Periodontal attachment loss in HIV-infected patients is associated with the major histocompatibility complex 8.1 haplotype (HLA-A1,B8,DR3)

Periodontal attachment loss is mediated by overproduction of tumour necrosis factor (TNF) and interleukin (IL)‐1, and appears to have a genetic component. The 8.1 major histocompatibility complex (MHC) ancestral haplotype (HLA‐A1,B8,TNFA‐308(2),DR3) is associated with elevated TNF production and pre...

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Published inTissue antigens Vol. 54; no. 4; pp. 391 - 399
Main Authors Price, P., Calder, D.M., Witt, C.S., Allcock, R.J.N., Christiansen, F.T., Davies, G.R., Cameron, P.U., Rogers, M., Baluchova, K., Moore, C.B., French, M.A.
Format Journal Article
LanguageEnglish
Published Copenhagen Munksgaard International Publishers 01.10.1999
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Online AccessGet full text
ISSN0001-2815
1399-0039
DOI10.1034/j.1399-0039.1999.540409.x

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Abstract Periodontal attachment loss is mediated by overproduction of tumour necrosis factor (TNF) and interleukin (IL)‐1, and appears to have a genetic component. The 8.1 major histocompatibility complex (MHC) ancestral haplotype (HLA‐A1,B8,TNFA‐308(2),DR3) is associated with elevated TNF production and predisposes carriers to several autoimmune/immunopathological disorders, including rapid progression of HIV disease, but not early onset periodontal disease in healthy individuals. Rather a high proportion of subjects with severe periodontal disease carry allele 2 at IL‐1A−889 and IL‐1B+3953. We predicted that genetic associations may be different or clearer in HIV patients, as they often show elevated production of TNF and IL‐1 and periodontal attachment loss. Hence periodontal parameters and IL‐1 polymorphisms were assessed in HIV‐positive subjects expressing HLA‐B8 with or without other markers of the 8.1 haplotype. Of 16 HLA‐B8 subjects, 13 demonstrated elevated probing pocket depth and clinical attachment loss. The difference was statistically significant and did not correlate with smoking, age, CD4 T‐cell counts, HIV viral load or levels of dental plaque. As TNFA‐308 (allele 2) was present in four non‐B8 subjects who had minimal attachment loss, it may not mediate the effect of the 8.1 haplotype. Moreover, polymorphisms at IL‐1A−889 and IL‐1B+3953 did not significantly affect periodontal parameters. Thus a central MHC gene characteristic of the 8.1 haplotype was the clearest determinant of periodontal attachment loss in HIV‐infected individuals.xm
AbstractList Periodontal attachment loss is mediated by overproduction of tumour necrosis factor (TNF) and interleukin (IL)‐1, and appears to have a genetic component. The 8.1 major histocompatibility complex (MHC) ancestral haplotype (HLA‐A1,B8,TNFA‐308(2),DR3) is associated with elevated TNF production and predisposes carriers to several autoimmune/immunopathological disorders, including rapid progression of HIV disease, but not early onset periodontal disease in healthy individuals. Rather a high proportion of subjects with severe periodontal disease carry allele 2 at IL‐1A−889 and IL‐1B+3953. We predicted that genetic associations may be different or clearer in HIV patients, as they often show elevated production of TNF and IL‐1 and periodontal attachment loss. Hence periodontal parameters and IL‐1 polymorphisms were assessed in HIV‐positive subjects expressing HLA‐B8 with or without other markers of the 8.1 haplotype. Of 16 HLA‐B8 subjects, 13 demonstrated elevated probing pocket depth and clinical attachment loss. The difference was statistically significant and did not correlate with smoking, age, CD4 T‐cell counts, HIV viral load or levels of dental plaque. As TNFA‐308 (allele 2) was present in four non‐B8 subjects who had minimal attachment loss, it may not mediate the effect of the 8.1 haplotype. Moreover, polymorphisms at IL‐1A−889 and IL‐1B+3953 did not significantly affect periodontal parameters. Thus a central MHC gene characteristic of the 8.1 haplotype was the clearest determinant of periodontal attachment loss in HIV‐infected individuals.xm
Periodontal attachment loss is mediated by overproduction of tumour necrosis factor (TNF) and interleukin (IL)-1, and appears to have a genetic component. The 8.1 major histocompatibility complex (MHC) ancestral haplotype (HLA-A1,B8,TNFA-308(2),DR3) is associated with elevated TNF production and predisposes carriers to several autoimmune/immunopathological disorders, including rapid progression of HIV disease, but not early onset periodontal disease in healthy individuals. Rather a high proportion of subjects with severe periodontal disease carry allele 2 at IL-1A-889 and IL-1B+3953. We predicted that genetic associations may be different or clearer in HIV patients, as they often show elevated production of TNF and IL-1 and periodontal attachment loss. Hence periodontal parameters and IL-1 polymorphisms were assessed in HIV-positive subjects expressing HLA-B8 with or without other markers of the 8.1 haplotype. Of 16 HLA-B8 subjects, 13 demonstrated elevated probing pocket depth and