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ABSTRACT
Paget's disease of bone is a disorder of bone, primarily affecting elderly population. The disease causes a structural disorganisation of of bone tissue in affected sites. The etiology is unknown. Microrganisms and/or genetic tendecy are clamied to play role in the etiopathogenesis. Evidence exists to support the genetic etiologies such as familial clustering and HLA linkage or chromosomal abnormalities. To demonstrat e the genetic linkage we performed HLA typing of 15 patients with Paget's disease of bone and 60 control subjects. A total of seventyone antigens were studied in various loci (Class I antigens: 53, Class II antigens: 18). Statistical analysis revealed that the HLA Q8 was a more prominent antigen in patients ( 2 test; p:0.02).
Our findings did not support previous studies where HLA DR2 was addressed as the responsible antigen, however, did reveal an antigen which belongs to Class II HLA loci which harbors the HLA-DR2, DR6 antigens, previously shown to play role in etiopathogenesis of the disease. Our results must be confirmed by larger samples.
Paget's disease of bone is a disorder of bone, primarily affecting elderly population. The disease causes a structural disorganisation of of bone tissue in affected sites. The etiology is unknown. Microrganisms and/or genetic tendecy are clamied to play role in the etiopathogenesis. Evidence exists to support the genetic etiologies such as familial clustering and HLA linkage or chromosomal abnormalities. To demonstrat e the genetic linkage we performed HLA typing of 15 patients with Paget's disease of bone and 60 control subjects. A total of seventyone antigens were studied in various loci (Class I antigens: 53, Class II antigens: 18). Statistical analysis revealed that the HLA Q8 was a more prominent antigen in patients ( 2 test; p:0.02).
Our findings did not support previous studies where HLA DR2 was addressed as the responsible antigen, however, did reveal an antigen which belongs to Class II HLA loci which harbors the HLA-DR2, DR6 antigens, previously shown to play role in etiopathogenesis of the disease. Our results must be confirmed by larger samples.