Evidence for Borrelia burgdorferi in morphea and lichen sclerosus

Özkan, Şebnem; Atabey, Neşe; Fetil, Emel; Erkizan, Verda; Güneş, Ali

doi:10.1046/j.1365-4362.2000.00912.x

Cited by 64 publications

(33 citation statements)

References 53 publications

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“…Some authors consider these diseases separate entities, and others suggest that lichen sclerosus is a superficial variant of morphea. [28][29][30] This suggestion is strengthened by observations that both morphea and lichen sclerosus may be induced by infection with Borrelia burgdorferi [31][32][33][34] and similar changes are associated with graftversus-host-disease (GVHD). In chronic GVHD the initial skin lesions are of lichen planus type, followed by sclerotic plaques mimicking morphea and/or lichen sclerosus, sometimes generalized morphea, occasionally even with internal involvement.…”

mentioning

confidence: 97%

Alterations of Basement Membrane Zone and Cutaneous Microvasculature in Morphea and Extragenital Lichen Sclerosus

Kowaléwski

Kozłowska²,

Górska³

et al. 2005

The American Journal of Dermatopathology

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The aim of this study was to compare alterations of the basement membrane zone (BMZ) and to visualize changes within the skin vascular network in morphea and extragenital lichen sclerosus with the use of laser scanning confocal microscopy. This work was performed in eight plaques of morphea (three active and five inactive) and eight of lichen sclerosus (three of short duration and five long-lasting). Biopsy specimens from six healthy individuals served as controls. The biopsies were cut into 40-microm-thick sections, labeled with antibodies against beta4-intergin (a lamina lucida marker), collagen IV, and the N-terminal end of collagen VII (lamina densa markers) and C-terminal end of collagen VII (a sublamina densa marker) and studied using laser scanning confocal microscopy. Three-dimensional reconstruction of various regions of the BMZ showed a decreased number and size of the dermal papillae both in morphea and lichen sclerosus compared with normal skin. In morphea, the continuity of the BMZ at the level of lamina lucida, lamina densa, and sublamina densa was preserved whereas in LS numerous invaginations and holes were present in the BMZ at the level of the lamina lucida and lamina densa. Thus the alterations of the BMZ in morphea differ from those in lichen sclerosus. Three-dimensional reconstruction of the skin vascular network showed increased angiogenesis only in the early inflammatory stage of morphea, whereas in inactive morphea and lichen sclerosus various numbers of enlarged vessels were visible. The changes in the vascular network in morphea appear to be related to the activity of the disease.

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mentioning

confidence: 97%

Alterations of Basement Membrane Zone and Cutaneous Microvasculature in Morphea and Extragenital Lichen Sclerosus

Kowaléwski

Kozłowska²,

Górska³

et al. 2005

The American Journal of Dermatopathology

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“…Concerning the association between Borrelia and lichen, in 1985, Asbrink wrote that “a Borrelia infection may result in lichen sclerosus et atrophicus-like reactions” (54), a claim that was subsequently supported by others (55–59). Although the debate remains open, a pathogenic link between borreliosis and lichen seems to exist in some cases (60).…”

Section: Resultsmentioning

confidence: 99%

Thyroid Autoimmunity and Lichen

et al. 2017

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Lichen planus (LP) and lichen sclerosus (LS) are cutaneous-mucous diseases with uncertain epidemiology. Current data, which are likely to be underestimated, suggest a prevalence in the general population of 0.1–4% for cutaneous LP, 1.27–2.0% for oral LP, and 0.1–3.3% for LS. While etiology of lichen is still unknown, clinical and histological evidence show an (auto)immune pathogenesis. Association of lichen with autoimmune thyroid disease (AITD) has been investigated in few studies. This association appears better defined in the case of LS, while is more controversial for LP. In both situations, the frequency of the association is higher in females. We review the available literature on the correlation between the different types of lichen and AITD, and the literature on the genetic risk factors which are shared by both conditions. Such data suggest that a common pathogenic mechanism could be the cause for co-occurrence of lichen and AITD, at least in some patients. Additionally, analyzing literature data and in continuity with our previous work on other autoimmune diseases, we suggest that molecular mimicry could trigger both diseases, and thus explain their co-occurrence.

