We read with interest the Review Article "Rotator cuff tendinopathy: A review", by Lewis, doi:10.1136/bjsm.2008.052175.
This manuscript may have been submitted before the publication of our investigations. Nevertheless, we would like to call your attention to the fact that we have performed several studies on the aetiology, histopathology and management of rotator cuff tendinopathy.
We read with interest the Review Article "Rotator cuff tendinopathy: A review", by Lewis, doi:10.1136/bjsm.2008.052175.
This manuscript may have been submitted before the publication of our investigations. Nevertheless, we would like to call your attention to the fact that we have performed several studies on the aetiology, histopathology and management of rotator cuff tendinopathy.
We investigated supraspinatus tendon samples obtained from patients undergoing arthroscopic repair of a rotator cuff tear to examine the distribution of tendinopathic changes associated with this condition. At arthroscopy, a full thickness supraspinatus tendon biopsy was harvested
close to the tear edge. We found more frequent tendon changes on the articular side of the rotator cuff[4]. We found more cartilage-like changes in patients affected by rotator cuff tears, but not in our control group. Recent biomechanical data suggest that the stress-shielded and
transversely-compressed side of the enthesis has a distinct tendency to develop cartilage-like or atrophic changes in response to the lack of tensile load [2,7,9,10]. Over a long period, this process may develop into a primary degenerative lesion in that area of the tendon. This may explain why the tendinopathy is not always clearly activity related, and can be strongly correlated with age. In this manner, it could almost be considered an ‘‘underuse’’ injury rather than an overuse injury as a result of stress-shielding [7,9,10]. The formation of cartilage-like changes
in the enthesis in many ways can be considered a physiological adaptation to the compressive loads [12-14]. It may not allow the tendon to maintain its ability to withstand high tensile loads in that region of the tendon.
As the stress-shielding may have led to tensile weakening over time, an injury may occur more easily in this region. In this manner, insertional tendinopathy could be considered an overuse injury, but predisposed by pre
-existing weakening of the tendon [12-14].
In another study 3 to evaluate the histopathological features of macroscopic intact tendon portion of patients with rotator cuff tears, we demonstrated that the supraspinatus tendons of patients undergoing
arthroscopic repair for a rupture show profound histopathologic changes, while the tendons of aged persons with no known tendon abnormalities have, as a group, little histological evidence of pathological changes. Moreover, tendon changes are not only localized at the site of rupture, but also in the macroscopic intact tendon portion.
Several centres are undertaking studies on tendinopathy [11,16,17] and the individual studies are unlikely to be large enough to result in adequate power for reliable evaluation. Therefore, combining the data from those
studies with a similar study design will be essential. Consistent high-quality pathology data are thus remarkably important for the success of the studies. Two scoring systems can be used for classification of the histopathological findings of tendinopathy: the Movin score [15] and its validated modifications [4,6,12] and the Bonar score [1]. We performed a study to answer the question whether these two scores of abnormal tendon
tissue were comparable [8]. In our hands, Movin and Bonar scores assess the same characteristics of tendon pathology.
In an frequency-matched case-control study we determined the plasma glucose levels in non diabetic patients with rotator cuff tear [5]. We found that normal, but in the high range of normal, increasing plasma glucose levels may be a risk factor for rotator cuff tear.
Lastly, although it is likely that the histopathology of tendinopathy is similar, of not the same, regardless of its location, this has only been shown in a formal fashion in the Achilles and patellar tendons [12]: we were slightly surprised of the fact that a number of papers dealing with
pathology of other tendons (i.e., patellar tendon, Achilles Tendon, and extensor carpi radialis brevis tendon (tennis elbow) are quoted referring to rotator cuff tendinopathy (references n°23,24,25,26,81,94,96,97,98,147,148).
Nicola Maffulli
Umile Giuseppe Longo
Vincenzo Denaro
References
1. Cook, J.; Feller, J.; Bonar, S.; and Khan, K. Abnormal tenocyte morphology is more prevalent than collagen disruption in asymptomatic athletes' patellar tendons. J Orthop Res 2004;22:334-338.