clinical attachment loss. The difference was statistically significant and did not correlate with smoking, age, CD4 T-cell counts, HIV viral load or levels of dental plaque. As TNFA-308 (allele 2) was present in four non-B8 subjects who had minimal attachment loss, it may not mediate the effect of the 8.1 haplotype. Moreover, polymorphisms at IL-1A-889 and IL-1B+3953 did not significantly affect periodontal parameters. Thus a central MHC gene characteristic of the 8.1 haplotype was the clearest determinant of periodontal attachment loss in HIV-infected individuals.Periodontal attachment loss is mediated by overproduction of tumour necrosis factor (TNF) and interleukin (IL)-1, and appears to have a genetic component. The 8.1 major histocompatibility complex (MHC) ancestral haplotype (HLA-A1,B8,TNFA-308(2),DR3) is associated with elevated TNF production and predisposes carriers to several autoimmune/immunopathological disorders, including rapid progression of HIV disease, but not early onset periodontal disease in healthy individuals. Rather a high proportion of subjects with severe periodontal disease carry allele 2 at IL-1A-889 and IL-1B+3953. We predicted that genetic associations may be different or clearer in HIV patients, as they often show elevated production of TNF and IL-1 and periodontal attachment loss. Hence periodontal parameters and IL-1 polymorphisms were assessed in HIV-positive subjects expressing HLA-B8 with or without other markers of the 8.1 haplotype. Of 16 HLA-B8 subjects, 13 demonstrated elevated probing pocket depth and clinical attachment loss. The difference was statistically significant and did not correlate with smoking, age, CD4 T-cell counts, HIV viral load or levels of dental plaque. As TNFA-308 (allele 2) was present in four non-B8 subjects who had minimal attachment loss, it may not mediate the effect of the 8.1 haplotype. Moreover, polymorphisms at IL-1A-889 and IL-1B+3953 did not significantly affect periodontal parameters. Thus a central MHC gene characteristic of the 8.1 haplotype was the clearest determinant of periodontal attachment loss in HIV-infected individuals.
Periodontal attachment loss is mediated by overproduction of tumour necrosis factor (TNF) and interleukin (IL)-1, and appears to have a genetic component. The 8.1 major histocompatibility complex (MHC) ancestral haplotype (HLA-A1,B8,TNFA-308(2),DR3) is associated with elevated TNF production and predisposes carriers to several autoimmune/immunopathological disorders, including rapid progression of HIV disease, but not early onset periodontal disease in healthy individuals. Rather a high proportion of subjects with severe periodontal disease carry allele 2 at IL-1A-889 and IL-1B+3953. We predicted that genetic associations may be different or clearer in HIV patients, as they often show elevated production of TNF and IL-1 and periodontal attachment loss. Hence periodontal parameters and IL-1 polymorphisms were assessed in HIV-positive subjects expressing HLA-B8 with or without other markers of the 8.1 haplotype. Of 16 HLA-B8 subjects, 13 demonstrated elevated probing pocket depth and clinical attachment loss. The difference was statistically significant and did not correlate with smoking, age, CD4 T-cell counts, HIV viral load or levels of dental plaque. As TNFA-308 (allele 2) was present in four non-B8 subjects who had minimal attachment loss, it may not mediate the effect of the 8.1 haplotype. Moreover, polymorphisms at IL-1A-889 and IL-1B+3953 did not significantly affect periodontal parameters. Thus a central MHC gene characteristic of the 8.1 haplotype was the clearest determinant of periodontal attachment loss in HIV-infected individuals.
Author Price, P.
Calder, D.M.
Rogers, M.
Witt, C.S.
Allcock, R.J.N.
French, M.A.
Davies, G.R.
Christiansen, F.T.
Baluchova, K.
Moore, C.B.
Cameron, P.U.
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Snippet Periodontal attachment loss is mediated by overproduction of tumour necrosis factor (TNF) and interleukin (IL)‐1, and appears to have a genetic component. The...
Periodontal attachment loss is mediated by overproduction of tumour necrosis factor (TNF) and interleukin (IL)-1, and appears to have a genetic component. The...
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SubjectTerms Adult
Alleles
Haplotypes
histocompatibility antigen HLA
HIV
HIV Infections - complications
HIV Infections - genetics
HIV Infections - immunology
HLA Antigens - genetics
HLA Antigens - immunology
HLA-A1 Antigen - genetics
HLA-A1 Antigen - immunology
HLA-B8 Antigen - genetics
HLA-B8 Antigen - immunology
HLA-DR3 Antigen - genetics
HLA-DR3 Antigen - immunology
Human immunodeficiency virus
Humans
interleukin-1
Interleukin-1 - genetics
Male
MHC
Periodontal Attachment Loss - genetics
Periodontal Attachment Loss - immunology
Periodontal Attachment Loss - virology
periodontal disease
Phenotype
Polymorphism, Genetic
Severity of Illness Index
TNF
Tumor Necrosis Factor-alpha - genetics
Title Periodontal attachment loss in HIV-infected patients is associated with the major histocompatibility complex 8.1 haplotype (HLA-A1,B8,DR3)
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