Bone lesions are caused by an imbalance of regulatory factors, characterized by an increased depletion and resorption of old bone tissue and a decrease in bone rebuilding, known as bone remodeling. This imbalance is due to a flooding of regulatory factors released by specific tumors, thus overwhelming the tissue repair system and resulting in these lesions. The over-activity of osteoclasts can also cause hypercalcemia, which can cause damage to the kidneys and requires additional medication and monitoring.

In multiple myeloma, an increased number of myeloma cells block osteoblasts from creating new bone, while these cancerous cells also release factors that cause an upregulation on osteoclasts, causing an increasing in bone tissue resorption and an overall breakdown of bone integrity. This breakdown often begins in the bone marrow near tumor sites and spreads outward to the surface of the implicated bone.

The most common cancers that metastasize to osteolytic lesions are prostate, thyroid, lung and breast, though any cancer can cause bone lesions. Lesions are most often found in larger bones, such as the skull, pelvis, radius, and femur.

An osteolytic lesion (from the Greek words for "bone" (ὀστέον), and "to unbind" (λύειν)) is a softened section of a patient's bone formed as a symptom of specific diseases, including breast cancer and multiple myeloma. This softened area appears as a hole on X-ray scans due to decreased bone density. Osteolytic lesions can cause pain, increased risk of bone fracture, and spinal chord compression. These lesions can be treated using biophosphonates or radiation, though new solutions are being tested in clinical trials.

Age and gender have an effect on the incidence of these lesions; they are more prevalent in women than men (though still common in both genders), and they appear more frequently with age. Due to the standard of medical care and screening in developed countries, it is increasingly rare for primary hyperparathyroidism to present with accompanying bone disease. This is not the case in less developed nations, however, and the two conditions are more often seen together.

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

It is common in age group of 10–30 years. It is second most common tumor of spine and commonest benign tumor of pelvis in pediatric population. Incidence is slightly more in males than females (1.3:1).

In the US, Osteoblastomas account for only 0.5-2% of all primary bone tumors and only 14% of benign bone tumors making it a relatively rare form of bone tumor.

In regards to morbidity and mortality, conventional osteoblastoma is a benign lesion with little associated morbidity. However, the tumor may be painful, and spinal lesions may be associated with scoliosis and neurologic manifestations. Metastases and even death have been reported with the controversial aggressive variant, which can behave in a fashion similar to that of osteosarcoma. This variant is also more likely to recur after surgery than is conventional osteoblastoma.

Osteoblastoma affects more males than it does females, with a ratio of 2-3:1 respectively. Osteoblastoma can occur in persons of any age, although the tumors predominantly affect the younger population (around 80% of these tumors occurs in persons under the age of 30). No racial predilection is recognized.

It usually presents in the vertebral column or long bones. Approximately 40% of all osteoblastomas are located in the spine. The tumors usually involve the posterior elements, and 17% of spinal osteoblastomas are found in the sacrum. The long tubular bones are another common site of involvement, with a lower extremity preponderance. Osteoblastoma of the long tubular bones is often diaphyseal, and fewer are located in the metaphysis. Epiphyseal involvement is extremely rare. Although other sites are rarely affected, several bones in the abdomen and extremities have been reported as sites of osteoblastoma tumors.

The brown tumor is a bone lesion that arises in settings of excess osteoclast activity, such as hyperparathyroidism. It is not a true neoplasm, as the term "tumor" suggests; however, it may mimic a true neoplasm. It most commonly affects the maxilla and mandible, though any bone may be affected. Brown tumours are radiolucent on x-ray.

Gorham's disease (pronounced GOR-amz), also known as Gorham vanishing bone disease and phantom bone disease, is a very rare skeletal condition of unknown cause, characterized by the uncontrolled proliferation of distended, thin-walled vascular or lymphatic channels within bone, which leads to resorption and replacement of bone with angiomas and/or fibrosis. Current treatments are experimental only.

Acidosis is the increased acidity in a given location, whether it is blood, urine, or tissues. Osteoclasts generate extracellular protons, lowering the pH of the extracellular matrix (ECM) around the osteoclast to approximately 4.5. Nociceptors in the bone trigger a pain response in the brain in response to this acidosis. It is thought that this is the primary source of the dull, chronic pain experienced by patients with bone metastasis.

The uncoupled regulation of the osteoclasts and osteoblasts leads to malformation of the bone. Malformed bones are unable to withstand the normal mechanical stresses placed on them in day-to-day activity, leading to fractures, spinal compression, and spinal instability. Malformed bones may also mechanically trigger pain receptors both within the bone and in the surrounding tissue.

To date, the specific cause of Gorham's disease remains unknown.

Bone mass and strength are obtained and maintained through a process of bone destruction and replacement that occurs at the cellular level throughout a person's life. Cells called osteoclasts secrete enzymes that dissolve old bone, allowing another type of cells called osteoblasts to form new bone. Except in growing bone, the rate of breakdown equals the rate of building, thereby maintaining bone mass. In Gorham's disease that process is disrupted.

