There have been attempts to control the inflammation using drugs that work in other conditions where inflammation is a problem. The most successful of these are steroids, but they have side effects when used long term. Other medications, including methotrexate, colchicine and canakinumab, have been tried with some success. Otherwise, the treatment is supportive, or aimed solely at controlling symptoms and maximizing function.

Most patients suffering from KTS have epilepsy that is resistant to anti-epileptic agents. Some patients showed a partial response to treatment, but very few were able to stop their epilepsy through treatment. One case was responsive to treatment using Phenobartbital and vigabatrin which are both anti-epileptic agents. Spasticity can be treated with baclofen, but not all patients are responsive to the treatment.

Since interleukin 1β plays a central role in the pathogenesis of the disease, therapy typically targets this cytokine in the form of monoclonal antibodies (such as canakinumab), binding proteins/traps (such as rilonacept), or interleukin 1 receptor antagonists (such as anakinra). These therapies are generally effective in alleviating symptoms and substantially reducing levels of inflammatory indices. Case reports suggest that thalidomide and the anti-IL-6 receptor antibody tocilizumab may also be effective.

Overall, the prognosis for patients with NOMID is not good, though many (80%) live into adulthood, and a few appear to do relatively well. They are at risk for leukemia, infections, and some develop deposits of protein aggregated called amyloid, which can lead to kidney failure and other problems. The neurologic problems are most troubling. The finding that other diseases are related and a better understanding of where the disease comes from may lead to more effective treatments.

The most obvious, and often important part of treatment, is avoiding exposure to sunlight. This includes wearing protective clothing and using sunscreen (physical and chemical). Keratosis can also be treated using cryotherapy or fluorouracil. Theoretically, the condition could be completely corrected if functionally intact (non-mutated) endonuclease genes could be inserted into every cell into the body, and the most promising method to do this would be crispr. However, every cell in the body would have to be penetrated for a total cure, because the skin does not protect against other forms of radiation, like x-rays, even at low quantities harmless for those without xeroderma pigmentosa.

Donnai–Barrow syndrome is a genetic disorder first described by Dian Donnai and Margaret Barrow in 1993. It is associated with "LRP2". It is an inherited (genetic) disorder that affects many parts of the body.

There is no real treatment for Felty's syndrome, rather the best method in management of the disease is to control the underlying rheumatoid arthritis. Immunosuppressive therapy for RA often improves granulocytopenia and splenomegaly; this finding reflects the fact that Felty's syndrome is an immune-mediated disease. A major challenge in treating FS is recurring infection caused by neutropenia. Therefore, in order to decide upon and begin treatment, the cause and relationship of neutropenia with the overall condition must be well understood. Most of the traditional medications used to treat RA have been used in the treatment of Felty's syndrome. No well-conducted, randomized, controlled trials support the use of any single agent. Most reports on treatment regimens involve small numbers of patients.

Splenectomy may improve neutropenia in severe disease.

Use of rituximab and leflunomide have been proposed.

Use of gold therapy has also been described.

Prognosis is dependent on the severity of symptoms and the patient's overall health.

Adult-onset Still's disease is treated with anti-inflammatory drugs. Steroids such as prednisone are used to treat severe symptoms of Still's. Other commonly used medications include hydroxychloroquine, penicillamine, azathioprine, methotrexate, etanercept, anakinra, cyclophosphamide, adalimumab, rituximab, and infliximab.

Newer drugs target interleukin-1 (IL-1), particularly IL-1β. A randomized, multicenter trial reported better outcomes in a group of 12 patients treated with anakinra than in a group of 10 patients taking other disease-modifying antirheumatic drugs. Other anti-IL1β drugs are being developed, including canakinumab and rilonacept.

The condition "juvenile-onset Still's disease" is now usually grouped under juvenile rheumatoid arthritis. However, there is some evidence that the two conditions are closely related.

Kohlschütter-Tönz syndrome (KTS), also called Amelo-cerebro-hypohidrotic syndrome is a rare inherited syndrome characterized by epilepsy, dementia, intellectual disability, and yellow teeth caused by amelogenesis imperfecta (abnormal formation of tooth enamel). It is a type A ectodermal dysplasia.

It is autosomal recessive and symptoms appear in early childhood. The syndrome was first described in 1974 by Alfried Kohlschütter and colleagues. Only 24 affected individuals are known as of 2012. The disease has not been connected to any other known epileptic syndromes. Some but not all cases are associated with mutations in a gene called ROGDI. Another gene that has been associated with this condition is the SCL13A5 gene Diagnoses of this syndrome have occurred in Switzerland, Sicily, the Northern Israel Druze community as well as some other parts of Western Europe.

