Osteoma Cutis
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Strictly defined, osteoma cutis refers to the presence of bone within the skin in the absence of a preexisting or associated lesion. This is opposed to secondary types of cutaneous ossification that can occur in reaction to inflammatory, traumatic, and neoplastic processes. [1, 2]
Bone arises in skin and soft tissues through mesenchymal (membranous) ossification without cartilage precursors or models (as in endochondral ossification of the skeletal system).
The lesions of osteoma cutis differ from calcinosis cutis in that they represent bone formation (dermal deposition of hydroxyapatite crystals) versus calcium salt deposits.
The pathogenesis of primary osteoma cutis has the following two proposed mechanisms [3] :
Through mesenchymal cells differentiating into osteoblasts and then migrating to an abnormal location
Through an osteoblastic metaplasia of mesenchymal cells already in the dermis, such as fibroblasts
Osteoma cutis can be a feature of several groups of patients. In can be secondary to inflammatory skin diseases, trauma/scars, and cutaneous tumors. It can also occur with genetic syndromes or in isolation.
Albright hereditary osteodystrophy is due to an autosomal dominant defect in the alpha subunit of intracellular G proteins. [4] The characteristic phenotype includes short stature, round facies, defective teeth, mental retardation, brachydactyly (fourth and fifth metacarpals/”knuckle knuckle dimple dimple” of the Archibald sign), and osteomas of the soft tissue and the skin. Classically, it presents with pseudohypoparathyroidism (elevated parathyroid hormone [PTH], hypocalcemia, hyperphosphatemia secondary to renal PTH resistance). Tetany is often the presenting sign, secondary to the low calcium level. Albright hereditary osteodystrophy can cause osteoma cutis without endocrine abnormalities in the pseudo-pseudohypoparathyroidism variant.
Progressive osseous heteroplasia is also, like Albright hereditary osteodystrophy, associated with a defect in the alpha subunit of G proteins (GNAS1 gene). It is characterized by ossification of the dermis in infancy, with progression to the subcutaneous and deeper connective tissues throughout childhood. It is not associated with endocrine changes, but it can have a severe affect on growth and joint mobility. [5]
Congenital platelike osteomatosis, a type of primary osteoma cutis, meets the following criteria:
Lesion present at birth (or within first year of life)
No evidence of abnormal calcium or phosphorous metabolism
No evidence of trauma or infection
Presence of at least one bony plate
Congenital platelike osteomatosis is most commonly found on the scalp. It should be monitored, as its diagnosis could be representative of a slow-evolving progressive osseous heteroplasia (something with much more severe consequences). [6]
Fibrodysplasia ossificans heteroplasia and fibrodysplasia ossificans progressiva (stone man syndrome) are possible causes.
Osteoma cutis can be found in patients with Gardner syndrome, which includes colonic polyposis, retinal hyperplasia, and other osseous and soft tissue growths.
Multiple miliary osteomas of the face often present in patients with a history of severe acne, sunburn, neurotic excoriation, or dermabrasion. These small, hard papules can have a bluish hue, especially in patients who have been exposed to tetracycline treatment. [7, 8]
Although considered rare, with no well-defined data on incidence, a plethora of conditions and syndromes may be found in association with osteoma cutis. Hence, the frequency of its occurrence varies accordingly. Primary lesions with no underlying cause are even rarer, but they account for approximately 20% of all skin ossifications. Reported in 1977, of 20,000 consecutive skin biopsies, only 35 cutaneous osteomas were found. Ten of them were primary, while 25 appeared secondary to another abnormality (although long ago, this allows some insight into its rarity). [1, 2]
No particular race is predisposed to developing osteoma cutis.
Generally, no distinct sexual predominance exists. However, one cause of osteoma cutis, Albright hereditary osteodystrophy, occurs with a female-to-male ratio of 2:1.
Osteoma cutis may occur at any age. Of note, multiple miliary osteoma cutis classically presents in middle-aged white women. [7]
Osteoma cutis is not life threatening, although local discomfort and/or disfigurement may lead the patient to seek consultation. Osteosarcoma or other malignancies have not been reported to arise within osteoma cutis.
Burgdorf W, Nasemann T. Cutaneous osteomas: a clinical and histopathologic review. Arch Dermatol Res. 1977 Dec 12. 260(2):121-35. [Medline].
Roth SI, Stowell RE, Helwigeb. Cutaneous ossification. Report of 120 cases and review of the literature. Arch Pathol. 1963 Jul. 76:44-54. [Medline].
Talsania N, Jolliffe V, O’Toole EA, Cerio R. Platelike osteoma cutis. J Am Acad Dermatol. 2011 Mar. 64(3):613-5. [Medline].