Gorham and Stout found that vascular anomalies always occupied space that normally would be filled with new bone and speculated that the presence of angiomatosis may lead to chemical changes in the bone. Gorham and others speculated that such a change in the bone chemistry might cause an imbalance in the rate of osteoclast activity to osteoblast activity such that more bone is dissolved than is replaced. Beginning in the 1990s there were reports of elevated levels of a protein called interleukin-6 (IL-6) being detected in patients with the disease, leading some to suggest that increased levels of IL-6 and vascular endothelial growth factor (VEGF) may contribute to the chemical changes Gorham and others believed were the cause of this type of osteolysis.

In 1999 Möller and colleagues concluded, "The Gorham-Stout syndrome may be, essentially, a monocentric bone disease with a focally increased bone resorption due to an increased number of paracrine – or autocrine – stimulated hyperactive osteoclasts. The resorbed bone is replaced by a markedly vascularized fibrous tissue. The apparent contradiction concerning the presence or absence or the number of osteoclasts, may be explained by the different phases of the syndrome." They further stated that their histopathological study provided good evidence that osteolytic changes seen in Gorham's disease are the result of hyperactive osteoclastic bone. However, others have concluded that lymphangiomatosis and Gorham's disease should be considered as a spectrum of disease rather than separate diseases.

While there is consensus that Gorham's is caused by deranged osteoclastic activity, there is not yet conclusive evidence as to what causes this deranged behavior to begin.

A CT scan can detect bone metastases before becoming symptomatic in patients diagnosed with tumors with risk of spread to the bones. Even sclerotic bone metastases are generally less radiodense than enostoses, and it has been suggested that bone metastasis should be the favored diagnosis between the two for bone lesions lower than a cutoff of 1060 Hounsfield units (HU).

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%.

The first route of treatment in Osteoblastoma is via medical means. Although necessary, radiation therapy (or chemotherapy) is controversial in the treatment of osteoblastoma. Cases of postirradiation sarcoma have been reported after use of these modalities. However, it is possible that the original histologic diagnosis was incorrect and the initial lesion was an osteosarcoma, since histologic differentiation of these two entities can be very difficult.

The alternative means of treatment consists of surgical therapy. The treatment goal is complete surgical excision of the lesion. The type of excision depends on the location of the tumor.

- For stage 1 and 2 lesions, the recommended treatment is extensive intralesional excision, using a high-speed burr. Extensive intralesional resections ideally consist of removal of gross and microscopic tumor and a margin of normal tissue.

- For stage 3 lesions, wide resection is recommended because of the need to remove all tumor-bearing tissue. Wide excision is defined here as the excision of tumor and a circumferential cuff of normal tissue around the entity. This type of complete excision is usually curative for osteoblastoma.

In most patients, radiographic findings are not diagnostic of osteoblastoma; therefore, further imaging is warranted. CT examination performed with the intravenous administration of contrast agent poses a risk of an allergic reaction to contrast material.

The lengthy duration of an MRI examination and a history of claustrophobia in some patients are limiting the use of MRI. Although osteoblastoma demonstrates increased radiotracer accumulation, its appearance is nonspecific, and differentiating these lesions from those due to other causes involving increased radiotracer accumulation in the bone is difficult. Therefore, bone scans are useful only in conjunction with other radiologic studies and are not best used alone.

Extramammary Paget's disease is usually seen in isolation and is associated with an underlying invasive malignancy about 12% of the time. It is associated with an underlying adnexal malignancy about 24% of the time. Paget's disease of the breast is almost always associated with an underlying invasive malignancy, i.e. breast cancer (e.g. mammary ductal carcinoma).

Fibrocartilaginous mesenchymoma of bone is (FCMB) is an extremely rare tumor first described in 1984. Fewer than 20 cases have been reported, with patient ages spanning from 9 to 25 years, though a case in a male infant aged 1 year and 7 months has been reported. Quick growth and bulky size are remarkable features of this tumor.

Surgery is curative despite possible local relapses. Wide resection of the tumor and resection arthrodesis with an intramedullary nail, vertebrectomy and femoral head allograft replacement of the vertebral body, resection of the iliac wing and hip joint disarticulation have been among the performed procedures.

The close resemblance of FCMB to fibrocartilaginous dysplasia has suggested to some scholars that they might be closely related entities, although the latter features woven bone trabeculae without osteoblastic rimming, which is a quite distinctive aspect. Instead the occurrence of epiphyseal plate-like cartilage is peculiar of the former.

A bone cyst or geode is a cyst that forms in bone.

Types include:

- Unicameral bone cyst

- Aneurysmal bone cyst

- Traumatic bone cyst

Paget's disease of the vulva, a rare disease, may be a primary lesion or associated with adenocarcinoma originating from local organs such as the Bartholin gland, the urethra, or the rectum and thus be secondary. Patients tend to be postmenopausal.

