Abstract
BackgroundTelemore length (TL) shortening has been found in many diseases. However, clinical characteristics of TL shortening in osteonecrosis of the femoral head (ONFH) has not been investigated. Therefore, we studied whether TL changes have clinicopathological values in ONFH.MethodsThe TL in the synovial tissues of 36 ONFH and 127 control patients (femoral neck fracture) was examined by quantitative real-time PCR as relative length, Δ Ct value. In addition, the correlation between TL and clinical features of ONFH and controls was analyzed.ResultsThe average TL in the femoral tissues was 1.46 ± 3.12 (standard deviation). The average TL in the ONFH and control tissues was 1.92 ± 4.11 and 1.34 ± 2.78, respectively, however, the difference was absent (p = 0.324). Furthermore, a shorter TL was tended to be associated with erythrocyte sedimentation rate (100% vs. 61.5%, p = 0.073); however, the association was not statistically significant.ConclusionsIn this study, we demonstrated that there is no association between the TL and clinicopathologic characteristics of ONFH patients. However, further studies considering the genetic factors are needed to be performed.
Highlights
Telemore length (TL) shortening has been found in many diseases
A shorter TL was found to be associated with erythrocyte sedimentation rate (ESR, 100% vs. 61.5%, p = 0.073); Telomere length analysis The TL of each chromosome was analyzed by quantitative real-time polymerase chain reaction
Most studies on TL used the peripheral blood samples from patients with cancer, diabetes, and psychological diseases [15, 16]; we used DNA extracted from the synovial tissues of Osteonecrosis of the femoral head (ONFH) and femoral neck fracture
Summary
Telemore length (TL) shortening has been found in many diseases. Clinical characteristics of TL shortening in osteonecrosis of the femoral head (ONFH) has not been investigated. Telomeric repeats are lost during every cell division, because of lacking replication of the 3′-end of the chromosome. It induces critically short telomeres, occurring cellular senescence or crisis [2]. Telomere length (TL) declines progressively with aging. This decline is apparently accelerated in the presence of oxidative stress and inflammation. The TL is determined at birth in individuals and reflects the lifelong cumulative burden effect of inflammation and oxidative stress [3, 4]
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