The current knowledge on the cellular, host-response features in juvenile periodontitis (JP) has been reviewed. The chemotaxis of the polymorphonuclear leukocytes (PMNs), known to be defective in JP, is modulated by serum factors and bacteria. The interactions of the putative etiologic pathogen Actinobacillus actinomycetemcomitans (A.a.) and the enzyme lysozyme with PMNs modify the host defense. Data on the phagocytic capacity of the peripheral blood and gingival crevice PMNs in JP are still controversial. The monocytes exhibit similar alterations as PMNs in interaction with A.a., but the reports on defective monocyte chemotaxis are conflicting. Both bacterial challenge and genetic factors may regulate the lymphocyte response in JP.
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Leena Sandholm (1985) studied this question.
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