Medical management of OFC consists of Vitamin D treatment, generally alfacalcidol or calcitriol, delivered intravenously. Studies have shown that in cases of OFC caused by either end-stage renal disease or primary hyperparathyoidism, this method is successful not only in treating underlying hyperparathyoidism, but also in causing the regression of brown tumors and other symptoms of OFC.

In especially severe cases of OFC, parathyroidectomy, or the full removal of the parathyroid glands, is the chosen route of treatment. Parathyroidectomy has been shown to result in the reversal of bone resorption and the complete regression of brown tumors. In situations where parathyroid carcinoma is present, surgery to remove the tumors has also led to the regression of hyperparathyroidism as well as the symptoms of OFC.

Bone transplants have proven successful in filling the lesions caused by OFC. A report showed that in 8 out of 11 instances where cavities caused by OFC were filled with transplanted bone, the lesion healed and the transplanted bone blended rapidly and seamlessly with the original bone.

Medications that are sometimes required include estrogen replacement therapy in postmenopausal women and bisphosphonates. Bisphosphonates may improve bone turnover.

Newer medications termed "calcimimetics" used in secondary hyperparathyroidism are now being used in primary hyperparathyroidism. Calcimimetics reduce the amount of parathyroid hormone released by the parathyroid glands. They are recommended in patients in whom surgery is inappropriate.

Treatment is usually surgical removal of the gland(s) containing adenomas, but medication may also be required.

Treatment for renal osteodystrophy includes the following:

- calcium and/or native vitamin D supplementation

- restriction of dietary phosphate (especially inorganic phosphate contained in additives)

- phosphate binders such as calcium carbonate, calcium acetate, sevelamer hydrochloride or carbonate, lanthanum carbonate, sucroferric oxyhydroxide, ferric citrate among others

- active forms of vitamin D (calcitriol, alfacalcidol, paricalcitol, maxacalcitol, doxercalciferol, among others)

- cinacalcet

- renal transplantation

- haemodialysis five times a week is thought to be of benefit

- parathyroidectomy for symptomatic medication refractive end stage disease

Non-steroidal anti-inflammatory drugs (NSAIDs) and corticosteroids are most used in PDP treatment. These drugs inhibit cyclo-oxygenase activity and thereby prostaglandin synthesis. Since PGE is likely to be involved in periosteal bone formation and acroosteolysis, this is why these drugs can alleviate the polyarthritis associated with PDP. In addition, NSAIDs and corticosteroids decrease formation of inflammatory mediators, reducing inflammation and pain. In case of possible gastropathy, the COX-2 selective NSAID etorixocib is preferred.

Infliximab can reduce pain and arthritis in PDP. It is a monoclonal antibody that blocks the biological action of TNF-α (tumor necrosis factor-alpha). TNF-α is an inflammatory cytokine found in high levels in PDP and it is involved in the production of other inflammatory mediators which increase the expression of RANKL. RANKL is thought to increase bone resorption.

Five bisphosphonates are currently available. In general, the most commonly prescribed are risedronic acid, alendronic acid, and pamidronic acid. Etidronic acid and other bisphosphonates may be appropriate therapies for selected patients but are less commonly used. None of these drugs should be used by people with severe kidney disease.

- Etidronate disodium The approved regimen is once daily for six months; a higher dose is more commonly used. No food, beverage, or medications should be consumed for two hours before and after taking. The course should not exceed six months, but repeat courses can be given after rest periods, preferably of three to six months duration.

- Pamidronate disodium in intravenous form: the approved regimen uses an infusion over four hours on each of three consecutive days, but a more commonly used regimen is over two to four hours for two or more consecutive or nonconsecutive days.

- Alendronate sodium is given as tablets once daily for six months; patients should wait at least 30 minutes after taking before eating any food, drinking anything other than tap water, taking any medication, or lying down (patient may sit).

- Tiludronate disodium are taken once daily for three months; they may be taken any time of day, as long as there is a period of two hours before and after resuming food, beverages, and medications.

