Following a successful induction of remission, maintenance therapy might be given in some cases, for example when there is a high risk of relapse or in patients with organ-threatening manifestations. Common maintenancy therapy is prednisolone 2.5–5 mg per day, or use of a steroid-sparing agent instead.

In untreated patients with active disease, the recommended first-line agent for induction of remission is glucocorticoids unless contraindications exist. Glucocorticoids characteristically result in a rapid and often dramatic improvement in clinical features and often a resolution of radiographic features. However, where advanced fibrotic lesions have resulted in irreversible damage, the response to glucocorticoids and other current treatment options may be poor or even absent.

Although not validated yet in clinical trials, the common induction regime is prednisolone 30–40 mg per day for 2–4 weeks, then gradually tapered over 3 to 6 months. Recurrences during or after tapering of glucocorticoids are frequent however. Steroid-sparing immunosuppressive agents might be considered, depending on local availability of these drugs, for use in combination with glucocorticoids from the start of treatment. Steroid-sparing agents that have been used include rituximab, azathioprine, methotrexate, and cyclophosphamide, although trials are needed to ascertain the effectiveness of each drug in IgG4-RD.

Lupus is a condition with no known cure. Lupus cerebritis however is treated by suppressing the autoimmune activity.

When it is caused by infections, treatment consists of medication that will primarily cure the infection. For inflammation, steroids can be used to bring down the swelling. If the swelling appears to have increased to a dangerous level, surgery may be needed to relieve pressure on the brain. The formation of an abscess also calls for surgery as it will be necessary to drain the abscess.

The standard treatment for GPA is cyclophosphamide and high dose corticosteroids for remission induction and less toxic immunosuppressants like azathioprine, leflunomide, methotrexate or mycophenolate mofetil. Trimethoprim/sulfamethoxazole may also help prevent relapse. Rituximab may be substituted for cyclophosphamide in inducing remission.

A systematic review of 84 trials examined the evidence for various treatments in GPA. Many trials include data on pooled groups of people with GPA and microscopic polyangiitis. In this review, cases are divided between localised disease, non-organ threatening, generalized organ-threatening disease and severe kidney vasculitis and immediately life-threatening disease.

- In generalised non-organ-threatening disease, remission can be induced with methotrexate and steroids, where the steroid dose is reduced after a remission has been achieved and methotrexate used as maintenance.

- In case of organ-threatening disease, pulsed intravenous cyclophosphamide with steroids is recommended. Once remission has been achieved, azathioprine and steroids can be used to maintain remission.

- In severe kidney vasculitis, the same regimen is used but with the addition of plasma exchange.

- In pulmonary haemorrhage, high doses of cyclophosphamide with pulsed methylprednisolone may be used, or alternatively CYC, steroids, and plasma exchange.

Therapy for GPA and MPA has two main components: induction of remission with initial immunosuppressive therapy, and maintenance of remission with immunosuppressive therapy for a variable period to prevent relapse.

The mainstay of treatment for granulomatosis with polyangiitis (GPA) is a combination of corticosteroids and cytotoxic agents.

- Medications

- Side effect treatments

- Plasma exchange

- Kidney transplant

Exercise is a promising mechanism of prevention and treatment for various diseases characterized by neuroinflammation. Aerobic exercise is used widely to reduce inflammation in the periphery. Exercise has been shown to decreases proliferation of microglia in the brain, decrease hippocampal expression of immune-related genes, and reduce expression of inflammatory cytokines such as TNF-α.

Treatment options include antibiotic therapy (not a permanent solution), endodontic (root canal) therapy, or extraction.

Pancreatic enzyme replacement is often effective in treating the malabsorption and steatorrhea associated with chronic pancreatitis. Treatment of CP consists of administration of a solution of pancreatic enzymes with meals. Some patients do have pain reduction with enzyme replacement and since they are relatively safe, giving enzyme replacement to a chronic pancreatitis patient is an acceptable step in treatment for most patients. Treatment may be more likely to be successful in those without involvement of large ducts and those with idiopathic pancreatitis.

The different treatment options for management of chronic pancreatitis are medical measures, therapeutic endoscopy and surgery. Treatment is directed, when possible, to the underlying cause, and to relieve pain and malabsorption. Insulin dependent diabetes mellitus may occur and need long term insulin therapy. The abdominal pain can be very severe and require high doses of analgesics, sometimes including opiates. Alcohol cessation and dietary modifications (low-fat diet) are important to manage pain and slow the calcific process. Antioxidants may help but it is unclear if the benefits are meaningful.

