These results demonstrate that periodontal lesions induced with different A. actinomycetemcomitans serotypes elicited distinct alveolar bone resorption and immune response. In particular, serotype b was more pathogenic than the others and induced stronger Th1 and Th17 patterns of immune responses during experimental periodontitis.

No abstract

Detection of extracellular matrix component-derived fragments produced during periodontal tissue destruction, such as LMW-HA, could explain at least partly unsuccessful periodontal treatment and the chronicity of the disease.