The radiological features of myositis ossificans are ‘faint soft tissue calcification within 2–6 weeks, (may have well-defined

bony margins by 8 weeks) separated from periosteum by lucent zone and on CT, the characteristic feature is peripheral ossification’.

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

Ectopic calcification is a pathologic deposition of calcium salts in tissues or bone growth in soft tissues. This can be a symptom of hyperphosphatemia. Formation of osseous tissue in soft tissues such as the lungs, eyes, arteries, or other organs is known as ectopic calcification, dystrophic calcification, or ectopic ossification.

Calcification is typically depicted 2 weeks earlier by ultrasound (US) when compared to radiographs. The lesion develops in two distinct stages with different presentations at US. In the early stage, termed immature, it is depicts a non-specific soft tissue mass that ranges from a hypoechoic area with an outer sheet-like hyperechoic peripheral rim to a highly echogenic area with variable shadowing. In the late stage, termed mature, myositis ossificans is depicted as an elongated calcific deposit that is aligned with the long-axis of the muscle, exhibits acoustic shadowing, and has no soft tissue mass associated. US may suggest the diagnosis at early stage, but imaging features need to evolve with successive maturation of the lesion and formation of the characteristic late stage changes before they become pathognomonic.

The differential diagnosis includes many tumoral and nontumoral pathologies. A main concern is to differentiate early myositis ossificans from malignant soft-tissue tumors, and the latter is suggested by a fast-growing process. If clinical or sonographic findings are dubious and extraosseous sarcoma is suspected, biopsy should be performed. At histology, detection of the typical zonal phenomenon is diagnostic of myositis ossificans, though microscopic findings may be misleading during the early stage.

The most common type of calcinosis is dystrophic calcification. This type of calcification can occur as a response to any soft tissue damage, including that involved in implantation of medical devices.

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

Treatment may involve surgery, which is currently the only recommended intervention. Surgery should include the removal of even small nodules, to prevent the recurrence of the scrotal calcinosis.

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.

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%.

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.

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.

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.

Epidemiology

- Incidence: uncommon

- Age: children and young adults

Site

- Scrotal skin

Presentation

- Single or multiple hard, marble-like nodules of varying size affecting scrotal skin.

- Nodules vary in size from a few millimeters to a few centimeters.

- Usually start to appear in childhood or early adult life

- Over time, nodules increase in number and size

- Nodules may break down and discharge chalky material

- Rarely, lesions may be polypoid

- Usually asymptomatic

Treatment

- Symptomatic single or grouped nodules can be excised surgically

Prognosis

- Benign condition

- Slow progression throughout life

- Lesions remain discrete and do not become confluent

There is no diagnostic test for calciphylaxis. The diagnosis is a clinical one. The characteristic lesions are the ischemic skin lesions (usually with areas of skin necrosis). The necrotic skin lesions (i.e. the dying or already dead skin areas) typically appear as violaceous (dark bluish purple) lesions and/or completely black leathery lesions. They can be extensive. The suspected diagnosis can be supported by a skin biopsy. It shows arterial calcification and occlusion in the absence of vasculitis. Sometimes the bone scintigraphy can show increased tracer accumulation in the soft tissues. In certain patients, anti-nuclear antibody may play a role.

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

The most common locations are the shaft and epyphises of long bones (fibula and humerus) but the spine, metatarsal bones, and ilium have been involved as well. Radiologic examination evidences osteolytic areas with a lobulated framework comprising radiolucent and radiodense foci admixed to speckled calcification. Cortical destruction is a common finding with no soft tissue expansion in many cases. Histopathology of the lesion shows large areas of mature fibrous stroma undergoing hyaline cartilage metaplasia resulting in conspicuous lobules or gradual transformation into chondroid foci. Both hyaline cartilage and chondroid in turn undergo calcification and endochondral cancellous bone formation mimicking epiphyseal plate-like cartilage.

Differential diagnosis is concerned with fibrocartilaginous dysplasia of bone, desmoplastic fibroma, low-grade fibrosarcoma, chondromyxoid fibroma and low-grade chondrosarcoma.

A full account of imaging findings on radiography, bone scan, CT and magnetic resonance has been provided by Sumner et al.

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.

Metastatic calcification is deposition of calcium salts in otherwise normal tissue, because of elevated serum levels of calcium, which can occur because of deranged metabolism as well as increased absorption or decreased excretion of calcium and related minerals, as seen in hyperparathyroidism.

In contrast, dystrophic calcification is caused by abnormalities or degeneration of tissues resulting in mineral deposition, though blood levels of calcium remain normal. These differences in pathology also mean that metastatic calcification is often found in many tissues throughout a person or animal, whereas dystrophic calcification is localized.

Metastatic calcification can occur widely throughout the body but principally affects the interstitial tissues of the vasculature, kidneys, lungs, and gastric mucosa. For the latter three, acid secretions or rapid changes in pH levels contribute to the formation of salts.

Often Mönckeberg's arteriosclerosis is discovered as an incidental finding in an X-ray radiograph, on mammograms, in autopsy, or in association with investigation of some other disease, such as diabetes mellitus or chronic kidney disease. Typically calcification is observed in the arteries of the upper and lower limb although it has been seen in numerous other medium size arteries. In the radial or ulnar arteries it can cause "pipestem" arteries, which present as a bounding pulse at the end of the calcific zone. It may also result in "pulselessness." Epidemiological studies have used the ratio of ankle to brachial blood pressure (ankle brachial pressure index, ABPI or ABI) as an indicator of arterial calcification with ABPI >1.3 to >1.5 being used as a diagnostic criterion depending on the study.

Hydrops-ectopic calcification-moth-eaten skeletal dysplasia is a defect in cholesterol biosynthesis. It is also known as Greenberg dysplasia. Greenberg characterized the condition in 1988.

It has been associated with the lamin B receptor.

The diagnosis of hyperphosphatemia is made through measuring the concentration of phosphate in the blood. A phosphate concentration greater than 1.46 mmol/L (4.5 mg/dL) is indicative of hyperphosphatemia, though further tests may be needed to identify the underlying cause of the elevated phosphate levels.

The calcific deposits are visible on X-ray as discrete lumps or cloudy areas. The deposits look cloudy on X-ray if they are in the process of reabsorption, and this is also when they cause the most pain. The deposits are crystalline when in their resting phase and like toothpaste in the reabsorptive phase. However, poor correlation exists between the appearance of a calcific deposit on plain X-rays and its consistency on needling. Ultrasound is also useful to depict calcific deposits and closely correlates with the stage of disease.

Diagnosis is usually made upon inspection. Differential diagnosis of tonsilloliths includes foreign body, calcified granuloma, malignancy, an enlarged temporal styloid process or rarely, isolated bone which is usually derived from embryonic rests originating from the branchial arches.

Tonsilloliths are difficult to diagnose in the absence of clear manifestations, and often constitute casual findings of routine radiological studies.

Imaging diagnostic techniques can identify a radiopaque mass that may be mistaken for foreign bodies, displaced teeth or calcified blood vessels. Computed tomography (CT) may reveal nonspecific calcified images in the tonsillar zone. The differential diagnosis must be established with acute and chronic tonsillitis, tonsillar hypertrophy, peritonsillar abscesses, foreign bodies, phlebolites, ectopic bone or cartilage, lymph nodes, granulomatous lesions or calcification of the stylohyoid ligament in the context of Eagle syndrome (elongated styloid process).

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.

In those with calcific tendinitis of the shoulder high energy extracorporeal shock-wave therapy (which uses sound waves) can be useful. It is not useful in other types of tendinitis. This procedure may be known as .