*5.3.4 Hyperimmunoglobulinemia E syndrome*

Hyperimmunoglobulinemia E syndrome manifests with overhiked susceptibility to infections and thus contributing to the development of periodontitis. The process involved here is thought to be associated with a deficient host cellular and humoral immune response, comprising of an inadequate neutrophil chemotaxis secondary to alteration in the regulation of T cell cytokines. The rapid spike in circulating IgE leads to a reduced production of gamma-interferon, which intervenenes with anti-inflammatory and bone resorption-inhibiting processes. Thereby, the heightened inflammatory and resorptive phenomena noted in these patients, gives rise to early and advanced periodontitis. This disorder is associated with abundance of pathogenic microflora (*P. gingivalis, T. denticola, E. corrodens*) that results in severe periodontal damage in adults and in children [73]. The syndromes, mode of inheritance, function of responsible gene and periodontal manifestations are given in **Table 5**.
