Bisphosphonates are useful in decreasing the risk of future fractures in those who have already sustained a fracture due to osteoporosis. This benefit is present when taken for three to four years. Different bisphosphonates have not been directly compared, therefore it is unknown if one is better than another. Fracture risk reduction is between 25 and 70% depending on the bone involved. There are concerns of atypical femoral fractures and osteonecrosis of the jaw with long-term use, but these risks are low. With evidence of little benefit when used for more than three to five years and in light of the potential adverse events, it may be appropriate to stop treatment after this time. One medical organization recommends that after five years of medications by mouth or three years of intravenous medication among those at low risk, bisphosphonate treatment can be stopped. In those at higher risk they recommend up to ten years of medication by mouth or six years of intravenous treatment.

For those with osteoporosis but who have not had a fracture evidence does not support a reduction in fracture risk with risedronate or etidronate. Alendronate decreases fractures of the spine but does not have any effect on other types of fractures. Half stop their medications within a year. When on treatment with bisphosphonates rechecking bone mineral density is not needed. Another review found tentative evidence of benefit in males with osteoporosis.

Fluoride supplementation does not appear to be effective in postmenopausal osteoporosis, as even though it increases bone density, it does not decrease the risk of fractures.

Teriparatide ( a recombinant parathyroid hormone ) has been shown to be effective in treatment of women with postmenopausal osteoporosis. Some evidence also indicates strontium ranelate is effective in decreasing the risk of vertebral and nonvertebral fractures in postmenopausal women with osteoporosis. Hormone replacement therapy, while effective for osteoporosis, is only recommended in women who also have menopausal symptoms. It is not recommended for osteoporosis by itself. Raloxifene, while effective in decreasing vertebral fractures, does not affect the risk of nonvertebral fracture. And while it reduces the risk of breast cancer, it increases the risk of blood clots and strokes. Denosumab is also effective for preventing osteoporotic fractures but not in males. In hypogonadal men, testosterone has been shown to improve bone quantity and quality, but, as of 2008, no studies evaluated its effect on fracture risk or in men with a normal testosterone levels. Calcitonin while once recommended is no longer due to the associated risk of cancer and questionable effect on fracture risk.

Certain medications like alendronate, etidronate, risedronate, raloxifene and strontium ranelate can be helpful for the preventing of osteoporotic fragility fractures in postmenopausal women with osteoporosis.

Weight-bearing endurance exercise and/or exercises to strengthen muscles improve bone strength in those with osteoporosis. Aerobics, weight bearing, and resistance exercises all maintain or increase BMD in postmenopausal women. Fall prevention can help prevent osteoporosis complications. There is some evidence for hip protectors specifically among those who are in care homes.

Treatment for secondary juvenile osteoporosis focuses on treating any underlying disorder.

The treatment of osteopenia is controversial. Currently, candidates for therapy include those at the highest risk of osteoporotic bone fracture based on bone mineral density and clinical risk factors. As of 2008, recommendations from the US National Osteoporosis Foundation (NOF) are based on risk assessments from the World Health Organization (WHO) Fracture Risk Assessment Tool (FRAX). According to these recommendations, consideration of therapy should be made for postmenopausal women, and men older than 50 years of age, if any one of the following is present:

1. Prior hip or vertebral fracture

2. T-score of −2.5 at the femoral neck or spine, excluding secondary causes

3. T-score between −1.0 and −2.5 at the femoral neck or spine "and" a 10-year probability of hip fracture ≥3% "or" a 10-year probability of major osteoporotic fracture ≥20%

4. Clinicians' judgment in combination with patient preferences indicate treatment for people with 10-year fracture probabilities above or below these levels.

When medical therapy is pursued, treatment includes medications with a range of actions. Commonly used drugs are bisphosphonates including alendronate, risedronate, and ibandronate; selective estrogen receptor modulators (SERMs) such as raloxifene; estrogen; calcitonin; and teriparatide.

