Microbiological, immunological and genetic factors in family members with periodontitis as a manifestation of systemic disease, associated with hematological disorders

Abstract

The microflora, immunological profiles of host defence functions, and human leukocyte antigen (HLA) findings are reported for a mother, son and daughter who were diagnosed as having 'periodontitis as a manifestation of systemic diseases, associated with hematological disorders'. Examinations were made of the bacterial flora from the periodontal pocket, neutrophil chemotaxis, neutrophil phagocytosis, and the genotypes (DQB1) and serotypes (DR locus) of HLA class II antigens. Phenotypic analyses of the peripheral lymphocytes were also conducted. The subgingival microflora from the mother was dominated by Gram-negative rods, especially Porphyromonas endodontalis, Prevotella intermedia/Prevotella nigrescens and Fusobacterium nucleatum. Subgingival microflora samples from the son and daughter were dominated by Gram-positive cocci and Gram-positive rods. Through the use of polymerase chain reaction, Campylobacter rectus and Capnocytophaga gingivalis were detected in all subjects, whereas Porphyromonas gingivalis, P. intermedia, and Treponema denticola were not detected in any subjects. All three subjects showed a remarkable level of depressed neutrophil chemotaxis to N-formyl-methionyl-leucyl-phenylalanine, although their phagocyte function levels were normal, in comparison to healthy control subjects. Each subject had the same genotype, HLA-DQB1*0601, while the mother had HLA-DR2 and HLA-DR8, and the son and daughter had HLA-DR2 only. In summary, the members of this family showed a similar predisposition to periodontitis with regard to certain host defence functions. It is suggested that the depressed neutrophil chemotaxis that was identified here could be a significant risk factor for periodontitis in this family.

Relationship of neutrophil phagocytosis and oxidative burst with the subgingival microbiota of generalized aggressive periodontitis

“…Similar findings have been reported by other investigators (4, 11, 21, 46). In contrast, some studies have not observed any significant difference in PMN phagocytosis between patients with periodontitis and controls (28, 41). Regarding the oxidative burst activity, available data suggest that peripheral PMNs from patients with different forms of periodontitis are ‘hyperactive’, and therefore release greater amounts of lysosomal enzymes and ROS than PMNs from individuals with periodontal health (12, 13, 16, 17, 19, 34, 35).…”

“…It should be pointed out that our main goal in this study was not to evaluate the direct effects of the subgingival microbiota on PMN functions, but rather to determine whether an intrinsic impairment in these cells would be associated with a pathogenic periodontal microbiota and disease. To date, very few studies have correlated the subgingival microbiota with PMN activities in individuals with aggressive disease (28, 36). Moreover, there is not a unique test to measure phagocytic or microbicidal functions of PMNs in the gingival sulcus because a wide variety of subgingival pathogens interact simultaneously with a large number of different components on the surface of these cells, eliciting distinct responses.…”

“…There is clear evidence of the importance of this protective PMN barrier, as patients with abnormalities in the numbers and/or functions of these cells often experience rapid and severe periodontal destruction (7). Several authors have reported a significant reduction in the chemotaxis, phagocytosis, and/or killing of bacteria by PMNs in patients with aggressive periodontitis (4, 11, 21, 28, 36, 45, 46). PMN dysfunctions have also been associated with recurrence of disease after treatment (25).…”

Site‐based versus subject‐based periodontal diagnosis

“…In one study (44), periodontal therapy seemed to reduce the presence of key pathogens at the site level but failed to confirm the results at the subject level. Although sampling from one site only per subject would provide subject‐based information such processing may not be representative for the subjects (11, 148). It appears that, at the subject level, there are few studies that have presented data on periodontal infection as part of a periodontal diagnosis.…”

Multidisciplinary Clinical Management of a Localized Aggressive Periodontitis diagnosed in a Child with Glanzmann\'s Thrombasthenia

“…Thus, it seems to be also associated with monocyte deficiency, such as disrupted neutrophil differentiation or chemotaxis. 9 Furthermore, the affected patients have been shown to have inflammatory hyperresponsive phenotype. 10 This genetic predisposition to disease is also found in the expression of major histocompatibility complex, human leukocyte antigen (HLA) genes or cytokines.…”