The aetiology of morphoea and lichen sclerosus ct atrophicus is still unkno
wn. Since the detection of Borrelia burgdorferi (B. burgdorferi) as the cau
sative agent of Lyme disease, there has been debate about a possible associ
ation between B. burgdorferi and morphoea. Initial serological and cultural
studies showed controversial results, The introduction of polymerase chain
reaction (PCR) initially suggested an association between B. burgdorferi a
nd morphoea. We reviewed the literature on B. burgdorferi (specific serolog
y, immunohistology culture, lymphocyte stimulation and DNA detection by PCR
) since 1983, using Medline and Current Contents, Histological and immunohi
stological detection of B. burgdorferi was reported in 0-40% (20 of 82) of
the cases with morphoea and in 46-50% (17 of 36) of the cases with lichen s
clerosus et atrophicus. Cultivation of spirochetes from lesional skin succe
eded in five patients (five of 68) with morphoea, but failed in patients wi
th lichen sclerosus ct atrophicus. In Europe and Asia, serological detectio
n of antibodies against B. burgdorferi was described in 0-60% (138 of 609)
of patients with morphoea and in 19% (six of 32) in the U.S.A. For lichen s
clerosus et atrophicus 0-25% of the published cases (three of 23) in Europe
and Asia were seropositive. DNA from B. burgdorferi was detected by PCR in
0-100% (17 of 82) of the tissues of patients with morphoea in Europe and A
sia, but not a single case among 98 patients was reported to be positive fr
om the U.S.A. In Europe and Asia, borrelial DNA was detected in 0-100% (nin
e of 38) of the cases with lichen sclerosus ct atrophicus, whereas in the U
.S.A. none of 48 patients was positive. There are two possible explanations
for these contradictory findings: the most likely is that B. burgdorferi i
s not a causative agent for morphoea. Another possible explanation could be
that a subset of morphoea is caused by a special subspecies of B. burgdorf
eri that is present in Europe and Asia but does not occur In the U.S.A.