Paget's disease of the penis may also be primary or secondary, and is even rarer than genital Paget’s disease in women. At least one case has been misdiagnosed as Bowen's disease. Isolated Paget's disease of the penis is extremely rare.

Treatment consists of wide resection or amputation. Metastases are rare at presentation but may occur in up to 30% of patients during the disease course. Prognosis is excellent, with overall survival of 85% at 10 years, but is lower when wide surgical margins cannot be obtained. This tumor is insensitive to radiation so chemotherapy is not typically used unless the cancer has metastasized to the lungs or other organs.

Adamantinoma (from the Greek word "adamantinos", meaning "very hard") is a rare bone cancer, making up less than 1% of all bone cancers. It almost always occurs in the bones of the lower leg and involves both epithelial and osteofibrous tissue.

The condition was first described by Fischer in 1913.

Simple (Unicameral) Bone Cyst

Some unicameral bone cysts may spontaneously resolve without medical intervention. Specific treatments are determined based on size of the cyst, strength of the bone, medical history, extent of the disease, activity level, symptoms an individual is experiencing, and tolerance for specific medications, procedures, or therapies. The types of methods used to treat this type of cyst are curettage and bone grafting, aspiration, steroid injections, and bone marrow injections. Watchful waiting and activity modifications are the most common nonsurgical treatments that will help resolve and help prevent unicameral bone cysts from occurring and reoccurring.

Aneurysmal Bone Cyst

The aneurysmal bone cyst can be treated with a variety of different methods. These methods include open curettage and bone grafting with or without adjuvant therapy, cryotheraphy, sclerotherapy, ethibloc injections, radionuclide ablation, and selective arterial embolization. En-block resection and reconstruction with strut grafting are the most common treatments and procedures that prevent recurrences of this type of cyst.

Traumatic Bone Cyst

The traumatic bone cyst treatment consists of surgical exploration, curettage of the osseous socket and bony walls, subsequent filling with blood, and intralesional steroid injections. Young athletes can reduce their risk of traumatic bone cyst by wearing protective mouth wear or protective head gear.

Actinic keratosis is very common, with an estimated 14% of dermatology visits related to AKs. It is seen more often in fair-skinned individuals, and rates vary with geographical location and age. Other factors such as exposure to ultraviolet (UV) radiation, certain phenotypic features, and immunosuppression can also contribute to the development of AKs.

Men are more likely to develop AK than women, and the risk of developing AK lesions increases with age. These findings have been observed in multiple studies, with numbers from one study suggesting that approximately 5% of women ages 20–29 develop AK compared to 68% of women ages 60–69, and 10% of men ages 20–29 develop AK compared to 79% of men ages 60–69.

Geography seems to play a role in the sense that individuals living in locations where they are exposed to more UV radiation throughout their lifetime have a significantly higher risk of developing AK. Much of the literature on AK comes from Australia, where prevalence of AK is estimated at 40–50% in adults over 40, as compared to the United States and Europe, where prevalence is estimated at under 11–38% in adults. One study found that those who immigrated to Australia after age 20 had fewer AKs than native Australians in all age groups.

The color of peripheral ossifying fibromas ranges from red to pink, and is frequently ulcerated. It can be sessile or pedunculated with the size usually being less than 2 cm. Weeks or months may pass by before it is seen and diagnosed.

There is a gender difference with 66% of the disease occurring in females. The prevalence of peripheral ossifying fibromas is highest around 10 – 19 years of age. It appears only on the gingiva, more often on the maxilla rather than the mandible, and is frequently found in the area around incisors and canines. The adjacent teeth are usually not affected.

Peripheral ossifying fibromas appear microscopically as a combination of a mineralized product and fibrous proliferation. The mineralized portion may be bone, cementum-like, or dystrophic calcifications. Additionally, highly developed bone or cementum is more likely to be present when the peripheral ossifying fibroma has existed for a longer period of time.

The exact cause of the condition is unknown. There is most evidence to support vascular infarction and ischemic necrosis of salivary gland lobules as a mechanism for the condition. Experimentally, local anaesthetic injections and tying of the arteries is reported to trigger the development of tissue changes similar to NS in lab rats. Factors which are thought to cause this ischemia are listed below, however sometimes there is no evident predisposing factor or initiating event.

- Trauma e.g. during intubation, or surgical procedures

- Local anesthetic injection

- Smoking

- Alcohol

- Diabetes mellitus

- Vascular disease, (e.g. arteriosclerosis)

- Pressure from a dental prosthesis

- Allergy

- Bulimia

- Infection

- Ionizing radiation

Nodular fasciitis, also known as nodular pseudosarcomatous fasciitis, pseudosarcomatous fasciitis, and subcutaneous pseudosarcomatous fibromatosis, is a benign soft tissue lesion most commonly found in the superficial fascia. The lesion commonly occurs in the first three decades of life. Upper extremities and trunk are the most common affected anatomical sites. Previous history of trauma may be present. Clinically and histologically, nodular fasciitis may be mistaken for a sarcoma.