Lyme Disease
Lyme Disease
Lyme Disease
The transition to
an advanced lesion signals the change to a chronic and successful defensive reaction to a destructive immunopathological mechanism, or periodontitis. Two schools of
thought seek to explain this progression: (1) involvement
of a host immune response and (2) involvement of a specific
microorganism in the plaque or a change in the organisms
virulence. The factors responsible for destructive periodontitis developing from reversible gingivitis are unknown.
Advanced periodontal lesions include pocket formation,
ulceration of the pockets epithelium, destruction of the
collagenous periodontal ligament, and bone resorption.
Teeth become mobile and can be lost. The inflammatory
infiltrate extends apically and laterally, reducing collagen
content and accumulating a dense population of lymphocytes, plasma cells, and macrophages. Reparative fibrosis is
noted peripherally, with destruction of the epithelial barrier
between plaque and periodontal connective tissue. As a
result, the loss of attachment becomes irreversible, with
loss of the periodontal ligament and bone and increased
pocket formation. Gingival crevicular fluid contains high
concentrations of IgG, IgA, IgM, complement, and polymorphs. Other notable changes include the inconsistent
invocation of antibodies that seem unable to protect from
disease, rising antibody titers during treatment related to
instrumentation inoculating antigens, and intrinsic mitogenicity or immunogenicity of plaque antigens rather than a
concentration of a single organism as the cause of disease.
The mediation of tissue damage relies more on
hypersensitivity-like responses such as antibody-mediated
cellular cytotoxicity and IgE-mediated hypersensitivity-like
reactions.
Bacteria can directly or indirectly damage tissues. Tissue
destruction can be caused by cytotoxic cellular immune responses to self or pro-inflammatory responses, such as the
release of interleukin 1b (IL-1b), tumor necrosis factor a
(TNF-a), and interleukin 6 (IL-6).
Clinical Significance.Future treatment strategies should take advantage of all that has
been learned about the pathogenesis of periodontal disease. Because the disease appears
to involve an imbalance between host and microbial influences, efforts should be made to
bolster host immune responses and other factors that will reduce the pathogenicity of oral
microorganisms. Many other possible courses
of action also suggest ways to avoid tissue
destruction and promote a healthy oral
environment.
Oral Medicine
Lyme disease
Background.The multisystemic inflammatory condition Lyme disease is caused by the spirochete Borrelia burgdorferi, which is carried on ticks and transmitted via their
bite. The facts about this disease are useful to dentists who
may be called on to manage oral manifestations (Table 1).
Incidence and Prevalence.Between 1992 and 1998
the US Centers for Disease Control and Prevention (CDC)
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Fig 1.Characteristic presentation of Borrelia burgdorferi tick bite. (Courtesy of Rhodus NL: Lyme disease. Northwest Dent 93:23-25, 2014.)
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Dental Abstracts
Clinical Significance.Dentists can take simple steps to help manage patients with Lyme
disease. Patients with suspicious symptoms
should be referred to their primary care provider for assessment. Patients who have been
diagnosed and are under treatment should
be asked about what medications they are taking and if their symptoms are sufficiently
controlled. Refractory responses to analgesics,
allergic reactions, excessive bleeding when
the patient is taking aspirin or non-steroidal
anti-inflammatory drugs, and the possibility
of cardiac disorders may complicate the delivery of dental care. Chair position may need to
be altered to make the patient comfortable. In
addition, surgical plans should include supplemental measures to control bleeding.
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