Studies have shown that the actual benefits of these drugs may be marginal. Approximately 270 women with osteopenia might need to be treated with drugs for three years so that one of them could avoid a single vertebral fracture.

Strontium ranelate has been approved in 27 European countries, having been found to build bone both by slowing the work of osteoclasts and by stimulating osteoblasts. On January 10, 2014, the European Pharmacovigilance Risk Assessment Committee recommended that strontium ranelate, marketed as Protelos or Protos by Servier, should be treated with caution when used to treat osteoporosis, as randomised trials have shown an increased risk of non-fatal myocardial infarction in patients with ischemic heart disease or uncontrolled hypertension patients. There is no increased risk of non-fatal myocardial infarction in healthy patients.

Other (natural) forms of available strontium include strontium lactate, strontium gluconate, strontium carbonate, and strontium citrate. Food sources include spices (especially basil), seafood, whole grains, root and leafy vegetables, and legumes. Strontium should not be taken with calcium supplements, to improve absorption.

Even though more studies are necessary for an efficient evaluation of the role played by zinc in senile osteoporosis, doctors recommend a proper supplementation of dietary zinc.

Replacement estrogen has proved to be an efficient way to combat the loss of bone mass in women when such treatment is started in the menopausal stage of their lives. John R. Lee, a Harvard graduate who wrote a book on the subject, came to the conclusion that by adding supplementation with natural progesterone to an existing natural osteoporosis treatment program, bone density was increased every year by 3-5% until it stabilized at the bone density levels expected for a 35-year-old woman, this after studies in 100 women between 38 and 83 with an average of 62 years old.

Initial and general approach for AGL patients are to treat the metabolic complications such as leptin-replacement therapy and/or to control the abnormal levels of lipids or glucose levels. Anti-diabetic medications such as insulin, metformin, or thiazolidinediones are used for insulin-resistance or high glucose levels, or statins or fibrates are used for hyperlipidemia. If symptoms persist, metreleptin can be prescribed.

Metreleptin (MYALEPT) is a recombinant human leptin analog and was approved by FDA in 2014 for generalized lipodystrophy as an adjunct therapy to diet to treat the complication of leptin deficiency. It is the only drug option approved for generalized lipodystrophy-related symptoms and is not intended to use for patients with HIV-related lipodystrophy or complications of partial lipodystrophy. Although it is a recombinant human leptin analog, it is not completely the same as natural leptin as it is produced in "e. coli" and has added methionine residues at is amino terminus. It works by binding to the human leptin receptor, ObR, and activates the receptor. The receptor belongs to the Class I cytokine family and signals the JAK/STAT pathway. It is available as 11.3 mg powder in a vial for subcutaneous injection upon reconstitution and needs to be protected from the light. For treatment, patients and their doctors need to be enrolled and certified in the Myalept Risk Evaluation and Mitigation Strategy (REMS) Program because people on this treatment has a risk of developing anti-metreleptin antibodies that decrease the effectiveness of metreleptin, and increased risk of lymphoma. Clinical study with GL patients who took metreleptin had increased insulin sensitivity, as indicated by decreased HbA1c and fasting glucose level, and reduced caloric intake as well as fasting triglyceride levels.

Plasmapheresis was previously an option for lowering extremely high triglyceride levels for preventing pancreatitis and painful xanthoma, but its use has been decreased after the approval of metreleptin.

Cosmetic treatments, such as facial reconstruction or implants, can be done to replace adipose tissues.

Lifestyle modifications are also recommended, including changes into less fat diet and exercise.

The prognosis of the disease is unknown as of December, 2017.

In severe cases of PM and DM with systemic signs, an initial three to five days on intravenous corticosteroid (methylprednisolone) may be used; but normally treatment begins with a single daily (after breakfast) high dose of oral corticosteroid (prednisone). After a month or so the strength of every second day's dose is very gradually reduced over three to four months, to minimize the negative effects of the prednisone. When a high dose of prednisone cannot be reduced without losing muscle strength, or when prednisone is effective but it is producing significant complications, "steroid sparing" oral immunosuppressants such as azathioprine, mycophenolate mofetil, methotrexate and cyclosporine, may be used in combination with reduced prednisone. Some of these steroid sparing drugs can take several months to demonstrate an effect.

