Riley G P, Harrall R L, Constant C R, Cawston T E, Hazleman B L
Rheumatology Research Unit, Addenbrookes Hospital, Cambridge, United Kingdom.
Ann Rheum Dis. 1996 Feb;55(2):109-15. doi: 10.1136/ard.55.2.109.
To investigate the prevalence of calcium phosphate mineral salt accumulation in degenerative supraspinatus 'tendinitis' compared with a normal sample of human tendons, and to determine whether there is an association of calcium salt deposition with pathological changes in the tendon extracellular matrix.
Cadaver tendons (supraspinatus and common biceps tendons, n = 96) and fragments of supraspinatus tendons obtained during shoulder surgery (n = 31) were analysed for calcium content by atomic absorption spectroscopy, phosphorous content using a spectrophotometric assay, and matrix composition (collagen, glycosaminoglycans and DNA) using standard biochemical techniques.
We established baseline values of calcium concentration in macroscopically normal cadaver tendons (mean 1.1 (SD 0.35) micrograms/mg dry wt, n = 60) and found that 33% (nine of 27) of ruptured tendons from patients with 'degenerative tendinitis' contained an excess of calcium (more than 2SD greater than the normal sample mean). Five of these specimens had increased concentrations of phosphorous and calcium:phosphorous (molar) ratios consistent with a variety of possible calcium crystals, including calcium pyrophosphate, hydroxyapatite, and tricalcium phosphate, in addition to mixed or amorphous calcium phosphate deposits. Four of these specimens contained normal concentrations of phosphorous, consistent with deposits of calcium oxalate or calcium carbonate, although this was not confirmed biochemically. In contrast, surgical specimens (n = 4) from patients with 'calcifying tendinitis' (radiographically detected calcium deposits) all contained salts with a mineral composition consistent with hydroxyapatite. The presence and identity of crystal deposits was subsequently confirmed in five specimens by radiographic microanalysis. Analysis of the tendon matrix demonstrated a number of significant differences between normal and degenerate (ruptured) tendons, including a reduction in collagen content, an increase in sulphated glycosaminoglycans (predominantly dermatan sulphate) and an increase in DNA (cellular) content. However, there were no significant differences between degenerate tendons that were 'calcified' and those degenerate specimens that contained normal concentrations of calcium.
Although there was a relatively high prevalence of calcium salts in degenerate tendons, which might contribute to the pathological process (such as increased matrix collagen degradation), these data are consistent with the hypothesis that 'dystrophic calcification' of degenerate tendon matrix is a pathological entity distinct from cell mediated 'calcifying tendinitis'. Calcification is probably one possible outcome (or end point) of chronic tendon injury, although the possibility exists that in many cases, the presence of calcium salts may contribute to the tendon matrix degeneration.
与正常人体肌腱样本相比，研究磷酸钙矿物盐在退行性冈上肌腱炎中的积聚情况，并确定钙盐沉积与肌腱细胞外基质病理变化之间是否存在关联。
通过原子吸收光谱法分析尸体肌腱（冈上肌腱和肱二头肌肌腱，n = 96）以及肩部手术中获取的冈上肌腱碎片（n = 31）中的钙含量，采用分光光度法测定磷含量，并使用标准生化技术分析基质成分（胶原蛋白、糖胺聚糖和DNA）。
我们确定了宏观正常尸体肌腱中钙浓度的基线值（平均1.1（标准差0.35）微克/毫克干重，n = 60），并发现“退行性肌腱炎”患者的33%（27例中的9例）破裂肌腱中钙含量过高（比正常样本平均值高出2个标准差以上）。其中5个标本的磷浓度以及钙：磷（摩尔）比升高，与多种可能的钙晶体一致，包括焦磷酸钙、羟基磷灰石和磷酸三钙，此外还有混合或无定形磷酸钙沉积物。其中4个标本的磷浓度正常，与草酸钙或碳酸钙沉积物一致，尽管这未通过生化方法得到证实。相比之下，“钙化性肌腱炎”（影像学检测到钙沉积）患者的手术标本（n = 4）均含有矿物成分与羟基磷灰石一致的盐。随后通过放射学微分析在5个标本中证实了晶体沉积物的存在和特性。对肌腱基质的分析表明，正常肌腱和退变（破裂）肌腱之间存在一些显著差异，包括胶原蛋白含量减少、硫酸化糖胺聚糖（主要是硫酸皮肤素）增加以及DNA（细胞）含量增加。然而，“钙化”的退变肌腱与钙浓度正常的退变标本之间没有显著差异。
尽管退变肌腱中钙盐的患病率相对较高，这可能导致病理过程（如基质胶原蛋白降解增加），但这些数据与以下假设一致，即退变肌腱基质的“营养不良性钙化”是一种与细胞介导的“钙化性肌腱炎”不同的病理实体。钙化可能是慢性肌腱损伤的一种可能结果（或终点），尽管在许多情况下，钙盐的存在可能导致肌腱基质退变。