Treatment is often started without confirmation of infection because of the serious complications that may result from delayed treatment. Treatment depends on the infectious agent and generally involves the use of antibiotic therapy. If there is no improvement within two to three days, the patient is typically advised to seek further medical attention. Hospitalization sometimes becomes necessary if there are other complications. Treating sexual partners for possible STIs can help in treatment and prevention.

For women with PID of mild to moderate severity, parenteral and oral therapies appear to be effective. It does not matter to their short- or long-term outcome whether antibiotics are administered to them as inpatients or outpatients. Typical regimens include cefoxitin or cefotetan plus doxycycline, and clindamycin plus gentamicin. An alternative parenteral regimen is ampicillin/sulbactam plus doxycycline. Erythromycin-based medications can also be used. Another alternative is to use a parenteral regimen with ceftriaxone or cefoxitin plus doxycycline. Clinical experience guides decisions regarding transition from parenteral to oral therapy, which usually can be initiated within 24–48 hours of clinical improvement.

Because neuroinflammation has been associated with a variety of neurodegenerative diseases, there is increasing interest to determine whether reducing inflammation will reverse neurodegeneration. Inhibiting inflammatory cytokines, such as IL-1β, decreases neuronal loss seen in neurodegenerative diseases. Current treatments for multiple sclerosis include interferon-B, Glatiramer actetate, and Mitoxantrone, which function by reducing or inhibiting T Cell activation, but have the side effect of systemic immunosuppression In Alzheimer's disease, the use of non-steroidal anti-inflammatory drugs decreases the risk of developing the disease. Current treatments for Alzheimer's disease include NSAIDs and glucocorticoids. NSAIDs function by blocking conversion of prostaglandin H2 into other prostaglandins (PGs) and thromboxane (TX). Prostoglandins and thromboxane act as inflammatory mediators and increase microvascular permeability.

Costochondritis may be treated with physical therapy (including ultrasonic, TENS, with or without nerve stimulation) or with medication. Treatment may involve the use of nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen or other pain relief medications (analgesics) such as acetaminophen. Severe cases of costochondritis may call for the use of opioid medications such as hydrocodone or oxycodone, tricyclic antidepressant medications such as amitriptyline for pain from chronic costochondritis, or anti-epileptic drugs such as gabapentin may be used. Oral or injected corticosteroids may be used for cases of costochondritis unresponsive to treatment by NSAIDs; however, this treatment has not been the subject of study by rigorous randomized controlled trials and its practice is currently based on clinical experience. Rest from stressful physical activity is often advised during the recovery period.

Before modern treatments, the 2-year mortality was over 90% and average survival five months. Death usually resulted from uremia or respiratory failure.

With corticosteroids and cyclophosphamide, 5-year survival is over 80%. Long-term complications are common (86%), mainly chronic kidney failure, hearing loss and deafness.

Today, drug toxicity is managed more carefully and long-term remissions are possible. Some patients are able to lead relatively normal lives and remain in remission for 20+ years after treatment.

Bacterial overgrowth is usually treated with a course of antibiotics although whether antibiotics should be a first line treatment is a matter of debate. Some experts recommend probiotics as first line therapy with antibiotics being reserved as a second line treatment for more severe cases of SIBO. Prokinetic drugs are other options but research in humans is limited. A variety of antibiotics, including tetracycline, amoxicillin-clavulanate, fluoroquinolones, metronidazole, neomycin, cephalexin, trimethoprim-sulfamethoxazole, and nitazoxanide have been used; however, the best evidence is for the use of rifaximin.

A course of one week of antibiotics is usually sufficient to treat the condition. However, if the condition recurs, antibiotics can be given in a cyclical fashion in order to prevent tolerance. For example, antibiotics may be given for a week, followed by three weeks off antibiotics, followed by another week of treatment. Alternatively, the choice of antibiotic used can be cycled.

The condition that predisposed the patient to bacterial overgrowth should also be treated. For example, if the bacterial overgrowth is caused by chronic pancreatitis, the patient should be treated with coated pancreatic enzyme supplements.

Probiotics are bacterial preparations that alter the bacterial flora in the bowel to cause a beneficial effect. Animal research has demonstrated that probiotics have barrier enhancing, antibacterial, immune modulating and anti-inflammatory effects which may have a positive effect in the management of SIBO in humans. "Lactobacillus casei" has been found to be effective in improving breath hydrogen scores after 6 weeks of treatment presumably by suppressing levels of a small intestinal bacterial overgrowth of fermenting bacteria. The multi-strain preparation VSL#3 was found to be effective in suppressing SIBO. "Lactobacillus plantarum", "Lactobacillus acidophilus", and "Lactobacillus casei" have all demonstrated effectiveness in the treatment and management of SIBO. Conversely, "Lactobacillus fermentum" and "Saccharomyces boulardii" have been found to be ineffective. A combination of "Lactobacillus plantarum" and "Lactobacillus rhamnosus" has been found to be effective in suppressing bacterial overgrowth of abnormal gas producing organisms in the small intestine.