Ward S, Sugo E, Verge CF, Wargon O. Three cases of osteoma cutis occurring in infancy. A brief overview of osteoma cutis and its association with pseudo-pseudohypoparathyroidism. Australas J Dermatol. 2011 May. 52(2):127-31. [Medline].
Coutinho I, Teixeira V, Cardoso JC, Reis JP. Plate-like osteoma cutis: nothing but skin and bone?. BMJ Case Rep. 2014 May 5. 2014:[Medline].
Worret WI, Burgdorf W. [Congenital, plaque-like osteoma of the skin in an infant]. Hautarzt. 1978 Nov. 29(11):590-6. [Medline].
Chabra IS, Obagi S. Evaluation and management of multiple miliary osteoma cutis: case series of 11 patients and literature review. Dermatol Surg. 2014 Jan. 40(1):66-8. [Medline].
Riahi RR, Cohen PR. Multiple miliary osteoma cutis of the face after initiation of alendronate therapy for osteoporosis. Skinmed. 2011 Jul-Aug. 9(4):258-9. [Medline].
Cohen PR, Tschen JA, Schulze KE, Martinelli PT, Nelson BR. Dermal plaques of the face and scalp. Platelike osteoma cutis. Arch Dermatol. 2007 Jan. 143(1):109-14. [Medline].
Wang JF, O’Malley DP. Extramedullary acute leukemia developing in a pre-existing osteoma cutis. J Cutan Pathol. 2014 Jul. 41 (7):606-11. [Medline].
Altman JF, Nehal KS, Busam KJ, Halpern AC. Treatment of primary miliary osteoma cutis with incision, curettage, and primary closure. J Am Acad Dermatol. 2001 Jan. 44(1):96-9. [Medline].
Kim SY, Park SB, Lee Y, Seo YJ, Lee JH, Im M. Multiple miliary osteoma cutis: treatment with CO(2) laser and hook. J Cosmet Laser Ther. 2011 Oct. 13(5):227-30. [Medline].
Cohen AD, Chetov T, Cagnano E, Naimer S, Vardy DA. Treatment of multiple miliary osteoma cutis of the face with local application of tretinoin (all-trans-retinoic acid): a case report and review of the literature. J Dermatolog Treat. 2001 Sep. 12(3):171-3. [Medline].
Baskan EB, Turan H, Tunali S, Toker SC, Adim SB, Bolca N. Miliary osteoma cutis of the face: treatment with the needle microincision-extirpation method. J Dermatolog Treat. 2007. 18(4):252-4. [Medline].
Weedon D, ed. Skin Pathology. 2nd ed. New York, NY: Churchill Livingstone; 2002. 355-7.
Luke Lennox, MD Resident Physician, Department of Dermatology, Case Western Metro Health Medical Center
Disclosure: Nothing to disclose.
Thomas N Helm, MD Clinical Professor of Dermatology and Pathology, University of Buffalo, State University of New York School of Medicine and Biomedical Sciences; Director, Buffalo Medical Group Dermatopathology Laboratory
Thomas N Helm, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Society for Dermatologic Surgery, American Society of Dermatopathology
Disclosure: Nothing to disclose.
David F Butler, MD Former Section Chief of Dermatology, Central Texas Veterans Healthcare System; Professor of Dermatology, Texas A&M University College of Medicine; Founding Chair, Department of Dermatology, Scott and White Clinic
David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Society for MOHS Surgery, Association of Military Dermatologists, Phi Beta Kappa
Disclosure: Nothing to disclose.
Rosalie Elenitsas, MD Herman Beerman Professor of Dermatology, University of Pennsylvania School of Medicine; Director, Penn Cutaneous Pathology Services, Department of Dermatology, University of Pennsylvania Health System
Rosalie Elenitsas, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, American Society of Dermatopathology, Pennsylvania Academy of Dermatology
Disclosure: Received royalty from Lippincott Williams Wilkins for textbook editor.
William D James, MD Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine
William D James, MD is a member of the following medical societies: American Academy of Dermatology, Society for Investigative Dermatology
Disclosure: Received income in an amount equal to or greater than $250 from: Elsevier; WebMD.
James W Patterson, MD Professor of Pathology and Dermatology, Director of Dermatopathology, University of Virginia Medical Center
James W Patterson, MD is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, American Society of Dermatopathology, Royal Society of Medicine, Society for Investigative Dermatology, United States and Canadian Academy of Pathology
Disclosure: Nothing to disclose.
Kevaghn P Fair, DO Consultant Pathologist and Founder, Dominion Pathology Laboratories
Kevaghn P Fair, DO is a member of the following medical societies: American Society for Clinical Pathology, American Society of Dermatopathology, and College of American Pathologists
Disclosure: Nothing to disclose.
Osteoma Cutis
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