The effects of aging on quantitative sonographic features of rotator cuff tendons.

PURPOSE: Grayscale analysis is a practical, objective, and easy way to quantify echogenicity during ultrasonography. The purpose of the current study was to measure the changes in thickness and echogenicity that result from aging of the rotator cuff and long head of the biceps tendons. METHODS: The study comprised 45 volunteers, aged between 20 and 84 years and without history of shoulder pain. Participants were divided into three groups: young, middle-aged, and old. All subjects underwent standard ultrasonography of both shoulders. Tendon thickness and tear were recorded, and images in both transverse and longitudinal scans were taken for grayscale analysis. To reduce the attenuation effect from skin and subcutaneous fat, we used the ratio of echogenicity of the tendon to that of the reference muscle and compared the tendon echogenicity among the different age groups. Sonographic findings were also correlated with age. RESULTS: The supraspinatus tendon was significantly thicker in elderly participants and this was positively correlated with age. Moreover, the echogenicity ratio of the supraspinatus tendon decreased in the elderly group and showed a negative correlation with age. There was a higher prevalence of supraspinatus tendon tears in the older participants. CONCLUSIONS: Our results indicate that supraspinatus tendons became thickened, hypoechogenic, and more likely to tear with age. The study presents a simple and useful method to investigate the echogenicity of the rotator cuff quantitatively.

The effect of aging on migration, proliferation, and collagen expression of tenocytes in response to ciprofloxacin.

Quinolone-induced tendinopathy or tendon rupture tends to be age-related. However, the synergistic effects of quinolone and aging on tenocytes remained to be explored. Tenocytes intrinsic to rat Achilles tendon from two age groups (young: 2 months; and near senescent (old): 24 months) were treated with ciprofloxacin. Tenocyte migration and proliferation were assessed by transwell filter migration assay and MTT (3-[4,5-Dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide) assay, respectively. Messenger RNA and protein expressions of types I and III collagen were determined by reverse transcription-polymerase chain reaction (RT/PCR) and Western blot analysis, respectively. Transwell filter migration assay revealed that ciprofloxacin inhibited tenocytes migration, which became more significant in old tenocytes (p < 0.05). The results of MTT assay revealed that tenocytes proliferation decreased after ciprofloxacin treatment (p < 0.05), which also became more significant in old tenocytes. The results of RT-PCR and Western blot analysis revealed that mRNA and protein expressions of type I collagen remained unchanged in either young or old tenocytes with ciprofloxacin treatment, whereas the expressions of type III collagen were down-regulated by ciprofloxacin, which was more significant in old tenocytes. In conclusion, aging potentiated the ciprofloxacin-mediated inhibition of migration, proliferation, and expression of type III collagen of tenocytes.

Fluoroquinolone-associated tendinopathy.

The fluoroquinolones (FQs) are used to treat a wide range of infections because of their excellent gastrointestinal absorption, superior tissue penetration and broad-spectrum activity. Recently, FQ-associated tendinopathy and tendon rupture have been reported, especially in the elderly and patients with diabetes and renal failure. However, these adverse effects do not appear to be widely known among physicians. Because of the frequent use of FQs in clinical practice, physicians should be aware of their potential for severe disability from tendon rupture. Achilles tendinopathy or rupture is among the most serious side effects associated with FQ use, with reports markedly increasing, especially with the use of ciprofloxacin. The histopathologic findings include degenerative lesions, fissures, interstitial edema without cellular infiltration, necrosis and neovascularization. There are possible molecular mechanisms accounting for FQ-associated tendinopathy. First, ciprofloxacin mediates inhibition of cell proliferation and G2/M cell cycle arrest in tendon cells by down-regulation of cyclin B and cyclin-dependent kinase 1. Second, ciprofloxacin inhibits the spead and migration of tenocytes by down-regulation of focal adhesion kinase phosphorylation. Third, ciprofloxacin enhances the enzymatic activity of matrix metalloproteinase-2 with degradation of type I collagen. Management of FQ-associated tendinopathy includes immediate discontinuation of FQs, rest, non-steroidal anti-inflammatory drugs, physical modalities and eccentric strengthening exercise. Tendon rupture may require surgical intervention.