- Risedronate sodium tablet taken once daily for 2 months is the prescribed regimen; patients should wait at least 30 minutes after taking before eating any food, drinking anything other than tap water, taking any medication, or lying down (patient may sit).

- Zoledronic acid is given as an intravenous infusion; a single dose is effective for two years. This is recommended for most people at high risk with active disease.

The effective treatment for PDP is currently unknown due to the lack of controlled data and is largely based on case reports. Although the HPGD enzyme is likely to be involved into the pathogenesis of PDP, no strategies against this mutation have been reported yet, since it is hard to tackle a defective enzyme. Gene therapy could be a solution for this, although this has not been reported yet in literature.

Conventional PDP drug treatment to decrease inflammation and pain includes NSAIDs and corticosteroids. Other drugs used by PDP patients target bone formation or skin manifestations. Surgical care is used to improve cosmetic appearance.

Calcitonin, also called calcitonin-salmon, is a synthetic copy of a polypeptide hormone secreted by the ultimobranchial gland of salmon. Miacalcin is administered by injection, three times per week or daily, for 6–18 months. Repeat courses can be given after brief rest periods. Miacalcin may be appropriate for certain patients, but is seldom used. Calcitonin is also linked to increased chance of cancer. Due to the increased risk of cancer, the European Medicines Agency (EMA) recommended that calcitonin be used only on a short-term basis for 3 conditions for which it had previously been approved in the European Union: Paget's disease, acute bone loss resulting from sudden immobilization, and hypercalcemia caused by cancer.

The EMA said it based its recommendations on a review of the benefits and risks of calcitonin-containing medicines. Conducted by the agency's Committee for Medicinal Products for Human Use (CHMP), the review encompassed available data from the companies that market these drugs, postmarketing safety data, randomized controlled studies, 2 studies of unlicensed oral calcitonin drugs, and experimental cancer studies, among other sources.

CHMP found that "a higher proportion of patients treated with calcitonin for long periods of time develop cancer of various types, compared with patients taking placebo." The increase in cancer rates ranged from 0.7% for oral formulations to 2.4% for the nasal formulation. CHMP concluded that the benefits of calcitonin for osteoporosis did not exceed the risks. The nasal spray's only indication is for osteoporosis, thus justifying the drug's removal from the market.

As a solution for injection or infusion, calcitonin should be administered for no more than 4 weeks to prevent acute bone loss resulting from sudden immobilization, and normally for no more than 3 months to treat Paget's disease, the EMA said. The agency did not specify a time frame for the short-term use of calcitonin for treating hypercalcemia caused by cancer.

Bone lesions in multiple myeloma patients may be treated with low-dose radiation therapy in order to reduce pain and other symptoms. Used in combination with immunochemotherapy, radiation therapy can be used to treat certain cancers when aimed at areas of bone lesion and softened bone.

Biophosphonates are drugs that are used to prevent bone mass loss and are often used to treat osteolytic lesions. Zoledronic acid (Reclast) is a specific drug given to cancer patients to prevent the worsening of bone lesions and has been reported to have anti-tumor effects as well. Zoledronic acid has been clinically tested in conjunction with calcium and vitamin D to encourage bone health. Denosumab, a monoclonal antibody treatment RANKl inhibitor that targets the osteocyte apoptosis regualtory RANKL gene, is also prescribed to prevent bone metastases and bone lesions. Most biophosphonates are co-prescribed with disease-specific treatments, such as chemotherapy or radiation for cancer patients.

Recovery from renal osteodystrophy has been observed following kidney transplantation. Renal osteodystrophy is a chronic condition with a conventional hemodialysis schedule. Nevertheless, it is important to consider that the broader concept of CKD-MBD, which includes renal osteodystrophy, is not only associated with bone disease and increased risk of fractures but also with cardiovascular calcification, poor quality of life and increased morbidity and mortality in CKD patients (the so-called bone-vascular axis). Actually, bone may now be considered a new endocrine organ at the heart of CKD-MBD.