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“…Additionally, an earlier study found 38% of seropositive (n=5) and 23% of seronegative (n=26) patients with morphea exhibited elevated B.burgdorferi induced lymphocyte proliferation, supporting a causal role, at least for some patients with morphea [26]. One study in Western Turkey (n=10 subjects with morphea and n=12 subjects with lichen sclerosus) found the presence of Bb DNA in 30% of morphea and 50% of lichen sclerosus patients suggesting a potential role in both conditions [27]; whereas, another study conducted in the U.S.A. (n = 35) did not find Bb spirochete in the pathogenesis of morphea and lichen sclerosus [28]. A more recent study reviewing the causal role of Bb in morphea concluded that previous conflicting results of European and American scientists could either be due to the fact that Bb is not a causative agent for morphea or that a subset of morphea is caused by a special subspecies of Bb present in Europe and Asia but not the U.S.A [29].…”

Section: Introductionmentioning

confidence: 94%

Infections Are Not Increased in Scleroderma Compared to Non-Inflammatory Musculoskeletal Disorders Prior to Disease Onset

Pope¹,

Goodwin²,

Ouimet³

et al. 2007

TORJ

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Abstract:The etiology of scleroderma (SSc) is unknown; immunogenic stimuli such as infections and vaccinations could theoretically be risk factors for scleroderma. Our objective was to assess the relationship between viral and bacterial infections, and vaccinations, prior to diagnosis of SSc compared to non-inflammatory controls. Methods: A questionnaire was sent to individuals with SSc (n =83) and controls (n=351) with non-inflammatory musculoskeletal (MSK) disorders (osteoarthritis, n = 204; tendonitis, n = 58; fibromyalgia, n= 89) from a rheumatology practice. Questions ascertained past infections, exposure to infectious agents and vaccination history. Results: The response rate was 78% (SSc) and 56% (MSK controls). The mean age was 56 ± 1.6 (SSc) and 58 ± 0.9 (MSK); 88% (SSc) and 82% (MSK) were female. No association between prior infections and SSc was observed. In fact, controls were more likely than SSc subjects to report any infection within 1-year prior to disease diagnosis (35% vs. 16%, p<0.006), or to have suffered a trauma to affected joints prior to diagnosis (44% vs. 19%, p<0.0002). Within the 1-year prior to disease diagnosis, controls reported slightly more streptococcal infections (p<0.2), infections with diarrhea and vomiting (p<0.3), and antibiotic use (p<0.09), although none of these results were statistically significant. Histories of any hepatitis, rubella, any bacterial infection, and having had a previous positive tuberculosis skin test were not significantly different between groups and were actually more often reported by the control subjects. SSc reported slightly more hepatitis B (p<0.08), more rheumatic fever (p<0.8) in past, and herpes zoster (p<0.4), although no differences reached significance. Conclusion: This study does not support that self-report of symptomatic infections are more likely to occur ever (prior to diagnosis) or within 1-year prior to symptom onset of SSc, or that vaccinations in adulthood trigger SSc.

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Evidence for Borrelia burgdorferi in morphea and lichen sclerosus

Abstract: The data obtained in this study suggest that Bb may play a role in the etiopathogenesis of both morphea and lichen sclerosus at least in the western parts of Turkey.

Cited by 64 publications

References 53 publications

Alterations of Basement Membrane Zone and Cutaneous Microvasculature in Morphea and Extragenital Lichen Sclerosus

Alterations of Basement Membrane Zone and Cutaneous Microvasculature in Morphea and Extragenital Lichen Sclerosus

Thyroid Autoimmunity and Lichen

Infections Are Not Increased in Scleroderma Compared to Non-Inflammatory Musculoskeletal Disorders Prior to Disease Onset

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