Curettage is performed on some patients, and is sufficient for inactive lesions. The recurrence rate with curettage is significant in active lesions, and marginal resection has been advised. Liquid nitrogen, phenol, methyl methacrylate are considered for use to kill cells at margins of resected cyst.

The treatment for CGCG is thorough curettage. A referral is made to an oral surgeon. Recurrence ranges from 15%–20%. In aggressive tumors, three alternatives to surgery are undergoing investigation:

- corticosteroids;

- calcitonin (salmon calcitonin);

- interferon α-2a.

These therapeutic approaches provide positive possible alternatives for large lesions. The long term prognosis of giant-cell granulomas is good and metastases do not develop.

Corticosteroids, typically high-dose prednisone (1 mg/kg/day), must be started as soon as the diagnosis is suspected (even before the diagnosis is confirmed by biopsy) to prevent irreversible blindness secondary to ophthalmic artery occlusion. Steroids do not prevent the diagnosis from later being confirmed by biopsy, although certain changes in the histology may be observed towards the end of the first week of treatment and are more difficult to identify after a couple of months. The dose of prednisone is lowered after 2–4 weeks, and slowly tapered over 9–12 months. Tapering may require two or more years. Oral steroids are at least as effective as intravenous steroids, except in the treatment of acute visual loss where intravenous steroids appear to offer significant benefit over oral steroids. It is unclear if adding a small amount of aspirin is beneficial or not as it has not been studied.

Treatment usually involves surgical removal of the lesion down to the bone. If there are any adjacent teeth, they are cleaned thoroughly with scaling and root planing (SRP) to remove any possible source of irritation. Recurrence is around 10%.

Treatment usually involves surgical removal of the lesion down to the bone. If there are any adjacent teeth, they are cleaned thoroughly to remove any possible source of irritation. Recurrence is around 16%.

Treatment is by surgical excision (complete removal) of the fibrous tissue overgrowth and addressing the causative factor to prevent recurrence of the lesion. Other sources suggest that surgical excision may not be required in all cases. Common techniques for removal of the excess tissue include traditional removal with a surgical scalpel, electrical scalpel, or laser excision with a laser scalpel, e.g. a carbon dioxide laser, , Neodymium-YAG laser, or diode laser. The poorly fitting denture can be adapted to fit better (a "reline") or a new denture constructed. Alternatively, the section of flange that is sharp/over-extended can be smoothed and reduced with a drill.

Chondroblastoma has not been known to spontaneously heal and the standard treatment is surgical curettage of the lesion with bone grafting. To prevent recurrence or complications it is important to excise the entire tumor following strict oncologic criteria. However, in skeletally immature patients intraoperative fluoroscopy may be helpful to avoid destruction of the epiphyseal plate. In patients who are near the end of skeletal growth, complete curettage of the growth plate is an option. In addition to curettage, electric or chemical cauterization (via phenol) can be used as well as cryotherapy and wide or marginal resection. Depending on the size of the subsequent defect, autograft or allograft bone grafts are the preferred filling materials. Other options include substituting polymethylmethacrylate (PMMA) or fat implantation in place of the bone graft. The work of Ramappa "et al" suggests that packing with PMMA may be a more optimal choice because the heat of polymerization of the cement is thought to kill any remaining lesion.

Both radiotherapy and chemotherapy are not commonly used. Radiotherapy has been implemented in chondroblastoma cases that are at increased risk of being more aggressive and are suspected of malignant transformation. Furthermore, radiofrequency ablation has been used, but is typically most successful for small chondroblastoma lesions (approximately 1.5 cm). Treatment with radiofrequency ablation is highly dependent on size and location due to the increased risk of larger, weight-bearing lesions being at an increased risk for articular collapse and recurrence.

Overall, the success and method of treatment is highly dependent upon the location and size of the chondroblastoma.

As the condition is quite rare, opinions among experts about how to treat OKCs differ.

Treatment options:

- Wide (local) surgical excision.

- Marsupialization - the surgical opening of the (OKC) cavity and a creation of a marsupial-like pouch, so that the cavity is in contact with the outside for an extended period, e.g. three months.