Treatment in fibrous dysplasia is mainly palliative, and is focused on managing fractures and preventing deformity. There are no medications capable of altering the disease course. Intravenous bisphosphonates may be helpful for treatment of bone pain, but there is no clear evidence that they strengthen bone lesions or prevent fractures. Surgical techniques that are effective in other disorders, such as bone grafting, curettage, and plates and screws, are frequently ineffective in fibrous dysplasia and should be avoided. Intramedullary rods are generally preferred for management of fractures and deformity in the lower extremities. Progressive scoliosis can generally be managed with standard instrumentation and fusion techniques. Surgical management in the craniofacial skeleton is complicated by frequent post-operative FD regrowth, and should focus on correction of functional deformities. Prophylactic optic nerve decompression increases the risk of vision loss and is contraindicated.

Managing endocrinopathies is a critical component of management in FD. All patients with fibrous dysplasia should be evaluated and treated for endocrine diseases associated with McCune–Albright syndrome. In particular untreated growth hormone excess may worsen craniofacial fibrous dysplasia and increase the risk of blindness. Untreated hypophosphatemia increases bone pain and risk of fractures.

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.

Specific treatment for enchondroma is determined by a physician based on the age, overall health, and medical history of the patient. Other considerations include:

- extent of the disease

- tolerance for specific medications, procedures, or therapies

- expectations for the course of the disease

- opinion or preference of the patient

Treatment may include:

- surgery (in some cases, when bone weakening is present or fractures occur)

- bone grafting - a surgical procedure in which healthy bone is transplanted from another part of the patient's body into the affected area.

If there is no sign of bone weakening or growth of the tumor, observation only may be suggested. However, follow-up with repeat x-rays may be necessary. Some types of enchondromas can develop into malignant, or cancerous, bone tumors later. Careful follow-up with a physician may be recommended.

Prevention of osteomalacia rests on having an adequate intake of vitamin D and calcium. Vitamin D3 Supplementation is often needed due to the scarcity of Vitamin D sources in the modern diet.

Nutritional osteomalacia responds well to administration of 2,000-10,000 IU of vitamin D3 by mouth daily. Vitamin D3 (cholecalciferol) is typically absorbed more readily than vitmin D2 (ergocalciferol). Osteomalacia due to malabsorption may require treatment by injection or daily oral dosing of significant amounts of vitamin D3.

One of the major concerns is bone density and bone loss. Non-hormonal bisphosphonates increase bone strength and are available as once-a-week prescription pills. Metastron also known as strontium-89 chloride is an intravenous medication given to help with the pain and can be given in three month intervals. Generic Strontium Chloride Sr-89 Injection UPS, manufactured by Bio-Nucleonics Inc., it is the generic version of Metastron. Astra zantec is currently under review as to the benefits in bone cancer.

Treatment of Gorham's disease is for the most part palliative and limited to symptom management.

Sometimes the bone destruction spontaneously ceases and no treatment is required. But when the disease is progressive, aggressive intervention may be necessary. Duffy and colleagues reported that around 17% of patients with Gorham's disease in the ribs, shoulder, or upper spine experience extension of the disease into the chest, leading to chylothorax with its serious consequences, and that the mortality rate in this group can reach as high as 64% without surgical intervention.

A search of the medical literature reveals multiple case reports of interventions with varying rates of success as follows:

Cardiothoracic (heart & lung):

- Pleurodesis

- Ligation of thoracic duct

- Pleurperitoneal shunt

- Radiation therapy

- Pleurectomy

- Surgical resection

- Thalidomide

- Interferon alpha-2b

- TPN (total parenteral nutrition)

- Thoracentesis

- Diet rich in medium-chain triglycerides and protein

- Chemotherapy

- Sclerotherapy

- Transplantation

Skeletal:

- Interferon alpha-2b

- Bisphosphonate (e.g. pamidronate)

- Surgical resection

- Radiation therapy

- Sclerotherapy

- Percutaneous bone cement

- Bone graft

- Prosthesis

- Surgical stabilization

- Amputation

To date, there are no known interventions that are consistently effective for Gorham's and all reported interventions are considered experimental treatments, though many are routine for other conditions. Some patients may require a combination of these approaches. Unfortunately, some patients will not respond to any intervention.