No treatment has been found to be routinely effective. NSAIDs and COX-2 inhibitors are not generally helpful other than for general pain relief. They do not seem to help reduce effusions or prevent their occurrence. Low-dose colchicine (and some other ‘anti-rheumatic’ therapies e.g. hydroxychloroquine) have been used with some success. (Use of methotrexate and intramuscular gold have not been reported in the literature). More aggressive treatments such as synovectomy, achieved using intra-articular agents (chemical or radioactive) can provide good results, with efficacy reported for at least 1 year.

Reducing acute joint swelling:

Arthrocentesis (or drainage of joint) may be useful to relieve joint swelling and improve range of motion. Local steroid injections can also reduce fluid accumulation short-term, but do not prevent onset of episodes. These treatments provide temporary relief only. Bed rest, ice packs splints and exercise are ineffective.

A single case report of a patient with treatment-refractory IH describes the use of anakinra, an interleukin 1 receptor antagonist. At the first sign of any attack, a single 100 mg dose was given. With this dosing at onset of attacks, each episode of effusion was successfully terminated.

Reducing frequency and severity of IH episodes:

Case reports indicate some success using long-term, low-dose colchicine (e.g. 0.5 mg to 1 mg daily). A recent single case report has shown hydroxychloroquine (300 mg daily) to be effective too.

Small-sized clinical trials have shown positive results with (1) chemical and (2) radioactive synovectomy. (1) Setti et al. treated 53 patients with rifampicin RV (600 mg intra-articular injections weekly for approximately 6 weeks) with good results at 1 year follow-up. (2) Top and Cross used single doses of intra-articular radioactive gold in 18 patients with persistent effusions of mixed causes including 3 with IH. All 3 patients with IH responded well to treatment at one-year follow-up.

Few clinical outcome studies exist regarding the treatment of central polydactyly. Tada and colleagues note that satisfactory surgical correction of central polydactyly is difficult to achieve and that outcomes are generally poor. In Tada’s study, 12 patients were reviewed. All patients required secondary surgical procedures to address flexion contractures and angular deviation at the IP joint level.

However, several primary factors contribute to the complexity of central polydactyly reconstruction. Hypoplastic joints and soft tissues that predispose the reconstructed finger to joint contracture, and angular deformities as well as complex tendon anomalies, are often difficult to address. Therefore, treatment is wholly dependent on the anatomic components present, the degree of syndactyly, and the function of the duplicated finger.

Because neither of the two thumb components is normal, a decision should be taken on combining which elements to create the best possible composite digit. Instead of amputating the most hypoplastic thumb, preservation of skin, nail, collateral ligaments and tendons is needed to augment the residual thumb. Surgery is recommended in the first year of life, generally between 9 and 15 months of age.

Surgical options depend on type of polydactyly.

Popliteal pterygium syndrome (PPS) is an inherited condition affecting the face, limbs, and genitalia. The syndrome goes by a number of names including the "popliteal web syndrome" and, more inclusively, the "facio-genito-popliteal syndrome". The term PPS was coined by Gorlin "et al.." in 1968 on the basis of the most unusual anomaly, the popliteal pterygium (a web behind the knee).

Complications of treatment may include joint stiffness and scar formation. Recurrence of the lesion is more common following excision of a volar ganglion cyst in the wrist. Incomplete excision that fails to include the stalk or pedicle also may lead to recurrence, as will failing to execute a layered closure of the incision.

Besides the frequent choice to leave the cyst in place, surgical treatments remain the primary elective option for treatment of ganglion cysts. The progression of ganglion surgery worldwide is to use an arthroscopic or mini-opening method. Alternatively, a hypodermic needle may be used to drain the fluid from the cyst (via aspiration) and a corticosteroid may be injected after the cyst is empty; however, if the fluid has thickened, owing to the passage of time, this treatment is not always effective.

There is a recurrence rate of approximately 50% following needle drainage (via aspiration) of ganglion cysts.

One common and traditional method of treatment for a ganglion cyst was to strike the lump with a large and heavy book, causing the cyst to rupture and drain into the surrounding tissues. Historically, a Bible was the largest or only book in any given household, and was often employed for this treatment. This led to the former nickname of "Bible bumps" or "Gideon's disease" for these cysts. This treatment risks injuring the patient.

This disorder is characterized by unusual facial features, including prominent, wide-set eyes with outer corners that point downward; a short bulbous nose with a flat nasal bridge; ears that are rotated backward; and a widow's peak hairline.

Individuals with Donnai–Barrow syndrome have severe hearing loss caused by abnormalities of the inner ear (sensorineural hearing loss). In addition, they often experience vision problems, including extreme nearsightedness (high myopia), detachment or deterioration of the light-sensitive tissue in the back of the eye (the retina), and progressive vision loss. Some have a gap or split in the colored part of the eye (iris coloboma).