- Curettage (simple excision & scrape-out of cavity).

- Peripheral ostectomy after curettage and/or enucleation.

- Simple excision.

- Carnoy's solution - usually used in conjunction with excision.

- Enucleation and cryotherapy

Treatment is not needed in the asymptomatic patient. Symptomatic patients may benefit from surgical debulking of the tumor. Complete tumor removal is not usually needed and can be difficult due to the tumor location.

General treatment regimens have not changed much in the past 30 years, in part due to the lack of randomized clinical trials. Surgery is the treatment of choice if the tumor is determined to be resectable. Curettage is a commonly used technique. The situation is complicated in a patient with a pathological fracture. It may be best to immobilize the affected limb and wait for the fracture to heal before performing surgery.

Patients with tumors that are not amenable to surgery are treated with radiation therapy. However caution is employed since a majority of recurrent tumors with transformations to the malignant sarcoma phenotype have been in patients receiving radiotherapy for their primary benign lesion. Pharmacotherapy for GCTOB, includes bisphosphonates such as Zoledronate, which are thought to induce apoptosis in the MNGC fraction, preventing tumor-induced osteolysis. Indeed, "in vitro" studies have shown zolidronate to be effective in killing osteoclast-like cells. More recently, humanized monoclonal antibodies such as Denosumab targeting the RANK ligand have been employed in treatment of GCTOB in a phase II study. This is based on the notion that increased expression of RANK-ligands by stromal cells plays a role in tumor pathogenesis.

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

Usually, treatment of a lipoma is not necessary, unless the tumor becomes painful or restricts movement. They are usually removed for cosmetic reasons, if they grow very large, or for histopathology to check that they are not a more dangerous type of tumor such as a liposarcoma. This last point can be important as the characteristics of a "bump" are not known until after it is removed and medically examined.

Lipomas are normally removed by simple excision. The removal can often be done under local anaesthetic, and takes less than 30 minutes. This cures the great majority of cases, with about 1–2% of lipomas recurring after excision. Liposuction is another option if the lipoma is soft and has a small connective tissue component. Liposuction typically results in less scarring; however, with large lipomas it may fail to remove the entire tumor, which can lead to regrowth.

New methods under development are supposed to remove the lipomas without scarring. One is removal by injecting compounds that trigger lipolysis, such as steroids or phosphatidylcholine.

Corticosteroids are the mainstay of therapy with a 90% response rate in some studies. Appropriate duration of steroid treatment is unknown and relapse often necessitates long term treatment. Various steroid sparing agents e.g. sodium cromoglycate (a stabilizer of mast cell membranes), ketotifen (an antihistamine), and montelukast (a selective, competitive leukotriene receptor antagonist) have been proposed, centering on an allergic hypothesis, with mixed results. An elimination diet may be successful if a limited number of food allergies are identified.

Villonodular synovitis is a type of synovial swelling.

Types include:

- Pigmented villonodular synovitis (PVNS)

- Giant cell tumor of the tendon sheath (GCTS)

Though they have very different names, they have the same histology, and stain positive for CD68, HAM56, and vimentin.

They are sometimes discussed together.

The mainstay of treatment is surgical excision. Two adjuvant therapeutic strategies are Stereotactic surgery (SRS) and fractionated convention radiotherapy (FCRT). Both are highly effective means of treatment.

If the causative factor persists, tissue will become more fibrous over time.

Treatment is targeted to the underlying cause. However, most vasculitis in general are treated with steroids (e.g. methylprednisolone) because the underlying cause of the vasculitis is due to hyperactive immunological damage. Immunosuppressants such as cyclophosphamide and azathioprine may also be given.

A systematic review of antineutrophil cytoplasmic antibody (ANCA) positive vasculitis identified best treatments depending on whether the goal is to induce remission or maintenance and depending on severity of the vasculitis.

Treatment may include the following:

- Surgery with or without radiation

- Radiotherapy

Fast neutron therapy has been used successfully to treat salivary gland tumors, and has shown to be significantly more effective than photons in studies treating unresectable salivary gland tumors.

