of invasive candidiasis, such as infections in the bones, joints, heart, or central nervous system, usually need to be treated for a longer period. Retrospective observational studies suggest that prompt presumptive antifungal therapy (based on symptoms or biomarkers) is effective and can reduce mortality.

If mucormycosis is suspected, amphotericin B therapy should be immediately administered due to the rapid spread and high mortality rate of the disease. Amphotericin B is usually administered for an additional 4–6 weeks after initial therapy begins to ensure eradication of the infection. Isavuconazole was recently FDA approved to treat invasive aspergillosis and invasive mucormycosis.

After administration of either amphotericin B or posaconazole, surgical removal of the "fungus ball" is indicated. The disease must be monitored carefully for any signs of reemergence.

Surgical therapy can be very drastic, and in some cases of disease involving the nasal cavity and the brain, removal of infected brain tissue may be required. In some cases surgery may be disfiguring because it may involve removal of the palate, nasal cavity, or eye structures. Surgery may be extended to more than one operation. It has been hypothesized that hyperbaric oxygen may be beneficial as an adjunctive therapy because higher oxygen pressure increases the ability of neutrophils to kill the organism.

If cause-specific measures are insufficient, soft-tissue graft surgery may be used to create more gingiva. The tissue used may be autologous tissue from another site in the patient's mouth, or it can be freeze-dried tissue products or synthetic membranes. New research is focused on using stem cells to culture the patients' own gums to replace receded gums.

The exact cause of the condition is unknown. There is most evidence to support vascular infarction and ischemic necrosis of salivary gland lobules as a mechanism for the condition. Experimentally, local anaesthetic injections and tying of the arteries is reported to trigger the development of tissue changes similar to NS in lab rats. Factors which are thought to cause this ischemia are listed below, however sometimes there is no evident predisposing factor or initiating event.

- Trauma e.g. during intubation, or surgical procedures

- Local anesthetic injection

- Smoking

- Alcohol

- Diabetes mellitus

- Vascular disease, (e.g. arteriosclerosis)

- Pressure from a dental prosthesis

- Allergy

- Bulimia

- Infection

- Ionizing radiation

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.

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.

In necrotizing fasciitis, aggressive surgical debridement (removal of infected tissue) is always necessary to keep it from spreading and is the only treatment available. Diagnosis is confirmed by visual examination of the tissues and by tissue samples sent for microscopic evaluation.

Amputation of the affected limb(s) may be necessary. Repeat explorations usually need to be done to remove additional necrotic tissue. Typically, this leaves a large open wound, which often requires skin grafting, though necrosis of internal (thoracic and abdominal) viscera such as intestinal tissue is also possible. The associated systemic inflammatory response is usually profound, and most people will require monitoring in an intensive care unit. Because of the extreme nature of many of these wounds and the grafting and debridement that accompanies such a treatment, a burn center's wound clinic, which has staff trained in such wounds, may be utilized.

Treatment is targeted to the underlying cause. However, most vasculitis in general are treated with steroids (e.g. methylprednisolone) because the underlying cause of the vasculitis is due to hyperactive immunological damage. Immunosuppressants such as cyclophosphamide and azathioprine may also be given.

A systematic review of antineutrophil cytoplasmic antibody (ANCA) positive vasculitis identified best treatments depending on whether the goal is to induce remission or maintenance and depending on severity of the vasculitis.

The oral lesion itself is benign and self-limiting, however this may not necessarily be the case for the underlying cause of immunocompromise. For instance, OHL with HIV/AIDS is a predictor of bad prognosis, (i.e. severe immunosuppression and advanced disease).

Treatment for eosinophilic granulomatosis with polyangiitis includes glucocorticoids (such as prednisolone) and other immunosuppressive drugs (such as azathioprine and cyclophosphamide). In many cases, the disease can be put into a type of chemical remission through drug therapy, but the disease is chronic and lifelong.

A systematic review conducted in 2007 indicated all patients should be treated with high-dose steroids, but in patients with a five-factor score of one or higher, cyclophosphamide pulse therapy should be commenced, with 12 pulses leading to fewer relapses than six. Remission can be maintained with a less toxic drug, such as azathioprine or methotrexate.

On December 12, 2017, the FDA approved mepolizumab, the first drug therapy specifically indicated for the treatment of eosinophilic granulomatosis with polyangiitis. Patients taking mepolizumab experienced a "significant improvement" in their symptoms.

There are no prospective randomized controlled trials studying therapies for relapsing polychondritis. Evidence for efficacy of treatments is based on case reports and series of small groups of patients.

For mild cases limited to joint pain or arthritis, oral nonsteroidal anti-inflammatory drugs (NSAIDs) may be used. Other treatments typically involve medications to suppress the immune system. Corticosteroids are frequently used for more serious disease. Steroid-sparing medications such as azathioprine or methotrexate may be used to minimize steroid doses and limit the side effects of steroids. For severe disease cyclophosphamide is often given in addition to high dose intravenous steroids.

Depending on the shape of the gum recession and the levels of bone around the teeth, areas of gum recession can be regenerated with new gum tissue using a variety of gum grafting "periodontal plastic surgery" procedures performed by a specialist in periodontics (a periodontist). These procedures are typically completed under local anesthesia with or without conscious sedation, as the patient prefers. This may involve repositioning of adjacent gum tissue to cover the recession (called a pedicle graft) or use of a free graft of gingival or connective tissue from the roof of the mouth (called a "free gingival graft" or a Subepithelial connective tissue graft). Alternatively, a material called acellular dermal matrix (processed donated human skin allograft) may be used instead of tissue from the patient's own palate.

Preventative antifungal treatment is supported by studies, but only for specific high-risk groups in intensive care units with conditions that put them at high risk for the disease. For example, one group would be patients recovering from abdominal surgery that may have gastrointestinal perforations or anastomotic leakage. Antifungal prophylaxis can reduce the incidence of fungemia by approximately 50%, but has not been shown to improve survival. A major challenge limiting the number of patients receiving prophylaxis to only those that can potentially benefit, thereby avoiding the creation of selective pressure that can lead to the emergence of resistance.

No specific cure is known. Treatment is largely supportive. Nonsteroidal anti-inflammatory drugs (NSAIDs) are indicated for tender lymph nodes and fever, and corticosteroids are useful in severe extranodal or generalized disease.

Symptomatic measures aimed at relieving the distressing local and systemic complaints have been described as the main line of management of KFD. Analgesics, antipyretics, NSAIDs, and corticosteroids have been used. If the clinical course is more severe, with multiple flares of bulky enlarged cervical lymph nodes and fever, then a low-dose corticosteroid treatment has been suggested.

For generations, the disease was treated with an application of the antiseptic gentian violet. Today, topical or oral antibiotics are usually prescribed. Mild cases may be treated with bactericidal ointment, such as mupirocin. In 95% of cases, a single antibiotic course results in resolution in children. It has been advocated that topical disinfectants are not nearly as efficient as antibiotics, and therefore should be avoided.

More severe cases require oral antibiotics, such as dicloxacillin, flucloxacillin, or erythromycin. Alternatively, amoxicillin combined with clavulanate potassium, cephalosporins (first-generation) and many others may also be used as an antibiotic treatment. Alternatives for people who are seriously allergic to penicillin or infections with MRSA include doxycycline, clindamycin, and SMX-TMP. When streptococci alone are the cause, penicillin is the drug of choice.

When the condition presents with ulcers, valacyclovir, an antiviral, may be given in case a viral infection is causing the ulcer.