etiology period on tit is
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8/2/2019 Etiology Period on Tit Is
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Foods Food Ingredients J. Jpn., Vol. 210, No.4, 2005
Pa th ogenesis an d Symptoms of Hu ma n P eriodont al Diseases
Shigenobu KimuraDepartment of Oral Microbiology, Iwate Medical University School of Dentistry
1-3-27, Chu odori, m orioka-shi, Iwa te 020-8505, J apa n
Summary
Although periodontal diseases are initiated by oral bacteria, it is also evident that the host
response plays a ma jor r ole in th e out come of th ese infections. This review addressed t hose un ique
host-para site intera ctions in t he pat hogenesis and sympt oms of human periodont al diseases.
Early studies on the pathogenic potential of plaque bacteria incriminated some selected
gram-negative organisms (periodontopathogens), especially Porphyromonas gingivalis and
Actinobacillus actinomycetemcomitans as major pathogens of adult and juvenile periodontitis,
respectively. However, our cross-sectional study in periodontally healthy children indicated the
colonizat ion of ma ny pu ta tive periodont opath ogens (with out clinical signs of periodont al disea se)
against the host defense mechan ism by saliva. Thus, it is possible th at th e saliva a s a host defense
mechan ism could in hibit more effectively the proliferat ion of colonized pat hogens t ha n th e initia l
colonization of organisms to gingival crevices. The polymorphonuclear leucocyte (PMNL) that is
the predominant cell of the gingival crevicular and pocket exudates acts as another host defense
mechan ism in gingival crevices. Substant ial reports indicat ed th at patients with P MNL disorders
have unusually rapid and severe periodontitis. We previously demonstrated that about 50% of the
pat ients wit h localized juvenile and gener alized juvenile periodontitis, but not a dult periodont itis,
exhibited depression of phagocytic function of the peripheral blood PMNL. Therefore, defective
PMNL function could be implicated in the pathogenesis of periodontitis, especially in juvenile
periodontitis.
The colonized periodont opat hogens could in vade/penetra te t he epith elial cells into gingival t issues.
In gingival tissues, the evasive action by the virulent components, such as lipopolysaccharide
(LPS) and proteases, of periodontopathogens against host defense mechanisms might be crucial
steps in leading tissue destruction and alveolar bone resorption. We indicated the unique
activation pathways of B cells by P. gingivalis LPS and the impairment in regulatory T cell
fun ction in adu lt periodont itis. Fur th er, th e alter at ion in r egulat ory T cell fun ction could be relat ed
to senescence.
The precise basis for the host-parasite interaction is still not understood, however, evidence
indicates th e cent ra l role of th e relationsh ip between the host defense mecha nism a nd virulence of
periodont al pat hogens in initiat ion an d development of periodont al diseases.