Pathogenesis: Primary forms of osteoma cutis show intramembranous ossification that is centered within the dermis. There is no preceding cartilage formation to act as a scaffolding for the bone to form. The exact cause is unknown. The G protein that is defective in Albright’s hereditary osteodystrophy has been found to be important in bone regulation. The precise reason why some areas of skin are involved while others are left intact in this genetic disease is not well understood.
Histology: Areas of bone formation are seen ectopically in the dermis or subcutaneous tissue. The bone is formed by an intramembranous mechanism without the assistance of a preceding cartilage scaffolding.
Treatment: Secondary osteoma cutis can be removed with a number of surgical techniques. Creation of a small, nick-like incision over the area of osteoma formation and removal with a small curette or laser resurfacing has produced the best results. This treatment can be very time-consuming and labor intensive in cases of multiple secondary osteoma cutis (e.g., in some cases of acne-associated osteoma cutis).
The treatment of primary plaque-like osteoma cutis is surgical removal. Albright’s heriditary osteodystrophy and fibrodysplasia ossificans progressiva are rare diseases that require a multidisciplinary approach at centers with experience treating these conditions.
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