Abstract
Osteoprotegerin (OPG; official gene symbol: TNFRSF11B) is considered a negative regulator of bone resorption via inhibition of osteoclast differentiation. Further, OPG expression has been detected in Prosthetic Joint Infection (PJI) a serious complication limiting the overall outcome of total joint arthroplasty (TJA). As OPG may be a candidate molecule for PJI pathogenesis, we investigated whether genetic variation in the OPG promoter, namely the SNP at position -163 was associated with PJI. OPG -163 T/C SNP (rs3102735) was genotyped by polymerase chain reaction with sequence specific primers (PCR-SSP) in 98 Czech patients with PJI and two Czech control groups: 1) aseptic TJA control [251 patients with TJA who did not develop PJI at least 6 yrs. after the surgery] and 2) population control (185 healthy control subjects without TJA). The distribution of OPG -163 SNP genotypes complied with the Hardy-Weinberg equilibrium in all three groups. The allele frequencies of OPG -163 SNP were similar in patients with PJI (minor allele frequency: 0.14), those with aseptic TJA (0.13) and population controls (0.14, P>0.05). Further, there was no significant difference in genotype or phenotype frequency (carriage rate) between patients with PJI and both control groups (P>0.05). In a Czech population, the OPG -163 T/C SNP has not been found to be associated with PJI.
Highlights
Prosthetic joint infection (PJI) is a serious complication threatening both the early and late period after total joint arthroplasty (TJA)
The allele frequencies of OPG -163 SNP were similar in the patients with PJI, those with aseptic TJA (0.13) and population controls as well (0.14, P>0.05)
When the patients with PJI were stratified according to the affected joint, there was no association between OPG -163 SNP and PJI of Total Hip Arthroplasty – C allele frequency was equal in both aseptic THA and in THA/PJI groups: 0.12; P>0.05)
Summary
Prosthetic joint infection (PJI) is a serious complication threatening both the early and late period after total joint arthroplasty (TJA). Significant reduction in bone mineral density shortly after the beginning of Staphylococcus aureus infection of the bone has been revealed4 This was effectively prevented by inhibition of RANKL (receptor activator of nuclear factor – kappa B ligand) signalling. This and other experiments support the clinical observation of a tight association between the development of infection and increased resorption of periprosthetic bone. This and other experiments support the clinical observation of a tight association between the development of infection and increased resorption of periprosthetic bone5 For this reason, cytokine ligands and the corresponding receptors that regulate osteoclast accumulation, maturation and viability, are probably involved in the complex pathogenesis of PJI. In a Czech population, the OPG -163 T/C SNP has not been found to be associated with PJI
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