Management often includes the use of beta blockers such as propranolol or if not tolerated calcium channel blockers or ACE inhibitors.

Since angiotensin II receptor antagonists (ARBs) also reduce TGF-β, these drugs have been tested in a small sample of young, severely affected people with Marfan syndrome. In some, the growth of the aorta was reduced. However, a recent study published in NEJM demonstrated similar cardiac outcomes between the ARB, losartan, and the more established beta blocker therapy, atenolol.

As there is no known cure, Loeys–Dietz syndrome is a lifelong condition. Due to the high risk of death from aortic aneurysm rupture, patients should be followed closely to monitor aneurysm formation, which can then be corrected with interventional radiology or vascular surgery.

Previous research in laboratory mice has suggested that the angiotensin II receptor antagonist losartan, which appears to block TGF-beta activity, can slow or halt the formation of aortic aneurysms in Marfan syndrome. A large clinical trial sponsored by the National Institutes of Health is currently underway to explore the use of losartan to prevent aneurysms in Marfan syndrome patients. Both Marfan syndrome and Loeys–Dietz syndrome are associated with increased TGF-beta signaling in the vessel wall. Therefore, losartan also holds promise for the treatment of Loeys–Dietz syndrome. In those patients in which losartan is not halting the growth of the aorta, irbesartan has been shown to work and is currently also being studied and prescribed for some patients with this condition.

If an increased heart rate is present, atenolol is sometimes prescribed to reduce the heart rate to prevent any extra pressure on the tissue of the aorta. Likewise, strenuous physical activity is discouraged in patients, especially weight lifting and contact sports.

There is no cure for Marfan syndrome, but life expectancy has increased significantly over the last few decades and is now similar to that of the average person. Regular checkups by a cardiologist are needed to monitor the health of the heart valves and the aorta. The syndrome is treated by addressing each issue as it arises and, in particular, preventive medication even for young children to slow progression of aortic dilation. The goal of treatment is to slow the progression of aortic dilation and damage to heart valves by eliminating arrythmias, minimizing the heart rate, and minimizing blood pressure.

There is no medical treatment for either syndrome but there are some recommendations that can help with prevention or early identification of some of the problems. Children with either syndrome should have their hearing tested, and adults should be aware that the hearing loss may not develop until the adult years. Yearly visits to an ophthalmologist or other eye care professional who has been informed of the diagnosis of Stickler or Marshall syndrome is important for all affected individuals. Children should have the opportunity to have myopia corrected as early as possible, and treatment for cataracts or detached retinas may be more effective with early identification. Support for the joints is especially important during sports, and some recommend that contact sports should be avoided by those who have very loose joints.

The treatment of arterial tortuosity syndrome entails possible surgery for aortic aneurysms, as well as, follow ups which should consist of EGC. The prognosis of this condition has it at about 12% mortality

Pediatric FMD medical and surgical treatments or interventions are available. Treatment is determined by factors such as age and disease location but routinely involve controlling hypertension, re-establishing vascular flow, clot prevention, and improving lifestyle such as diet, exercise and smoking cessation.

Medical therapy for pediatric population may involve the use of angiotensin-converting enzyme inhibitor (ACE inhibitors) and/or angiotensin II receptor blockers, multiple anti-hypertensive medications, diuretics, calcium channel blockers, and beta-blockers. Prevention of thrombosis of affected arteries may be taken through administration of an antiplatelet medication such as aspirin.

Percutaneous transluminal renal angioplasty (PTRA) remains the gold standard for renal-artery FMD. This treatment is useful when hypertension is difficult to control; patient is intolerant to the anti-hypertensive medications, non-complainant to medication regime and patient loss of renal volume due to ischemia. PTRA can also aide in preventing a lifelong dependency on a medication for such a young patient. According to Meyers, “effective PTRAs result in cured or controlled blood pressure, which is often signified by reductions in plasma renin activity and angiotensin II levels, and when compared with surgery, percutaneous balloon angioplasty is less costly, able to be performed on an outpatient basis, results in lower morbidity, and the use of stenting is not primarily necessary.” However, there is a subset of the pediatric population that are resistant to PTRA. Adverse events may include, “recurrent stenosis, arterial occlusion with renal loss, and arterial rupture with extravasations and pseudo aneurysm formation and may require surgical intervention.

There is no known cure for FMD. However, treatment focuses on relieving symptoms associated with it. Medical management is the most common form of treatment. The best approach to medically managing these patients is constantly being reevaluated as more information is learned about the disease.

Medication is not the primary treatment for hypermobility, but can be used as an adjuct treatment for related joint pain. NSAIDS are the primary medications of choice. Narcotics are not recommended for primary or long term treatment and are reserved for short term use after acute injury.

