J Periodontol 2002 May;73(5):511-6
Shapira L, Ayalon S, Brenner T.
Department of Periodontology, Faculty of Dental Medicine, Hadassah University Hospital and Hebrew University Medical Center, Jerusalem, Israel.
Several studies have suggested that peripheral inflammation may be involved in the etiology of multiple sclerosis (MS), a demyelinating disease of the central nervous system (CNS). T-cells activated in the periphery enter the CNS, leading to demyelination and axonal loss. We hypothesized that peripheral infection by Porphyromonas gingivalis can affect pathological processes in the CNS and aggravate MS.
Glial cells derived from rat brains were cultured and stimulated with P. gingivalis or P. gingivalis lipopolysaccharide (LPS). Secretion of nitric oxide (NO) and prostaglandin E2 (PGE2) was determined. In addition, we examined the proliferation of lymphocytes harvested from P. gingivalis-immunized mice in response to stimulation by echephalitogenic proteins. The effect of peripheral inflammation induced by P. gingivalis on the clinical course of the disease was tested in experimental autoimmune encephalomyelitis (EAE), a mouse model used for the study of MS.
P. gingivalis LPS and heat-killed bacteria induced secretion of the proinflammatory mediators NO and PGE2 by CNS glial cells. Lymphocytes derived from P. gingivalis-immunized mice proliferated in the presence of the echephalitogenic protein myelin basic protein. Injection of P. gingivalis into subcutaneous chambers in mice, followed by EAE induction led to aggravation of the disease.
The present study provides evidence that infection with a periodontal pathogen, such as P. gingivalis, may play a role in the pathogenesis of CNS inflammatory disorders such as MS.