To minimize side effects, patients on corticosteroids should follow a strict high-protein, low-carbohydrate, low-salt diet; and with long-term corticosteroid use a daily calcium supplement and weekly vitamin D supplement (and a weekly dose of Fosamax for postmenopausal women) should be considered.

For patients not responding to this approach there is weak evidence supporting the use of intravenous immunoglobulin, ciclosporin, tacrolimus, mycophenolate mofetil and other agents; and trials of rituximab have indicated a potential therapeutic effect.

There have been few randomized treatment trials, due to the relative rarity of inflammatory myopathies. The goal of treatment is improvement in activities of daily living and muscle strength. Suppression of immune system activity (immunosuppression) is the treatment strategy. Patients with PM or DM almost always improve to some degree in response to treatment, at least initially, and many recover fully with maintenance therapy. (If there is no initial improvement from treatment of PM or DM, the diagnosis should be carefully re-examined.) There is no proven effective therapy for IBM, and most IBM patients will need assistive devices such as a cane, a walking frame or a wheelchair. The later in life IBM arises, the more aggressive it appears to be.

Juvenile osteoporosis is osteoporosis in children and adolescents.Osteoporosis is rare in children and adolescents. When it occurs, it is usually secondary to some other condition, "e.g." osteogenesis imperfecta, rickets, eating disorders or arthritis. In some cases, there is no known cause and it is called idiopathic juvenile osteoporosis. Idiopathic juvenile osteoporosis usually goes away spontaneously.

Also, child abuse should be suspected in recurring cases of bone fracture.

JIA is best treated by a multidisciplinary team. The major emphasis of treatment for JIA is to help the child regain normal level of physical and social activities. This is accomplished with the use of physical therapy, pain management strategies, and social support. Another emphasis of treatment is to control inflammation and extra-articular symptoms quickly. Doing so should help to reduce joint damage and other symptoms, which will help reduce levels of permanent damage leading to disability.

Beneficial advances in drug treatment have been made over the last 20 years. Most children are treated with nonsteroidal anti-inflammatory drugs and intra-articular corticosteroid injections. Methotrexate, a disease-modifying antirheumatic drug (DMARD) is a powerful drug which helps suppress joint inflammation in the majority of JIA patients with polyarthritis (though less useful in systemic arthritis). Newer drugs have been developed recently, such as TNF alpha blockers, such as etanercept. No controlled evidence supports the use of alternative remedies such as specific dietary exclusions, homeopathic treatment, or acupuncture. However, an increased consumption of omega-3 fatty acids proved to be beneficial in two small studies.

Celecoxib has been found effective in one study.

Other aspects of managing JIA include physical and occupational therapy. Therapists can recommend the best exercise and also make protective equipment. Moreover, the child may require the use of special supports, ambulatory devices, or splints to help them ambulate and function normally.

Surgery is only used to treat the most severe cases of JIA. In all cases, surgery is used to remove scars and improve joint function.

Home remedies that may help JIA includes getting regular exercises to increase muscle strength and joint flexibility. Swimming is perhaps the best activity for all children with JIA. Stiffness and swelling can also be reduced with application of cold packs, but a warm bath or shower can also improve joint mobility.

In the future, genetic testing may be available allowing earlier detection of JIA. Early detection will help determine the severity of the disease in each child and help identify which therapies will be the most effective and beneficial treatment options.

The traditional medical management of scoliosis is complex and is determined by the severity of the curvature and skeletal maturity, which together help predict the likelihood of progression.

