By Gary M. White, MD

Osteoma cutis is bone formation in the skin. It most commonly occurs in a secondary form in association with a pre-existing inflammatory skin condition, e.g. pilomatricoma, acne, nevus or dermatomyositis. In its primary form, it may be related to inactivating mutations of the GNAS gene, which have been associated with several disorders such as progressive osseous heteroplasia, Albright hereditary osteodystrophy, pseudohypoparathyroidism and fibrodysplasia ossificans progressiva. See also multiple miliary osteoma cutis of the face.

One study of 6500 CT scans of the head and neck [Dermatology Online Journal 2016;22;1] showed 2.27% had osteoma cutis of some type, with the multiple disseminated lesions (miliary type) far and away the most common (2%). Other variants described were as follows: multiple plate-like lesions, a single nodule, a single, plate-like lesions and a deep thread-like lesion.


A firm, hard plaque is felt in the skin. The lesions may occur anywhere, but have a predilection for sites around large joints and at areas of trauma. The lesions initially may be pinpoint in size and then enlarge, becoming many centimeters in diameter.

Congenital Plate-like osteoma cutis (CPLOC) is a larger osseous lesion present at birth. Although the scalp and extremities are commonly affected, any site may be involved.

Progressive osseous heteroplasia (POH) is a very rare genetic condition of progressive ectopic ossification. Most cases are caused by mutations of GNAS, the gene encoding the alpha subunit of the G-stimulatory protein of adenylyl cyclase. Onset is most common in the first year of life. The child develops hard dermal areas that over time coalesce into plaques with spread into deeper connective tissues including fascia, skeletal muscle, tendon, and ligament. Extensive ossification of the deep connective tissues can result in ankylosis of affected joints and growth retardation of involved limbs.

A 50-year-old man presented to the dermatology clinic at the Charles C. Harris Skin and Cancer Pavilion in June, 2010, for evaluation of multiple, thick, crusted plaques on his scalp and face. The lesions first appeared as small growths approximately 31 years ago. Over the past several years, they had been increasing in size and had spread to his chest and legs.


Radiology and/or biopsy may be performed to confirm the diagnosis. Serum calcium and parathyroid hormone levels rule out Albright’s hereditary osteodystrophy.


Surgical excision is needed. Larger lesions have required a split-thickness skin graft after removal [Dermatology 1999;198;209].


A case of giant primary osteoma cutis successfully treated with tissue expansion and surgical excision Indian J Dermatol Venereol Leprol 2011;77:79-81

Idiopathic acquired platelike osteoma cutis in a 50 yo man. Dermatology Online Journal 17(10)

Progressive osseous heteroplasia: diagnosis, treatment, and prognosis Appl Clin Genet. 2015; 8: 37–48

A 10-year-old girl presented with a stone-hard, round, erythematous, crusted, alopetic plaque that measured 6×7 cm on the right parietal region . This lesion was neither painful nor pruritic and was slowly evolving since she was a few months old. BMJ Case Rep. 2014; 2014


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