Men and women are affected in equal number., reflecting the fact that osteopoikilosis attacks indiscriminately. Additionally, the disease is often associated with melorheostosis, despite the apparent lack of correlation between melorheostosis and genetic heritability. It has been tied to LEMD3. Buschke-Ollendorff syndrome is a similar condition, which is also associated with LEMD3.

The cause of the rare condition of tumoral calcinosis is not entirely understood. It is generally characterized by large, globular calcifications near joints.

The prevalence of Mönckeberg's arteriosclerosis increases with age and is more frequent in diabetes mellitus, chronic kidney disease, systemic lupus erythematosus, chronic inflammatory conditions, hypervitaminosis D and rare genetic disorders, such as Keutel syndrome. The prevalence of Monckeberg's arteriosclerosis in the general population has been estimated as 1.5; however the validity of this criterion is questionable.

Metastatic calcification involves a systemic calcium excess imbalance, which can be caused by hypercalcemia, kidney failure, milk-alkali syndrome, lack or excess of other minerals, or other causes.

Oncogenic osteomalacia or tumor-induced osteomalacia, also known as oncogenic hypophosphatemic osteomalacia or oncogenic osteomalacia, is an uncommon disorder resulting in increased renal phosphate excretion, hypophosphatemia and osteomalacia. It may be caused by a phosphaturic mesenchymal tumor.

The gene NT5E is related to the gene ENPP1, which when mutated is known to cause arterial calcification in infants. Treatments for the ENPP1 mutation, such as bisphosphonates, which are similar to phosphatase, and adenosine reuptake inhibitors, provide possible routes of treatment for the NT5E mutation, as the mechanism of both disorders are very similar.

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.

Tumor-induced osteomalacia is usually referred to as a paraneoplastic phenomenon, however, the tumors are usually benign and the symptomatology is due to osteomalacia or rickets. A benign mesenchymal or mixed connective tissue tumor (usually phosphaturic mesenchymal tumor and hemangiopericytoma) are the most common associated tumors. Association with mesenchymal malignant tumors, such as osteosarcoma and fibrosarcoma, has also been reported.

Locating the tumor can prove to be difficult and may require whole body MRI. Some of the tumors express somatostatin receptors and may be located by octreotide scanning.

A phosphaturic mesenchymal tumor is an extremely rare benign neoplasm of soft tissue and bone that inappropriately produces fibroblast growth factor 23. This tumor may cause tumor-induced osteomalacia, a paraneoplastic syndrome, by the secretion of FGF23, which has phosphaturic activity (by inhibition of renal tubular reabsorption of phosphate and renal conversion of 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D). The paraneoplastic effects can be debilitating and are only reversed on discovery and surgical resectionof the tumor.

Axial osteomalacia is a rare osteosclerotic disorder characterized by axial skeleton pain, coarsening of the trabecular bone pattern on radiographs of the axial but not appendicular skeleton.

Malignant infantile osteopetrosis, also known as infantile autosomal recessive osteopetrosis or simply infantile osteopetrosis is a rare osteosclerosing type of skeletal dysplasia that typically presents in infancy and is characterized by a unique radiographic appearance of generalized hyperostosis - excessive growth of bone.

The generalized increase in bone density has a special predilection to involve the medullary portion with relative sparing of the cortices. Obliteration of bone marrow spaces and subsequent depression of the cellular function can result in serious hematologic complications. Optic atrophy and cranial nerve damage secondary to bony expansion can result in marked morbidity. The prognosis is extremely poor in untreated cases. Plain radiography provides the key information to the diagnosis. Clinical and radiologic correlations are also fundamental to the diagnostic process, with additional gene testing being confirmatory.

Arterial calcification due to deficiency of CD73 (ACDC) is a rare genetic disorder that causes calcium buildup in the arteries and joints of the hands and feet, and other areas below the waist. Although patients exhibiting these symptoms have been identified as early as 1914, this disorder had not been studied extensively until recently. The identification of the specific ACDC gene and mutations occurred in 2011. ACDC is caused by a mutation in the NT5E gene, which prevents calcium-removing agents from functioning. Patients afflicted with this mutation suffer from chronic pain, difficulty moving, and increased risk of cardiovascular problems. In experiments at the molecular level, treatment with adenosine or a phosphatase inhibitor reversed and prevented calcification, suggesting they could be used as possible treatment methods. There is currently no cure for ACDC, and patients have limited treatment options which focus primarily on removal of blood calcium and improving mobility.