Probiotics are superior to antibiotics in the treatment of SIBO. A combination of probiotic strains has been found to produce better results than therapy with the antibiotic drug metronidazole and probiotics have been found to be effective in treating and preventing secondary lactase deficiency and small intestinal bacteria overgrowth in individuals suffering from post-infectious irritable bowel syndrome. Probiotics taken in uncomplicated cases of SIBO can usually result in the individual becoming symptom free. Probiotic therapy may need to be taken continuously to prevent the return of overgrowth of gas producing bacteria. A study by the probiotic yogurt producer Nestlé found that probiotic yogurt may also be effective in treating SIBO with evidence of reduced inflammation after 4 weeks of treatment.

An elemental diet taken for two weeks is an alternative to antibiotics for eliminating SIBO. An elemental diet works via providing nutrition for the individual while depriving the bacteria of a food source. Additional treatment options include the use of prokinetic drugs such as 5-HT4 receptor agonists or motilin agonists to extend the SIBO free period after treatment with an elemental diet or antibiotics. A diet void of certain foods that feed the bacteria can help alleviate the symptoms. For example, if the symptoms are caused by bacterial overgrowth feeding on indigestible carbohydrate rich foods, following a FODMAP restriction diet may help.

Even when the PID infection is cured, effects of the infection may be permanent. This makes early identification essential. Treatment resulting in cure is very important in the prevention of damage to the reproductive system. Formation of scar tissue due to one or episodes of PID can lead to tubal blockage, increasing the risk of the inability to get pregnant and long-term pelvic/abdominal pain. Certain occurrences such as a post pelvic operation, the period of time immediately after childbirth (postpartum), miscarriage or abortion increase the risk of acquiring another infection leading to PID.

Treatment should be sought immediately in order to avoid hospitalization. If not treated, hospitalization for an extended period of time (usually two weeks) is likely. During hospitalization, the patient is tested for signs of system degradation, especially of the skeletal structure and the digestive tract. By this time open sores will develop on the upper torso. Some will be the size of dimes, others will be large enough to stick a couple fingers into. They will crust up, causing cohesion to any fabric the sores touch, which is extremely painful to remove. It is recommended to sleep on one's sides until the cystic condition subsides, in order to avoid any uncomfortable situations. Debridement and steroid therapy is preferred over antibiotics. Recurrent AF is extremely rare. Bone lesions typically resolve with treatment, but residual radiographic changes, such as sclerosis and hyperostosis, may remain. Scarring and fibrosis may result from this acute inflammatory process.

The disease activates at the height of puberty, usually at around 13 years of age. Acne fulminans predominantly affects young males aged 13 to 22 years with a history of acne.

Treatment varies. In most cases, the best treatment is to remove the cause of compression by modifying patient behavior, in combination with medical treatment to relieve inflammation and pain. Whatever the cause, typical treatment takes several weeks to months—depending on the degree of nerve damage. Typical treatment options include:

- Active Release Technique (ART) soft tissue treatment

- Wearing looser clothing and suspenders rather than belts

- Weight loss if obesity is present

- Non-steroidal anti-inflammatory drugs (NSAIDs) to reduce inflammatory pain if pain level limits motion and prevents sleep

- Reducing physical activity in relation to pain level. Acute pain may require absolute bed rest

- Deep tissue massage to reduce tension in the gluteal muscles, most commonly the gluteus maximus. The tensor fasciae latae may also be implicated.

The lateral cutaneous nerve of the thigh can occasionally be damaged during laparoscopic hernia repair, or scarring from the operation can lead to meralgia paraesthetica.

For lower pain levels, treatment may involve having the patient:

- Seek appropriate physical therapy, such as stretching and massage, which plays a large role in the management of pain

- Learn to perform inguinal ligament stretching (from a physical therapist or from a YouTube video) which can rapidly relieve symptoms

- Use rest periods to interrupt long periods of standing, walking, cycling, or other aggravating activity

- Lose weight, and exercise to strengthen abdominal muscles

- Wear clothing that is loose at the upper front hip area

- Apply heat, ice, or electrical stimulation

- Take nonsteroidal anti-inflammatory medications for 7–10 days

- Remove hair in affected area (shave)

- Lidocaine patches (must shave area first)

- Titanium dioxide patches to interfere with the electrostatic effect of the nerves on the surface of the skin

Pain may take significant time (weeks) to stop and, in some cases, numbness persists despite treatment. In severe cases, the physician might perform a local nerve block at the inguinal ligament, using a combination of local anaesthetic (lidocaine) and corticosteroids to provide relief that may last several weeks. Pain modifier drugs for neuralgic pain (such as amitriptyline, carbamazepine or gabapentin) may be tried, but are often not as helpful in the majority of patients.