The conventional options for children and adolescents are:

1. Observation

2. Bracing

3. Surgery

For adults, treatment usually focuses on relieving any pain:

1. Painkilling medication

2. Bracing

3. Surgery

Treatment for idiopathic scoliosis also depends upon the severity of the curvature, the spine’s potential for further growth, and the risk that the curvature will progress. Mild scoliosis (less than 30 degrees deviation) may simply be monitored and treated with exercise. Moderately severe scoliosis (30–45 degrees) in a child who is still growing may require bracing. Severe curvatures that rapidly progresses may be treated surgically with spinal rod placement. Bracing may prevent a progressive curvature, but evidence for this is not very strong. In all cases, early intervention offers the best results.

A growing body of scientific research testifies to the efficacy of specialized treatment programs of physical therapy, which may include bracing.

An endocrine bone disease is a bone disease associated with a disorder of the endocrine system. An example is osteitis fibrosa cystica.

Most of the etiologic considerations regarding senile osteoporosis are not very clear for physicians yet. But based on the current evidence attached to clinical experimentation, it has been determined that the pathogenesis of the disease is clearly related to a deficiency of zinc. Such deficiency is known to lead to an increment of endogenous heparin, which is most likely caused by mast cell degranulation, and an increase in the bone resorption (calcium discharge in the bones) reaction of prostaglandin E2, which constrain the formation of more bone mass, making bones more fragile. These co-factors are shown to play an important role in the pathogenetic process attached to senile osteoporosis as they enhance the action of the parathyroid hormone.

The intake of calcium in elder people is quite low, and this problem is worsened by a reduced capability to ingest it. This, attached to a decrease in the absorption of vitamin D concerning metabolism, are also factors that contributes to a diagnosis of osteoporosis type II.

Osteopenia is a condition in which bone mineral density is lower than normal. It is considered by many doctors to be a precursor to osteoporosis. However, not every person diagnosed with osteopenia will develop osteoporosis. More specifically, osteopenia is defined as a bone mineral density T-score between −1.0 and −2.5.

The treatment of juvenile arthritis includes medications, physical therapy, splints and in severe cases surgery. These treatments are focused on reducing swelling, relieving pain and maintaining full movement of joints. Children are encouraged to be involved in extra-curricular activities, physical activity when possible, and to live a "normal" life.

Many researches for the treatment of lipodystrophy focus on the safety and efficacy of leptin replacement therapy and the outlook is positive in many studies.

According to a prospective, open-label clinical study at the NIH, metreleptin decreased the fasting glucose level from 180 mg/dL to 121 mg/dL, HbA1c from 8.4% to 6.4%, total cholesterol from 214 mg/dL to 146 mg/dL, and triglycerides from 467 (200-847)mg/dL to 180 (106-312)mg/dL after 12 months of use (p<0.001). Patients also had decreased use of anti-diabetic medications, lipid-lowering medications, and insulin (p<0.001). In other clinical reports studying 3 patients diagnosed with AGL accompanied by hypoleptinemia, uncontrolled diabetes, and hypertriglyceridemia who were treated with metreleptin for 12–168 weeks, patients had great reduction in HbA1c, from 10.9% to 5.8%, and had normalized serum triglycerides with a mean decline of 90%. Patients reported improved quality of life and reduced need for other medications without significant adverse effects.

One research published in 2017 reported an middle-aged patient developed AGL after treatment and recovery for autoimmune thrombocytopenia that included immunoglobulin therapy and prednisone, which suggests the autoimmune trigger may contribute to the development of AGL.

Other researches focus on genetics of lipodystrophy; however its relevance to acquired generalized lipodystrophy has not been confirmed so far. One clinical report published in July 2017 stated two brothers with juvenile-onset generalized lipodystrophy was due to lamin C-specific mutation but it is unknown at this point if this will fall into acquired or familial lipodystrophy.

There has been many published case reports. Meta-analysis of published case reports published within the decade will be very helpful in establishing patient demographic, etiologies, and prognosis of the diagnosis.

This disease has not been shown to be life-threatening or the cause of death in patients. However, treatment is necessary to maintain a healthy lifestyle.

Body braces showed benefit in a randomised controlled trial.

