1996
DOI: 10.1111/j.1600-051x.1996.tb01825.x
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Association between HLA antigens and early onset periodontitis

Abstract: HLA-A, B, C and DR antigen frequencies were determined in a group of patients with juvenile periodontitis and rapidly progressive periodontitis. In juvenile periodontitis patients, HLA-A24 and DR4 were found at a significantly higher level than in the control group, and in rapidly progressive periodontitis patients, A9 and DR4 were found at a significantly higher level than the control group. The presence of these antigens gives evidence as to the susceptibility of various forms of early onset periodontitis.

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Cited by 40 publications
(45 citation statements)
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“…Increased HLA-A9 frequency was observed in early onset periodontitis (Firatli et al 1996), juvenile periodontitis (Reinholdt et al 1977;Kaslick et al 1980;Cullinan et al 1980, Marggraf et al 1993, in rapidly progressive periodontitis (Kloude et al 1986;Shapira et al 1994) and in adult periodontitis (Reinholdt et al 1977;Kaslick et al 1980, Amer et al 1988. The suggestion by Amer et al (1988) regarding HLA-A10 as a marker for resistance does not hold good in the present study.…”
contrasting
confidence: 49%
See 1 more Smart Citation
“…Increased HLA-A9 frequency was observed in early onset periodontitis (Firatli et al 1996), juvenile periodontitis (Reinholdt et al 1977;Kaslick et al 1980;Cullinan et al 1980, Marggraf et al 1993, in rapidly progressive periodontitis (Kloude et al 1986;Shapira et al 1994) and in adult periodontitis (Reinholdt et al 1977;Kaslick et al 1980, Amer et al 1988. The suggestion by Amer et al (1988) regarding HLA-A10 as a marker for resistance does not hold good in the present study.…”
contrasting
confidence: 49%
“…Ethnicity and genetic predisposition is correlated wherein the association between HLA antigens and periodontal disease could be correspondingly different among various races. Previous studies have all been restricted to mainly the Caucasian (Amer et al 1988), Negroid (Cullinan et al 1980), Turkish (Firatli et al 1996) and Japanese (Ashikaga et al 1984) populations.…”
Section: Introductionmentioning
confidence: 99%
“…Studies [45] have shown the presence of periopathogenic bacteria in the synovium of patients with rheumatoid arthritis indicating that joint seeding and localized inflammatory amplification may be operative. Others [46,47] have shown common genetic risk factors including the Human Leukocyte Antigen (HLA)-DR shared epitope and polymorphisms and epigenetic modifications in cytokine genes, including a recent report showing similar interleukin-6 promoter methylation in rheumatoid arthritis and periodontal disease [48 ■ ]. …”
Section: Moving From Clinical Associations To Mechanismmentioning
confidence: 99%
“…There may be a non-causal association between PD and RA due to shared genetic and environmental risk factors, such as expression of the MHC class II HLA-DRB1 allele and smoking, respectively [1–5]. Despite differences in initiating etiological mechanisms, evidence emerging from numerous clinical and epidemiological studies suggests an association between RA and PD [6–9].…”
Section: Introductionmentioning
confidence: 99%