For some people with hypermobility, lifestyle changes decrease symptom severity. In general activity that increases pain is to be avoided. For example:

- Typing can reduce pain from writing.

- Voice control software or a more ergonomic keyboard can reduce pain from typing.

- Bent knees or sitting can reduce pain from standing.

- Unwanted symptoms are frequently produced by some forms of yoga and weightlifting.

- Use of low impact elliptical training machines can replace high-impact running.

- Pain-free swimming may require a kickboard or extra care to avoid hyperextending elbow and other joints.

- Weakened ligaments and muscles contribute to poor posture, which may contribute to other medical conditions.

- Isometric exercise avoids hyperextension and contributes to strength.

As with many musculoskeletal conditions, the management of de Quervain's disease is determined more by convention than scientific data. From the original description of the illness in 1895 until the first description of corticosteroid injection by Jarrod Ismond in 1955, it appears that the only treatment offered was surgery. Since approximately 1972, the prevailing opinion has been that of McKenzie (1972) who suggested that corticosteroid injection was the first line of treatment and surgery should be reserved for unsuccessful injections. A systematic review and meta-analysis published in 2013 found that corticosteroid injection seems to be an effective form of conservative management of de Quervain's syndrome in approximately 50% of patients, although more research is needed regarding the extent of any clinical benefits. Efficacy data are relatively sparse and it is not clear whether benefits affect the overall natural history of the illness.

Most tendinoses are self-limiting and the same is likely to be true of de Quervain's although further study is needed.

Palliative treatments include a splint that immobilized the wrist and the thumb to the interphalangeal joint and anti-inflammatory medication or acetaminophen. Systematic review and meta-analysis do not support the use of splinting over steroid injections.

Surgery (in which the sheath of the first dorsal compartment is opened longitudinally) is documented to provide relief in most patients. The most important risk is to the radial sensory nerve.

Some occupational and physical therapists suggest alternative lifting mechanics based on the theory that the condition is due to repetitive use of the thumbs during lifting. Physical/Occupational therapy can suggest activities to avoid based on the theory that certain activities might exacerbate one's condition, as well as instruct on strengthening exercises based on the theory that this will contribute to better form and use of other muscle groups, which might limit irritation of the tendons.

Some occupational and physical therapists use other treatments, in conjunction with Therapeutic Exercises, based on the rationale that they reduce inflammation and pain and promote healing: UST, SWD, or other deep heat treatments, as well as TENS, acupuncture, or infrared light therapy, and cold laser treatments. However, the pathology of the condition is not inflammatory changes to the synovial sheath and inflammation is secondary to the condition from friction. Teaching patients to reduce their secondary inflammation does not treat the underlying condition but may reduce their pain; which is helpful when trying to perform the prescribed exercise interventions.

Getting Physical Therapy before surgery or injections has been shown to reduce overall costs to patients and is a viable option to treat a wide array of musculoskeletal injuries.

Non-surgical interventions include three elements: weight control, exercise control, and medication. Canine massage may alleviate discomfort and help move lymph and nutrients through the system. Weight control is often "the single most important thing that we can do to help a dog with arthritis", and consequentially "reducing the dog's weight is enough to control all of the symptoms of arthritis in many dogs". Reasonable exercise stimulates cartilage growth and reduces degeneration (though excessive exercise can do harm too), and also regular long walks in early or mild dysplasia can help prevent loss of muscle mass to the hips. Medication can reduce pain and discomfort, and also reduce damaging inflammation.

Non-surgical intervention is usually via a suitable non-steroidal anti-inflammatory drug (NSAID) which doubles as an anti-inflammatory and painkiller. Typical NSAIDs used for hip dysplasia include carprofen and meloxicam (often sold as Rimadyl and Metacam respectively), both used to treat arthritis resulting from dysplasia, although other NSAIDs such as tepoxalin (Zubrin) and prednoleucotropin ("PLT", a combination of cinchophen and prednisolone) are sometimes tried. NSAIDs vary dramatically between species as to effect: a safe NSAID in one species may be unsafe in another. It is important to follow veterinary advice.

A glucosamine-based nutritional supplement may give the body additional raw materials used in joint repair. Glucosamine can take 3–4 weeks to start showing its effects, so the trial period for medication is usually at least 3–5 weeks. In vitro, glucosamine has been shown to have negative effects on cartilage cells.

It is also common to try multiple anti-inflammatories over a further 4–6 week period, if necessary, since an animal will often respond to one type but fail to respond to another. If one anti-inflammatory does not work, a vet will often try one or two other brands for 2–3 weeks each, also in conjunction with ongoing glucosamine, before concluding that the condition does not seem responsive to medication.

