Sandholm, L. The Cellular Host Response in Juvenile Periodontitis. A Review. J Periodontol, 56:359, 1985

Lit. Review: PMNs chemotaxis defects is modulated by serum factors and bacteria.

• AA and Lysozyme interaction with PMNs may modify the host defense.
• Monocytes exhibit similar alterations as PMNs in interaction with AA.
• Bacterial & genetic factors may regulate the lymphocyte response in JP.

Findings of PMNs defects

• Random migration & deformability are normal, adherence is normal or slightly elevated.
• 75% of LJP pats has depressed chemotaxis activity of PMNs. Defect is mostly intrinsic to the PMN cell, long lasting and found also in healthy siblings.
• The JP PMNs have a reduced number of binding sites for a chemotactic peptide (formyl-methionyl-leucyl-phenylalanine =FMLP).
• PMNs have reduced density of binding site for C5a.
• Drugs that appear to enhance PMN chemotaxis are: isobuttlmethylanthine, levamisole, bestadine.

Serum factors that seems to inhibit chemotaxis are:

• Cell -directed inhibitor (CDI). Related with polymeric IgA. Acts directly on PMNs in a reversible manner.
• Chemotactic Factor Inhibitor (CFI): Acts in an irreversible manner on the chemotactic factor itself.

Leukotoxin may cause irreversible damage to PMNs & monocytes ( lysosomal content is liberated after cell death producing more tissue damage).

It has been reported that lysosyme which may depress PMN chemotaxis, was elevated in saliva of JP pats.

* Phagocytic capacity of peripheral blood & gingival crevice PMNs in JP is still controversial. PMNs from healthy sites of JP pats. have had normal function indicating that environmental factors may be involved in the disease.

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