Persistent and severe cases may require surgery to decompress the nerve or, as a last resort, to resect the nerve. The latter treatment leaves permanent numbness in the area.

People with acute pyelonephritis that is accompanied by high fever and leukocytosis are typically admitted to the hospital for intravenous hydration and intravenous antibiotic treatment. Treatment is typically initiated with an intravenous fluoroquinolone, an aminoglycoside, an extended-spectrum penicillin or cephalosporin, or a carbapenem. Combination antibiotic therapy is often used in such situations. The treatment regimen is selected based on local resistance data and the susceptibility profile of the specific infecting organism(s).

During the course of antibiotic treatment, serial white blood cell count and temperature are closely monitored. Typically, the intravenous antibiotics are continued until the person has no fever for at least 24 to 48 hours, then equivalent antibiotics by mouth can be given for a total of 2–week duration of treatment. Intravenous fluids may be administered to compensate for the reduced oral intake, insensible losses (due to the raised temperature) and vasodilation and to optimize urine output. Percutaneous nephrostomy or ureteral stent placement may be indicated to relieve obstruction caused by a stone. Children with acute pyelonephritis can be treated effectively with oral antibiotics (cefixime, ceftibuten and amoxicillin/clavulanic acid) or with short courses (2 to 4 days) of intravenous therapy followed by oral therapy. If intravenous therapy is chosen, single daily dosing with aminoglycosides is safe and effective.

Treatment of xanthogranulomatous pyelonephritis involves antibiotics as well as surgery. Removal of the kidney is the best surgical treatment in the overwhelming majority of cases, although polar resection (partial nephrectomy) has been effective for some people with localized disease. Watchful waiting with serial imaging may be appropriate in rare circumstances.

In people suspected of having pyelonephritis, a urine culture and antibiotic sensitivity test is performed, so therapy can eventually be tailored on the basis of the infecting organism. As most cases of pyelonephritis are due to bacterial infections, antibiotics are the mainstay of treatment. The choice of antibiotic depends on the species and antibiotic sensitivity profile of the infecting organism, and may include fluoroquinolones, cephalosporins, aminoglycosides, or trimethoprim/sulfamethoxazole, either alone or in combination.

Conservative management of minor cases involves icing, a firm compression bandage, and avoidance of the aggravating activity. This can also be augmented with oral or topical anti-inflammatory medications such as NSAIDs. Elbow padding can also be used for symptomatic relief. Treatment for more severe cases may include the excess bursa fluid with a syringe (draining of the bursa), or injecting into the bursa a hydrocortisone type medication which is aimed at relieving the inflammation and preventing further accumulation of fluid.

In case of infection, the bursitis should be treated with an antibiotic.

There is no universally accepted treatment strategy, but, generally, treatments aim to prevent movement of the segments of the involved tooth so they do not move or flex independently during biting and grinding and so the crack is not propagated.

- Stabilization (core buildup) (a composite bonded restoration placed in the tooth or a band is placed around the tooth to minimize flexing)

- Crown restoration (to do the same as above but more permanently and predictably)

- Root Canal therapy (if pain persists after above)

- Extraction

IgG4-related ophthalmic disease (IgG4-ROD) is the recommended term to describe orbital (eye socket) manifestations of the systemic condition IgG4-related disease, which is characterised by infiltration of lymphocytes and plasma cells and subsequent fibrosis in involved structures. It can involve one or more of the orbital structures.

Frequently involved structures include the lacrimal glands, extraocular muscles, infraorbital nerve, supraorbital nerve and eyelids. It has also been speculated that ligneous conjunctivitis may be a manifestation of IgG4-related disease (IgG4-RD).

As is the case with other manifestations of IgG4-related disease, a prompt response to steroid therapy is a characteristic feature of IgG4-ROD in most cases, unless significant fibrosis has already occurred.

Orthotics and corticosteroid injections are widely used conservative treatments for Morton’s neuroma. In addition to traditional orthotic arch supports, a small foam or fabric pad may be positioned under the space between the two affected metatarsals, immediately behind the bone ends. This pad helps to splay the metatarsal bones and create more space for the nerve so as to relieve pressure and irritation. It may however also elicit mild uncomfortable sensations of its own, such as the feeling of having an awkward object under one's foot. Corticosteroid injections can relieve inflammation in some patients and help to end the symptoms. For some patients, however, the inflammation and pain recur after some weeks or months, and corticosteroids can only be used a limited number of times because they cause progressive degeneration of ligamentous and tendinous tissues.