The Milwaukee brace is one particular body brace that is often used to treat kyphosis in the US. Modern CAD/CAM braces are used in Europe to treat different types of kyphosis. These are much easier to wear and have better in-brace corrections than reported for the Milwaukee brace. Since there are different curve patterns (thoracic, thoracolumbar and lumbar), different types of brace are in use, with different advantages and disadvantages.

Surgery is usually recommended by orthopedists for curves with a high likelihood of progression (i.e., greater than 45 to 50° of magnitude), curves that would be cosmetically unacceptable as an adult, curves in patients with spina bifida and cerebral palsy that interfere with sitting and care, and curves that affect physiological functions such as breathing.

Surgery is indicated by the Society on Scoliosis Orthopaedic and Rehabilitation Treatment (SOSORT) at 45 degrees to 50 degrees and by the Scoliosis Research Society (SRS) at a Cobb angle of 45 degrees. SOSORT uses the 45-degree to 50-degree threshold as a result of the well-documented, plus or minus five degrees measurement error that can occur while measuring Cobb angles.

Surgeons that are specialized in spine surgery are the ones who perform surgery for scoliosis. To completely straighten a scoliotic spine is usually impossible, however for the most part, significant corrections are achieved.

The two main types of surgery are:

- Anterior fusion: This surgical approach is through an incision at the side of the chest wall.

- Posterior fusion: This surgical approach is through an incision on the back and involves the use of metal instrumentation to correct the curve.

One or both of these surgical procedures may be needed. The surgery may be done in one or two stages and, on average, takes four to eight hours.

Osteoporosis is due to causal factors like atrophy of disuse and gonadal deficiency. Hence osteoporosis is common in post menopausal women and in men above 50 yrs. Hypercorticism may also be causal factor, as osteoporosis may be seen as a feature of Cushing's syndrome.

Since about 2002, some patients with this disorder have been offered drug therapy with bisphosphonates (a class of osteoporosis drugs) to treat problems with bone resorption associated with the bone breakdown and skeletal malformations that characterize this disorder. Brand names include Actonel (risedronate/alendronate), made by Merck Pharmaceuticals. Other drugs include Pamidronate, made by Novartis and Strontium Ranelate, made by Eli Lilly. However, for more progressive cases, surgery and bone grafting are necessary.

Since this condition is generally agreed upon to be hereditary, nothing can be done to prevent HGF. However, in some cases where it can develop as a result of rare multi-system syndromes, such as: Zimmerman-Laband, Jones, Ramon Syndrome, Rutherford Syndrome, Juvenile Hyaline Fibromatosis, Systemic Infantile Hyalinosis, and Mannosidosis, it is best for one to simply monitors the possible progression for HGF with regular dental check-ups.

If the patient's disease is treated by means of surgery, it is recommended that the patient undergoes post-surgical therapies for maintenance and periodic monitoring of gums for the sake of the possibility of re-occurrence of HGF.

Metabolic bone disease is an umbrella term referring to abnormalities of bones caused by a broad spectrum of disorders.

Most commonly these disorders are caused by abnormalities of minerals such as calcium, phosphorus, magnesium or vitamin D leading to dramatic clinical disorders that are commonly reversible once the underlying defect has been treated. These disorders are to be differentiated from a larger group of genetic bone disorders where there is a defect in a specific signaling system or cell type that causes the bone disorder. There may be overlap. For example, genetic or hereditary hypophosphatemia may cause the metabolic bone disorder osteomalacia. Although there is currently no treatment for the genetic condition, replacement of phosphate often corrects or improves the metabolic bone disorder.

In Germany, a standard treatment for both Scheuermann's disease and lumbar kyphosis is the Schroth method, a system of physical therapy for scoliosis and related spinal deformities.

It involves lying supine, placing a pillow under the scapular region and posteriorly stretching the cervical spine.

Treatment involves having the person stop taking any calcium supplements and any other alkali agents they have been taking, and hydration.

In severe cases, hospitalization may be required, in which case saline may be administered intravenously.

If kidney failure is advanced then treatment for that is required, namely chronic dialysis.