Clinical and laboratory study
Borrelia burgdorferi DNA is undetectable by polymerase chain reaction in skin lesions of morphea, scleroderma, or lichen sclerosus et atrophicus of patients from North America

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Abstract

Background:, Borrelia burgdorferi has been linked to the pathogenesis of morphea and lichen sclerosus et atrophicus (LSA). However, considerable controversy still exists as to the actual role, if any, that this spirochete plays in the development of these diseases. Antibody titer determinations have been inconclusive and polymerase chain reaction (PCR) studies have yielded conflicting results.

Objective: We sought to show whether PCR analysis detected B. burgdorferi in archival tissue specimens from the involved skin of 20 North American patients with morphea, 10 patients with LSA, and four patients with scleroderma.

Methods: We used two different sets of PCR primers for the B. burgdoferi flagellin gene, one specific for European strains of B. burgdorferi, and another common to both European and American strains. A subset of these samples were further amplified with nested PCR primers.

Results: None of the samples showed PCR products with either primer sets, whereas purified B. burgdorferi DNA and lesional erythema chronicum migrans tissues, which were used as positive controls, yielded easily detectable products with all primer sets.

Conclusion: These data suggest that B. burgdorferi infection plays no role in the development of morphea, LSA, or scleroderma in North American patients; these findings further support the recent observations that B. burgdorferi strain variability is associated with differential spectra of disease in North America compared with that found in various parts of Europe.

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Presented at the Society for Investigative Dermatology annual meeting, Washington, D.C., April 28–May 1, 1993.

Dr. Dillon received a grant from the Henry Ford Hospital Medical Education Resident Research Award.

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