In almost all people with Donnai–Barrow syndrome, the tissue connecting the left and right halves of the brain (corpus callosum) is underdeveloped or absent. Affected individuals may also have other structural abnormalities of the brain. They generally have mild to moderate intellectual disability and developmental delay.

People with Donnai–Barrow syndrome may also have a hole in the muscle that separates the abdomen from the chest cavity (the diaphragm), which is called a diaphragmatic hernia. This potentially serious birth defect allows the stomach and intestines to move into the chest and possibly crowd the developing heart and lungs. An opening in the wall of the abdomen (an omphalocele) that allows the abdominal organs to protrude through the navel may also occur in affected individuals. Occasionally people with Donnai–Barrow syndrome have abnormalities of the intestine, heart, or other organs and scoliosis.

They are benign lesions and malignant degeneration is rare. They are usually treated with curettage which however have a high recurrence rate of 25%. As such if an en-bloc resection is possible this is advisable

Treatment requires treating the underlying condition with dental treatments, physical therapy, and passive range of motion devices. Additionally, control of symptoms with pain medications (NSAIDs), muscle relaxants, and warm compresses may be used.

Splints have been used.

Cryopyrin-associated periodic syndrome (CAPS) is a group of rare, heterogeneous autoinflammatory disease characterized by interleukin 1β-mediated systemic inflammation and clinical symptoms involving skin, joints, central nervous system, and eyes. It encompasses a spectrum of three clinically overlapping autoinflammatory syndromes including familial cold autoinflammatory syndrome (FCAS, formerly termed familial cold-induced urticaria), the Muckle–Wells syndrome (MWS), and neonatal-onset multisystem inflammatory disease (NOMID, also called chronic infantile neurologic cutaneous and articular syndrome or CINCA) that were originally thought to be distinct entities, but in fact share a single genetic mutation and pathogenic pathway.

Because any medication that could reduce the inflammation of CPPD bears a risk of causing organ damage, treatment is not advised if the condition is not causing pain.

For acute pseudogout, treatments include intra-articular corticosteroid injection, systemic corticosteroids, non-steroidal anti-inflammatory drugs (NSAIDs), or, on occasion, high-dose colchicine. In general, NSAIDs are administered in low doses to help prevent CPPD. However, if an acute attack is already occurring, higher doses are administered. If nothing else works, hydroxychloroquine or methotrexate may provide relief.

Research into surgical removal of calcifications is underway, however this still remains an experimental procedure.

Treatment of Foix–Chavany–Marie syndrome depends on the onset of symptoms and involves a multidisciplinary approach. Drugs are used in neurological recovery depending on the etiological classification of FCMS. FCMS caused by epilepsy, specifically resulting in the development of lesions in the bilateral and subcortical regions of the brain can be treated using antiepileptic drugs to reverse abnormal EEG changes and induce complete neurological recovery. In addition, a hemispherectomy can be performed to reverse neurological deficits and control the seizures. This procedure can result in a complete recovery from epileptic seizures. Physical therapy is also used to manage symptoms and improve quality of life. Classical FCMS resulting in the decline of ones ability to speak and swallow can be treated using neuromuscular electrical stimulation and traditional dysphagia therapy. Speech therapy further targeting dysphagia can strengthen oral musculature using modified feeding techniques and postures. Therapeutic feedings include practicing oral and lingual movements using ice chips. In addition, different procedures can be performed by a neurosurgeon to alleviate some symptoms.

Succinyl choline, phenothiazines and tricyclic antidepressants causes trismus as a secondary effect. Trismus can be seen as an extra-pyramidal side-effect of metoclopromide, phenothiazines and other medications.

Clinical expressions of PPS are highly variable, but include the following:

- Limb findings: an extensive web running from behind the knee down to the heel (90%), malformed toenails, and webbed toes.

- Facial findings: cleft palate with or without cleft lip (75%), pits in the lower lip (40%), and fibrous bands in the mouth known as syngnathia (25%).

- Genital findings (50%): hypoplasia of the labia majora, malformation of the scrotum, and cryptorchidism.

Treatment generally includes the following:

- Sometimes pharmacologic therapy for initial disease treatment

- Physical therapy

- Occupational therapy

- Use of appropriate assistive devices such as orthoses

- Surgical treatment

There is moderate quality evidence that manual therapy and therapeutic exercise improves pain in patients with thumb CMC

OA at both short- and intermediate-term follow-up, and low to moderate quality evidence that magneto therapy improves pain

and function at short-term follow-up. There is moderate evidence that orthoses (splints) can improve hand function at long-term follow-up. There is very low to low-quality evidence that other conservative interventions provide no significant improvement in pain and in function at short- and long-term follow-up. Some of the commonly performed conservative interventions performed in therapy have evidence to support their use to improve hand function and decrease hand pain in patients with CMC OA.