The medication(s) listed below have been approved by the Food and Drug Administration (FDA) as orphan products for treatment of this condition. Learn more orphan products.

Ectopic ossification of the heart valves is an indicator of future heart problems, hyperparathyroidism, and necrosis of tissues.

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.

Treatment is symptomatic, often addressing indicators associated with peripheral pulmonary artery stenosis. Laryngotracheal calcification resulting in dyspnea and forceful breathing can be treated with bronchodilators including the short and long-acting β2-agonists, and various anticholinergics. Prognosis is good, yet life expectancy depends on the severity and extent of diffuse pulmonary and arterial calcification.

Dystrophic calcification (DC) is the calcification occurring in degenerated or necrotic tissue, as in hyalinized scars, degenerated foci in leiomyomas, and caseous nodules. This occurs as a reaction to tissue damage, including as a consequence of medical device implantation. Dystrophic calcification can occur even if the amount of calcium in the blood is not elevated. (A systemic mineral imbalance would elevate calcium levels in the blood and all tissues and cause metastatic calcification.) Basophilic calcium salt deposits aggregate, first in the mitochondria, and progressively throughout the cell. These calcifications are an indication of previous microscopic cell injury. It occurs in areas of cell necrosis in which activated phosphatases bind calcium ions to phospholipids in the membrane.

Calcification can occur in dead or degenerated tissue.

Myositis ossificans comprises two syndromes characterized by heterotopic ossification (calcification) of muscle.

Most (i.e. 80%) ossifications arise in the thigh or arm, and are caused by a premature return to activity after an injury. Other sites include intercostal spaces, erector spinae, pectoralis muscles, glutei, and the chest. On planar x-ray, hazy densities are sometimes noted approximately one month after injury, while the denser opacities eventually seen may not be apparent until two months have passed.

Approximately eight to 40 children are born in the United States each year with the malignant infantile type of osteopetrosis. One in every 100,000 to 500,000 individuals is born with this form of osteopetrosis. Higher rates have been found in Denmark and Costa Rica. Males and females are affected in equal numbers.

The adult type of osteopetrosis affects about 1,250 individuals in the United States. One in every 200,000 individuals is affected by the adult type of osteopetrosis. Higher rates have been found in Brazil. Males and females are affected in equal numbers.

The odds are greater in the Russian region of Mari El (1 of every 14,000 newborns) and much greater in Chuvashia (1 of every 3,500—4,000 newborns) due to genetic features of the Mari people and Chuvash people, respectively.

Endocrine disorder is more common in women than men, as it is associated with menstrual disorders.

Calcinosis may result from a variety of causes such as:

- Trauma to the region

- Inflammation (bug bites, acne)

- Varicose veins

- Infections

- Tumors (malignant or benign)

- Diseases of connective tissue

- Hypercalcemia

- Hyperphosphatemia

Calicinosis cutis is associated with systemic sclerosis.

Bone disease is common among the elderly individual, but adolescents can be diagnosed with this disorder as well. There are many bone disorders such as osteoporosis, Paget's disease, hypothyroidism. Although there are many forms of bone disorders, they all have one thing in common; abnormalities of specific organs involved, deficiency in vitamin D or low Calcium in diet, which results in poor bone mineralization.

Absorption of calcium salts normally occurs in bony tissues and is facilitated by parathyroid hormone and vitamin D. However, increased amounts of parathyroid hormone in the blood result in the deposit of calcium in soft tissues. This can be an indication of hyperparathyroidism, arteriosclerosis, or trauma to tissues.

Calcification of muscle can occur after traumatic injury and is known as myositis ossificans. It can be recognized by muscle tenderness and loss of stretch in the affected area. To reduce the risk of calcification after an injury, initiate what is commonly known as "RICE" (rest, ice, compression, and elevation).

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.

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.