- Chemotherapy

Treatment is beta blockers, ASA, and NSAIDs (or corticosteroids if NSAIDs are ineffective).

Most histiocytomas will regress within two or three months. Surgical removal may be necessary if the tumor does not regress or if it is growing rapidly to a large size. Histiocytomas should never be treated with an intralesional injection of a corticosteroid, as remission relies on recognition of the tumour by the body's immune system which is suppressed by steroids.

Surgical excision of the central neurocytoma is the primary consensus among practicing physicians. The surgeons perform a craniotomy to remove the tumor. The ability to remove the tumor and to what extent it is removed is dependent upon the location of the tumor and surgeon experience and preference. The extent of the disease plays a large part in determining how effective the surgery will be. The main goal of a complete surgical resection, of the tumor, can also be hindered by the adherence of the tumor to adjoining structures or hemorrhages. If there is a recurrence of the central neurocytoma, surgery is again the most notable treatment.

Excision of the entire lesion, with adequate margin, will remove the lesion, allow full tissue diagnosis, and leave a planned surgical wound which can usually be repaired with a good cosmetic result. However, removing the entire lesion (especially on the face) may present difficult problems of plastic reconstruction. (On the nose and face, Mohs surgery may allow for good margin control with minimal tissue removal, but many insurance companies require the definitive diagnosis of a malignancy "before" they are prepared to pay the extra costs of Mohs surgery.) Especially in more cosmetically-sensitive areas, and where the clinical diagnosis is reasonably certain, alternatives to surgery may include no treatment (awaiting spontaneous resolution).

On the trunk, arms, and legs, electrodesiccation and curettage often suffice to control keratoacanthomas until they regress. Other modalities of treatment include cryosurgery and radiotherapy; intralesional injection of methotrexate or of 5-fluorouracil have also been used.

Recurrence after electrodesiccation and curettage can occur; it can usually be identified and treated promptly with either further curettage or surgical excision.

Treatment options include surgery, radiotherapy, radiosurgery, and chemotherapy.

The infiltrating growth of microscopic tentacles in fibrillary astrocytomas makes complete surgical removal difficult or impossible without injuring brain tissue needed for normal neurological function. However, surgery can still reduce or control tumor size. Possible side effects of surgical intervention include brain swelling, which can be treated with steroids, and epileptic seizures. Complete surgical excision of low grade tumors is associated with a good prognosis. However, the tumor may recur if the resection is incomplete, in which case further surgery or the use of other therapies may be required.

Standard radiotherapy for fibrillary astrocytoma requires from ten to thirty sessions, depending on the sub-type of the tumor, and may sometimes be performed after surgical resection to improve outcomes and survival rates. Side effects include the possibility of local inflammation, leading to headaches, which can be treated with oral medication. Radiosurgery uses computer modelling to focus minimal radiation doses at the exact location of the tumor, while minimizing the dose to the surrounding healthy brain tissue. Radiosurgery may be a complementary treatment after regular surgery, or it may represent the primary treatment technique.

Although chemotherapy for fibrillary astrocytoma improve overall survival, it is effective only in about 20% of cases. Researchers are currently investigating a number of promising new treatment techniques including gene therapy, immunotherapy, and novel chemotherapies.

Recurrence rate of solid form of tumour is lower than classic form.

Two related drugs have been shown to shrink or stabilize subependymal giant cell tumors: rapamycin and everolimus. These both belong to the mTOR inhibitor class of immunosuppressants, and are both contraindicated in patients with severe infections.

Rapamycin showed efficacy in five cases of SEGA in TSC patients, shrinking their tumor volumes by an average of 65%. However, after the drug was stopped, the tumors regrew.

Everolimus, which has a similar structure as rapamycin, but with slightly increased bioavailability and shorter half-life, was studied in 28 patients with SEGA. There was a significant reduction in SEGA size in 75% of the patients, and a mild improvement in their seizures. Everolimus was approved for the treatment of SEGA by the US Food and Drug Administration (FDA) in October, 2010.