Osteoma cutis is little bits of calcium deposits under the skin (mine is where I had acne when I was younger.) I had dermabrasion many years ago, but the condition recurred because of the time it took for healing...it forms in scar tissue.
I would like to hear from anyone who has knowledge of the rare skin disorder, osteoma cutis. And treatments.?
Osteoma Cutis
Last Updated: February 15, 2005 Rate this Article
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Synonyms and related keywords: bone in the skin, Albright hereditary osteodystrophy, Albright's hereditary osteodystrophy, miliary osteomas
AUTHOR INFORMATION Section 1 of 9
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Author: Kevaghn P Fair, DO, Consulting Staff, Department of Pathology, Dominion Pathology Laboratories
Kevaghn P Fair, DO, is a member of the following medical societies: American Osteopathic Association, American Society of Clinical Pathologists, American Society of Dermatopathology, and College of American Pathologists
Editor(s): James W Patterson, MD, Director of Dermatopathology, Professor of Pathology and Dermatology, Departments of Pathology and Dermatology, University of Virginia Medical Center; David F Butler, MD, Professor, Texas A%26amp;M University College of Medicine; Director, Division of Dermatology, Scott and White Clinic; Rosalie Elenitsas, MD, Associate Professor of Dermatology, University of Pennsylvania School of Medicine; Director, Penn Cutaneous Pathology Services, Department of Dermatology, University of Pennsylvania Health System; Catherine Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University; and William D James, MD, Paul R Gross Professor of Dermatology, University of Pennsylvania School of Medicine; Vice-Chair, Program Director, Department of Dermatology, University of Pennsylvania Health System
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INTRODUCTION Section 2 of 9
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Background: Strictly defined, osteoma cutis refers to the presence of bone within the skin in the absence of a preexisting or associated lesion, as opposed to secondary types of cutaneous ossification that occur by metaplastic reaction to inflammatory, traumatic, and neoplastic processes.
Pathophysiology: Bone arises in skin and soft tissues through mesenchymal (membranous) ossification without cartilage precursors or models (enchondral ossification, as in the skeletal system).
The lesions of osteoma cutis differ from tumoral calcinosis in that they represent bone formation, and calcinosis refers to calcium salt deposits.
In addition to colonic polyposis, epidermal cysts of the face and the scalp, and multiple fibromas, osteomatosis in the form of intraosseous (not cutaneous) osteomas may develop within the membranous bones of the head in Gardner syndrome.
Frequency:
In the US: Although said to be rare, with no well-defined data on the incidence, a plethora of conditions and syndromes may be found in association with osteoma cutis, and the frequency of its occurrence varies accordingly. Primary lesions with no underlying cause are even more rare, but they account for approximately 20% of all cases.
Mortality/Morbidity: Osteoma cutis is not life threatening, although local discomfort and/or disfigurement may lead the patient to seek consultation.
Race: No race is predisposed to develop osteoma cutis.
Sex: 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.
Age: Osteoma cutis may occur at any age.
CLINICAL Section 3 of 9
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History:
Patients may report having hard areas in the skin.
A familial occurrence of Albright hereditary osteodystrophy may be present.
Physical:
The presentations of osteoma cutis can be highly variable, with clinical entities that are defined by the number, the form, and the location of the lesions.
Osteomas may present as single or multiple, extremely hard nodules, plaques, or miliary tumors.
The face, the extremities, the scalp, the digits, and the subungual regions are the most commonly affected sites.
Causes: Osteoma cutis is a feature in several groups of patients.
Albright hereditary osteodystrophy, which includes most patients with pseudohypoparathyroidism and pseudopseudohypoparathyroidism, is due to an autosomal dominant defect in the alpha subunit of intracellular guanyl nucleotide-binding protein (G protein).
The characteristic phenotype includes short stature, a round face, defective teeth, mental retardation, brachydactyly, and osteomas of the soft tissue and the skin.
Tetany is often the presenting sign of pseudohypoparathyroidism, formerly called Albright hereditary osteodystrophy. In addition to skeletal system abnormalities, lesions of osteoma cutis are frequently observed.
Single, small osteomas, arising later in life, sometimes with transepidermal elimination of bony fragments may be a cause.
Multiple, miliary osteomas of the face, following acne, neurotic excoriation, or dermabrasion is a possible cause.
Congenital plaquelike osteomatosis or limited dermal ossification is generally present from birth; the skin of the scalp or the extremities is often affected.
Fibrodysplasia ossificans heteroplasia and fibrodysplasia ossificans progressiva are possible causes.
Miscellaneous rare disorders with or without cartilaginous elements include osteomas of the distal extremities and multiple osteomas of childhood unrelated to Albright hereditary osteodystrophy.
DIFFERENTIALS Section 4 of 9
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Calcinosis Cutis
Other Problems to be Considered:
Cartilaginous tumors of the skin
Foreign body
Gouty tophus
Myositis ossificans
Secondary (heterotopic) ossification
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WORKUP Section 5 of 9
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Lab Studies:
Serum calcium and parathyroid hormone (PTH) levels help to define Albright hereditary osteodystrophy.
Imaging Studies:
Plain radiographs demonstrate lesions but are not necessary for diagnosis.
Procedures:
Excisional biopsy for diagnosis, relief of discomfort, or cosmesis may be performed.
Histologic Findings: Small spicules to large masses of mature bone are found in the dermis or extend into the subcutaneous tissue. Spicules of bone may enclose areas of mature fat, recapitulating a medullary cavity, but hematopoietic elements are seldom observed (see Image 3).
TREATMENT Section 6 of 9
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Medical Care:
Removal by excision or laser resurfacing to unroof overlying skin may be performed. Treatment with the Er:YAG laser may result in less hypopigmentation and scarring than with the carbon dioxide laser.
Other reported treatments with unproven efficacy include the following:
Topical application of tretinoin to provoke transepidermal elimination
Etidronate disodium taken orally
Consultations: When several lesions are noted, especially in pediatric patients, evaluation for associated syndromes may be warranted. FOLLOW-UP Section 7 of 9
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Prognosis:
Osteosarcoma or other malignancies have not been reported to arise within osteoma cutis.
PICTURES Section 8 of 9
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Caption: Picture 1. Solitary nodule on the frontal part of the scalp.
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Caption: Picture 2. Miliary cutaneous osteomata. Multiple, small, bluish, stony-hard nodules in an acneiform distribution along the cheeks.
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Caption: Picture 3. A microscopic view of osteoma cutis shows well-formed mature trabecular bone just beneath the epidermis. Note the absence of hematopoietic elements in the medullary spaces.
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BIBLIOGRAPHY Section 9 of 9
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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].
Burgdorf W, Nasemann T: Cutaneous osteomas: a clinical and histopathologic review. Arch Dermatol Res 1977 Dec 12; 260(2): 121-35[Medline].
Cohen AD, Chetov T, Cagnano E, et al: 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].
Ragsdale BD: Lever's Histopathology of the Skin. Philadelphia, Pa: Lippincott-Raven; 1997: 965-7.
Roth SI, Stowell RE, Helwig EB: Cutaneous ossification. Report of 120 cases and review of the literature. Arch Pathol 1963; 76(1): 44-54[Medline].
Watsky KL: In: Arndt KA, ed. Cutaneous Medicine and Surgery. Philadelphia, Pa: WB Saunders; 1996: 1828-31.
Weedon D, ed: Skin Pathology. 2nd ed. New York, NY: Churchill Livingstone; 2002: 355-7.
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