Neutrophil chemotaxis in refractory cases of periodontitis

Oshrain, Herbert I.; Telsey, Bernard; Mandel, Irwin D.

doi:10.1111/j.1600-051x.1987.tb01514.x

Cited by 19 publications

(10 citation statements)

References 6 publications

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“…Some patients respond poorly to conventional treatment and suffer from recurrence, which results in progressive attachment loss (8,16). This recurrence might be associated with compromised function of polymorphonuclear neutrophils (PMN) (15,20).…”

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confidence: 99%

Relevance of immunoglobulin G Fc receptor polymorphism to recurrence of adult periodontitis in Japanese patients

et al. 1997

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Polymorphonuclear neutrophil (PMN) phagocytic function has been shown to be impaired in some patients with periodontitis. PMN constitutively express members of two immunoglobulin G receptor (Fc␥R) classes: Fc␥RIIa (CD32) and Fc␥RIIIb (CD16). Both receptors exhibit genetically determined structural and functional biallelic polymorphisms, which have been shown to influence PMN phagocytic function. In this study, we assessed the relevance of these Fc␥R polymorphisms to susceptibility to adult periodontitis and recurrence rate. The distribution of Fc␥RIIa and Fc␥RIIIb genotypes of 100 Japanese patients with adult periodontitis during follow-up was compared to the distribution of genotypes in 105 race-matched healthy controls. No significant skewing of distributions of Fc␥RIIa and Fc␥RIIIb genotypes was observed between patients and controls. Notably, however, a significant overrepresentation of the Fc␥RIIIb-NA2 allotype was found in patients with disease recurrence (P < 0.05; odds ratio, 4.29; 95% confidence interval, 1.19 to 16.24). Moreover, the annual rate of recurrence was significantly higher in patients with the Fc␥RIIIb-NA2/NA2 and Fc␥RIIIb-NA1/NA2 genotypes than in Fc␥RIIIb-NA1/NA1 individuals (P < 0.05). Fc␥RIIa-R/R131 individuals also exhibited higher recurrence rates, though the difference was not statistically significant (P ‫؍‬ 0.06). These results suggest that the Fc␥RIIIb-NA2 allotype represents a risk factor for recurrence of adult periodontitis.

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Relevance of immunoglobulin G Fc receptor polymorphism to recurrence of adult periodontitis in Japanese patients

et al. 1997

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“…59 A reduced chemotaxis and phagocytosis of neutrophils; a reduced CD4ϺCD8 ratio in peripheral blood; a failure to mount an antibody response to infecting pathogens; and elevated interleukin (IL)-1, IL-2, and IL-6 levels in gingival crevicular fluid have been reported in patients with periodontitis unresponsive to treatment. [63][64][65][66][67][68] The only studies on the incidence of periodontitis not responding to treatment on a tooth or periodontal site basis; i.e., annual incidence of CAL under therapy, are based on rather heterogeneous and mostly small study populations in which various treatment regimens were used. [69][70][71][72] Therefore, the data vary considerably between studies and need to be interpreted with caution.…”

Section: Refractory Adult Periodontitismentioning

confidence: 99%

Periodontitis

1999

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The purpose of this review was to assess the scientific and clinical bases for the proposed classification of periodontitis. The clinical and histopathological signs and the etiology of periodontitis were described. Cross-sectional studies were analyzed to determine when onset of periodontitis most frequently occurs in adults. In addition, the progression rates of periodontitis have been assessed from longitudinal studies. No clinical, histopathological, or microbiological features could be identified that would characterize different disease entities of chronic periodontitis. The prevalence, extent, and severity of periodontitis were found to increase continually with higher age and there was no age when onset of disease would most likely occur. The rate of periodontitis progression varies largely between patients and there is no natural threshold for distinguishing various rates of disease progression. The incidence of periodontitis unresponsive to treatment depends on pretreatment progression rate, extent and severity of disease, tooth type, smoking, high levels of putative periodontal pathogens, a deficient immune response, and the type of therapy provided. There is no scientific basis for the classification "adult periodontitis" and "refractory adult periodontitis." Extensive clinical examinations are required for the diagnosis of "rapidly progressive adult periodontitis." It appears unrealistic that these examinations can be performed routinely in clinical practice. Therefore, the classification proposed by the Organizing Committee to define adult, rapidly progressive, and refractory periodontitis as specific disease entities was replaced with a simplified classification of periodontitis based on the scientific data available.

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“…HafTajee et al emphasize the microbiological aspects of diseases in their patients, In the discussion, the authors do mention "'an inadequate host defense might also explain the refractory subject", and make reference to the need for adequate numbers of functioning polymorphonuclear leukocytes. We wish to point out that a beginning was made in investigation of PMN response in refractory periodontitis patients by Oshrain et al (1987). Using an in vivo procedure, they found there was a chemotactic defect in PMNs in refractory cases.…”

Section: Dear Sirmentioning

confidence: 99%