Carprofen, and other anti-inflammatories in general, whilst very safe for most animals, can sometimes cause problems for some animals, and (in a few rare cases) sudden death through liver toxicity. This is most commonly discussed with carprofen but may be equally relevant with other anti-inflammatories. As a result, it is often recommended to perform monthly (or at least, twice-annually) blood tests to confirm that the animal is not reacting adversely to the medications. Such side effects are rare but worth being aware of, especially if long-term use is anticipated.

This regimen can usually be maintained for the long term, as long as it is effective in keeping the symptoms of dysplasia at bay.

Some attempts have been made to treat the pain caused by arthritic changes through the use of "laser therapy", in particular "class IV laser therapy". Well-controlled clinical trials are unfortunately lacking, and much of the evidence for these procedures remains anecdotal.

Conservative therapies include NSAIDs, pain medication, weight management and exercise restriction. The problems with these therapies is that they do not work well, especially long-term.

Loeys–Dietz syndrome (LDS) is an autosomal dominant genetic connective tissue disorder. It has features similar to Marfan syndrome and Ehlers–Danlos syndrome. The disorder is marked by aneurysms in the aorta, often in children, and the aorta may also undergo sudden dissection in the weakened layers of the wall of aorta. Aneurysms and dissections also can occur in arteries other than the aorta. Because aneurysms in children tend to rupture early, children are at greater risk for dying if the syndrome is not identified. Surgery to repair aortic aneurysms is essential for treatment.

There are four types of the syndrome, labelled types I through IV, which are distinguished by their genetic cause. Type 1, Type 2, Type 3, and Type 4 are caused by mutations in "TGFBR1", "TGFBR2", "SMAD3", and "TGFB2" respectively. These four genes encoding transforming growth factors play a role in cell signaling that promotes growth and development of the body's tissues. Mutations of these genes cause production of proteins without function. Although the disorder has an autosomal pattern of inheritance, this disorder results from a new gene mutation in 75% of cases and occurs in people with no history of the disorder in their family.

Loeys-Dietz syndrome was identified and characterized by pediatric geneticists Bart Loeys and Harry Dietz at Johns Hopkins University in 2005.

Most people with Takayasu’s arteritis respond to steroids such as prednisone. The usual starting dose is approximately 1 milligram per kilogram of body weight per day (for most people, this is approximately 60 milligrams a day). Because of the significant side effects of long-term high-dose prednisone use, the starting dose is tapered over several weeks to a dose which controls symptoms while limiting the side effects of steroids.

Promising results are achieved with mycophenolate and tocilizumab. If treatment is not kept to a high standard, long-term damage or death can occur.

For patients who do not respond to steroids may require revascularization, either via vascular bypass or angioplasty and stenting. Outcomes following revascularization vary depending on the severity of the underlying disease

There is no complete cure, although there are many options to alleviate the clinical signs. The aim of treatment is to enhance quality of life. Crucially, this is an inherited, degenerative condition and so will change during the life of an animal, so any treatment is subject to regular review or re-assessment if the symptoms appear to get worse or anything significantly changes.

If the problem is relatively mild, then sometimes all that is needed to bring the symptoms under control are suitable medications to help the body deal better with inflammation, pain and joint wear. In many cases this is all that is needed for a long time.

If the problem cannot be controlled with medications, then often surgery is considered. There are traditionally two types of surgery - those which reshape the joint to reduce pain or help movement, and hip replacement which completely replaces the damaged hip with an artificial joint, similar to human hip replacements.

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

The treatment of FAI varies. Conservative treatment includes reducing levels of physical activity, anti-inflammatory medication and physiotherapy. Physical therapy may optimize alignment and mobility of the joint, thereby decreasing excessive forces on irritable or weakened tissues. It may also identify specific movement patterns that may be causing injury.

Due to the frequency of diagnosis in adolescents and young adults, various surgical techniques have been developed with the goal of preserving the hip joint. Surgery may be arthroscopic or open, peri-acetabular or rotational osteotomies being two common open surgical techniques employed when an abnormal angle between femur and acetabulum has been demonstrated. These primarily aim to alter the angle of the hip socket in such a way that contact between the acetabulum and femoral head are greatly reduced, allowing a greater range of movement. Femoral sculpting may be performed simultaneously, if required for a better overall shape of the hip joint. It is unclear whether or not these interventions effectively delay or prevent the onset of arthritis. Well designed, long term studies evaluating the efficacy of these treatments have not been done.

A 2011 study analyzing current surgical methods for management of symptomatic femoral acetabular impingement (FAI), suggested that arthroscopic method had surgical outcomes equal to or better than other methods with a lower rate of major complications when performed by experienced surgeons.

Post-traumatic wrist osteoarthritis can be treated conservatively or with a surgical intervention. In many patients, a conservative (non-surgical) approach is sufficient. Because osteoarthritis is progressive and symptoms may get worse, surgical treatment is advised in any stage.

