Steroid injection can be an effective way to treat plantar fasciitis, and injection under sonographic guidance is associated with lower recurrence of heel pain.

The reliability of sonographic examination of the thickness of the plantar fascia is high. Mean gray-level analysis of quantitative sonography can be used for the evaluation of echogenicity, which could reduce discrepancies in the interpretation of echogenicity by different sonographers. Longitudinal instead of transverse scanning is recommended for imaging the plantar fascia.

BackgroundMost tendon pathology is associated with degeneration, which is thought to involve cyclic loading and cumulative age-related changes in tissue architecture. However, the association between aging and degeneration of the extracellular matrix (ECM) in tendons has not been investigated extensively.MethodsWe examined tenocytes from Achilles tendons taken from rats of three different ages (2, 12, and 24 months). Tenocyte viability was assessed using the 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) assay. Quantitative real-time polymerase chain reaction (PCR) was used to determine the levels of mRNAs that encode type-I collagen, matrix metalloproteinase (MMP)-2 and −9, tissue inhibitor of metalloproteinase (TIMP)-1 and −2 and transforming growth factor (TGF)-β1. Gelatin zymography was used to evaluate the enzymatic activities of MMP-2 and −9. Furthermore, the concentration of TGF-β1 in conditioned medium was evaluated using enzyme-linked immunosorbent assay (ELISA).ResultsThe results of the MTT assay showed that the number of viable tenocytes decreased with age. No differences were observed in the levels of mRNAs that encode type-I collagen and TGF-β1 among the three age groups, and the TGF-β1 concentration did not change with age. However, mRNAs that encode MMP-2 and −9 were significantly more abundant in tenocytes from the aging group, and gelatin zymography revealed that the enzymatic activities of MMP-2 and −9 also increased significantly with age. Furthermore, as compared with young group, mRNAs that encode TIMP-1 and −2 were significantly decreased in tenocytes from the aging group.ConclusionsActivities of MMP-2 and MMP-9 in tenocytes increase with age. This might provide a mechanistic explanation of how aging contributes to tendinopathy or tendon rupture with age.

Symptomatic tendinopathy tends to be age-related. However, the molecular mechanisms of ageing and its effects on tenocyte proliferation and cell cycle progression are unknown. We examined tenocytes from Achilles tendons in rats from three age groups (young, 2 months; middle-aged, 12 months, and near senescence, 24 months). Tenocyte proliferation was assessed by 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry. Senescence-associated b-galactosidase (SA b-gal) staining was performed in all groups of tenocytes. mRNA and protein expression of cellular senescence-inhibited gene (CSIG) and p27 was measured by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot, respectively. The results of MTT assay revealed that tenocyte proliferation decreased with age (p < 0.05). Cell cycle progression was arrested at G0/G1 phase in senescent tenocytes. More senescent tenocytes expressed SA b-gal than young tenocytes did. By RT-PCR and Western blot analysis, the gene and protein expression of CSIG was found to be down-regulated, whereas that of p27 was up-regulated with age. In conclusion, the proliferation of tenocytes declines with age and is associated with the down-regulation of CSIG and up-regulation of p27. ß