Sclerosing alcohol injections are an increasingly available treatment alternative if the above management approaches fail. Dilute alcohol (4%) is injected directly into the area of the neuroma, causing toxicity to the fibrous nerve tissue. Frequently, treatment must be performed 2–4 times, with 1–3 weeks between interventions. A 60–80% success rate has been achieved in clinical studies, equal to or exceeding the success rate for surgical neurectomy with fewer risks and less significant recovery. If done with more concentrated alcohol under ultrasound guidance, the success rate is considerably higher and fewer repeat procedures are needed.

Radio Frequency Ablation is also used in the treatment of Morton's Neuroma The outcomes appear to be equally or more reliable than alcohol injections especially if the procedure is done under ultrasound guidance.

If such interventions fail, patients are commonly offered surgery known as neurectomy, which involves removing the affected piece of nerve tissue. Postoperative scar tissue formation (known as stump neuroma) can occur in approximately 20%-30% of cases, causing a return of neuroma symptoms. Neurectomy can be performed using one of two general methods. Making the incision from the dorsal side (the top of the foot) is the more common method but requires cutting the deep transverse metatarsal ligament that connects the 3rd and 4th metatarsals in order to access the nerve beneath it. This results in exaggerated postoperative splaying of the 3rd and 4th digits (toes) due to the loss of the supporting ligamentous structure. This has aesthetic concerns for some patients and possible though unquantified long-term implications for foot structure and health. Alternatively, making the incision from the ventral side (the sole of the foot) allows more direct access to the affected nerve without cutting other structures. However, this approach requires a greater post-operative recovery time where the patient must avoid weight bearing on the affected foot because the ventral aspect of the foot is more highly enervated and impacted by pressure when standing. It also has an increased risk that scar tissue will form in a location that causes ongoing pain.

Cryogenic neuroablation is a lesser known alternative to neurectomy surgery. Cryogenic neuroablation (also known as cryo injection therapy, cryoneurolysis, cryosurgery or cryoablation) is a term that is used to describe the destruction of axons to prevent them from carrying painful impulses. This is accomplished by making a small incision (~3 mm) and inserting a cryoneedle that applies extremely low temperatures of between −50 °C to −70 °C to the nerve/neuroma. This results in degeneration of the intracellular elements, axons, and myelin sheath (which houses the neuroma) with wallerian degeneration. The epineurium and perineurium remain intact, thus preventing the formation of stump neuroma. The preservation of these structures differentiates cryogenic neuroablation from surgical excision and neurolytic agents such as alcohol. An initial study showed that cryo neuroablation is initially equal in effectiveness to surgery but does not have the risk of stump neuroma formation.

Recently, an increasing number of procedures are being performed at specialist centers which offer a range of procedures to treat Morton's neuroma under ultrasound guidance. Recent studies have shown excellent results for the treatment of Morton's neuroma with ultrasound guided sclerosing alcohol injections, ultrasound guided radiofrequency ablation, and ultrasound guided cryo-ablation.

In approximately half of suspected nail fungus cases there is actually no fungal infection, but only some nail dystrophy. Before beginning oral antifungal therapy the health care provider should confirm a fungal infection. Administration of treatment to persons without an infection is unnecessary health care and causes needless exposure to side effects.

Steroid injections are helpful in the short term (first approximately 4 weeks) however, their long term effectiveness is not known, and quality of evidence for its use remains poor and controversial.

Other, more conservative and non-surgical, treatment options available for the management and treatment of tendinopathy include: rest, ice, massage therapy, eccentric exercise, NSAIDs, ultrasound therapy, LIPUS, electrotherapy, taping, sclerosing injections, blood injection, glyceryl trinitrate patches, and (ESWT) extracorporeal shockwave therapy. Studies with a rat model of fatigue-damaged tendons suggested that delaying exercise until after the initial inflammatory stage of repair could promote remodelling more rapidly. There is insufficient evidence on the routine use of injection therapies (Autologous blood, Platelet-rich plasma, Deproteinised haemodialysate, Aprotinin, Polysulphated glycosaminoglycan, Corticosteroid, Skin derived fibroblasts etc.) for treating Achilles tendinopathy. As of 2014 there was insufficient evidence to support the use of platelet-rich therapies for treating musculoskeletal soft tissue injuries such as ligament, muscle and tendon tears and tendinopathies.

There are several types of treatment for congenital trigger thumb, conservative and surgical.