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.

Diagnosis is through x-rays, arthroscopy or CT (computed tomography). In cases with significant lameness, surgery is the best option, especially with UAP. However, conservative treatment is often enough for cases of FMCP and OCD of the medial humeral epicondyle. The dogs are exercised regularly and given pain medication, and between the ages of 12 to 18 months the lameness will often improve or disappear. Control of body weight is important in all cases of elbow dysplasia, and prevention of quick growth spurts in puppies may help to prevent the disease.

Surgery for FMCP consists of removal of cartilage and bone fragments and correction of any incongruity of the joint. Reattachment of UAP with a screw is usually attempted before the age of 24 weeks, and after that age the typical treatment is removal of the UAP. Without surgery, UAP rapidly progresses to osteoarthritis, but with FMCP osteoarthritis typically occurs with or without surgery. Osteoarthritis is also a common sequela of OCD of the humerus despite medical or surgical treatment. Elbow replacement surgery has been developed and can be an option for treatment

The first-line treatment for arteritis is oral glucocorticoid (steroid) medication, such as prednisone, taken daily for a period of three months. After this initial phase, the medication may be reduced in dose or frequency, e.g. every other day, if possible. If the disease worsens with the new treatment schedule, a cytotoxic medication may be given, in addition to the glucocorticoid. Commonly used cytotoxic agents include azathioprine, methotrexate, or cyclophosphamide. The dose of glucocorticoid medication may be decreased if response to treatment is good. This medication may be reduced gradually once the disease becomes inactive, slowly tapering the dose (to allow the body time to adjust) until the medication may be stopped completely. Conversely, if the disease remains active, the medication will need to be increased. After six months, if the medication cannot be reduced in frequency to alternate days, or if in 12 months the medications cannot be stopped completely, then treatment is deemed to have failed.

Pulsed therapy is an alternative method of administering the medications above, using much higher doses over a short period of time (a pulse), to reduce the inflammation within the arteries. Methylprednisolone, a glucocorticoid, is often used for pulse therapy; cyclophosphamide is an alternative. This method has been shown to be successful for some patients. Immunosuppressive pulse therapy, such as with cyclophosphamide, has also demonstrated relief of symptoms associated with arteritis.

In this stage there are two surgical treatment options; total wrist arthroplasty and total wrist arthrodesis.

Total wrist arthrodesis has become the standard surgical treatment for patients with stage IV wrist osteoarthritis. During this procedure the carpal bones are all fused together and are then fastened to the distal radius. Patients who still want to undertake heavy labor benefit the most of this surgical approach, because after surgery and recovery this is still possible. However, the arc of motion is extremely diminished by this type of surgery.

The best option for those who wish for a motion-sparing procedure is total wrist arthroplasty. However, impact loading should be avoided, an object heavier than 4.5 kg should not be lifted. So, this surgical approach has postoperative activity restrictions. Nevertheless, patients with a total wrist arthrodesis on one side and a total wrist arthroplasty on the other, prefer the total wrist arthroplasty. The procedure exists of a couple of elements. First, the proximal row is removed and the distal row is fastened to the metacarpals. Then, one side of the arthroplasty is placed upon the distal row and the other side on the distal radius. Additionally, the head of the ulna is removed.

Marshall syndrome is a genetic disorder of the connective tissue which can cause hearing loss. The three most common areas to be affected are the eyes which are uncommonly large, joints and the mouth and facial structures. Marshall syndrome and Stickler syndrome closely resemble each other; in fact they are so similar, some say they are the same.

Most hand injuries are minor and can heal without difficulty. However, any time the hand or finger is cut, crushed or the pain is ongoing, it is best to see a physician. Hand injuries when not treated on time can result in long term morbidity.

Antibiotics in simple hand injuries do not typically require antibiotics as they do not change the chance of infection.

No definite standard treatment have been set. This is because treatments of the disease has been poorly studied as of 2014. Often in cases of inflammatory parenchymal disease, "corticosteroids should be given as infusions of

intravenous methylprednisolone followed by a slowly tapering course of oral steroids". It is suggested that therapy should be continued for a period of time even when the symptoms get suppressed because early relapse may occur. Sometimes, the medical doctors may suggest a different steroid depending on the nature of the disease, the severity, and the response to steroids. According to several studies, parenchymal NBD patients successfully suppress the symptoms with the prescribed steroids. As for non-parenchymal patients, there is no general consensus on how to treat the disease. The reason is that the mechanisms of cerebral venous thrombosis in BD are still poorly understood. Some doctors use anti-coagulants to prevent a clot. On the other hand, some doctors only give steroids and immunosuppressants alone.