The following are the most common treatments of elevated alkaline phosphatase.

- Treatment of the underlying condition

- Once doctors identifies the cause of elevated ALP and diagnose a treatment, the levels of alkaline phosphatase fluctuates back to normal

- Removal of medication - that is associated with increased levels of alkaline phosphatase

- Birth control pills

- Anti-inflammatory medication

- Narcotic medication

- Hormonal drug

- Steroid

- Antidepressant

- Dietary changes

- Include foods rich in vitamin D

- Lifestyle change

- Healthy diet in association with physical exercise

- Exposure to sunlight which increases the production of vitamin D

The only effective line of treatment for malignant infantile osteopetrosis is hematopoietic stem cell transplantation. It has been shown to provide long-term disease-free periods for a significant percentage of those treated; can impact both hematologic and skeletal abnormalities; and has been used successfully to reverse the associated skeletal abnormalities.

Radiographs of at least one case with malignant infantile osteopetrosis have demonstrated bone remodeling and recanalization of medullar canals following hematopoietic stem cell transplantation. This favorable radiographic response could be expected within one year following the procedure - nevertheless, primary graft failure can prove fatal.

There is no cure or approved treatment for FOP. Attempts to surgically remove the bone result in explosive bone growth. While under anesthesia, people with FOP may encounter difficulties with intubation, restrictive pulmonary disease, and changes in the electrical conduction system of the heart. Activities that increase the risk of falling or soft tissue injury should be avoided, as even minor trauma may provoke heterotopic bone formation.

The treatment should be tailored to the cause involved and the severity of the disease process. With oral osteoporosis the emphasis should be on good nutrient absorption and metabolic wastes elimination through a healthy gastro-intestinal function, effective hepatic metabolism of toxicants such as exogenous estrogens, endogenous acetaldehyde and heavy metals, a balanced diet, healthy lifestyle, assessment of factors related to potential coagulopathies, and treatment of periodontal diseases and other oral and dental infections.

In cases of advanced oral ischaemic osteoporosis and/or ONJ that are not bisphosphonates related, clinical evidence has shown that surgically removing the damaged marrow, usually by curettage and decortication, will eliminate the problem (and the pain) in 74% of patients with jaw involvement. Repeat surgeries, usually smaller procedures than the first, may be required. Almost a third of jawbone patients will need surgery in one or more other parts of the jaws because the disease so frequently present multiple lesions, i.e., multiple sites in the same or similar bones, with normal marrow in between. In the hip, at least half of all patients will get the disease in the opposite hip over time; this pattern occurs in the jaws as well. Recently, it has been found that some osteonecrosis patients respond to anticoagulation therapies alone. The earlier the diagnosis the better the prognosis. Research is ongoing on other non-surgical therapeutic modalities that could alone or in combination with surgery further improve the prognosis and reduce the morbidity of ONJ. A greater emphasis on minimizing or correcting known causes is necessary while further research is conducted on chronic ischaemic bone diseases such as oral osteoporosis and ONJ.

In patients with bisphosphonates-associated ONJ, the response to surgical treatment is usually poor. Conservative debridement of necrotic bone, pain control, infection management, use of antimicrobial oral rinses, and withdrawal of bisphosphonates are preferable to aggressive surgical measures for treating this form of ONJ. Although an effective treatment for bisphosphonate-associated bone lesions has not yet been established, and this is unlikely to occur until this form of ONJ is better understood, there have been clinical reports of some improvement after 6 months or more of complete cessation of bisphosphonate therapy.

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.

Chemotherapy and radiotherapy are effective in some tumors (such as Ewing's sarcoma) but less so in others (such as chondrosarcoma).

There is a variety of chemotherapy treatment protocols for bone tumors. The protocol with the best reported survival in children and adults is an intra-arterial protocol where tumor response is tracked by serial arteriogram. When tumor response has reached >90% necrosis surgical intervention is planned.