2. Gardner, K.; Arnoczky, S. P.; Caballero, O.; and Lavagnino, M. The effect of stress-deprivation and cyclic loading on the TIMP/MMP ratio in tendon cells: An in vitro experimental study. Disabil Rehabil 2008:1-7.
3. Longo, U. G.; Franceschi, F.; Ruzzini, L.; Rabitti, C.; Morini, S.; Maffulli, N.; and Denaro, V. Histopathology of the supraspinatus tendon in rotator cuff tears. Am J Sports Med 2008;36:533-8.
4. Longo, U. G.; Franceschi, F.; Ruzzini, L.; Rabitti, C.; Morini, S.; Maffulli, N.; Forriol, F.; and Denaro, V. Light microscopic histology of supraspinatus tendon ruptures. Knee Surg Sports Traumatol Arthrosc
2007;15:1390-4.
5. Longo, U. G.; Franceschi, F.; Ruzzini, L.; Spiezia, F.; Maffulli, N.; and Denaro, V. Higher fasting plasma glucose levels within the normoglycemic range and rotator cuff tears. Br J Sports Med 2008;
6. Maffulli, N.; Barrass, V.; and Ewen, S. W. Light microscopic histology of achilles tendon ruptures. A comparison with unruptured tendons. Am J Sports Med 2000;28:857-63.
7. Maffulli, N.; Khan, K. M.; and Puddu, G. Overuse tendon conditions: time to change a confusing terminology. Arthroscopy 1998;14:840-3.
8. Maffulli, N.; Longo, U. G.; Franceschi, F.; Rabitti, C.; and Denaro, V. Movin and Bonar scores assess the same characteristics of tendon histology. Clin Orthop Relat Res 2008;466:1605-11.
9. Maffulli, N.; Reaper, J.; Ewen, S. W.; Waterston, S. W.; and Barrass, V. Chondral metaplasia in calcific insertional tendinopathy of the Achilles tendon. Clin J Sport Med 2006;16:329-34.
10. Maffulli, N.; Sharma, P.; and Luscombe, K. L. Achilles tendinopathy: aetiology and management. J R Soc Med 2004;97:472-6.
11. Maffulli, N.; Testa, V.; Capasso, G.; Bifulco, G.; and Binfield, P. M.
Results of percutaneous longitudinal tenotomy for Achilles tendinopathy in middle- and long-distance runners. Am J Sports Med 1997;25:835-40.
12. Maffulli, N.; Testa, V.; Capasso, G.; Ewen, S. W.; Sullo, A.; Benazzo, F.; and King, J. B. Similar histopathological picture in males with Achilles and patellar tendinopathy. Med Sci Sports Exerc 2004;36:1470-5.
13. Maffulli, N.; Waterston, S. W.; and Ewen, S. W. Ruptured Achilles tendons show increased lectin stainability. Med Sci Sports Exerc 2002;34:1057-64.
14. Maffulli, N.; Wong, J.; and Almekinders, L. C. Types and epidemiology of tendinopathy. Clin Sports Med 2003;22:675-92.
15. Movin, T.; Gad, A.; Reinholt, F.; and Rolf, C. Tendon pathology in long-standing achillodynia. Biopsy findings in 40 patients. Acta Orthop
Scand 1997;68:170-5.
16. Murrell, G. A. Oxygen free radicals and tendon healing. J Shoulder Elbow Surg 2007;16:S208-14.
17. Murrell, G. A. Using nitric oxide to treat tendinopathy. Br J Sports Med 2007;41:227-31.
I have Type 2 diabetes. I'm 53 years old. My blood sugar level was 22
mml/L and I was obese. Now I have reached the ideal weight within 3 months
following a strict diabetes diet together with a 30 or 45 minute exercise
daily and Glucophage 850 twice a day.
Now I am off medication but still on dieting and exercise.
My fasting blood Sugar level is stable at around 5.6 - 5.8 every morning
and stays so after 3 hours of meals. T...
I have Type 2 diabetes. I'm 53 years old. My blood sugar level was 22
mml/L and I was obese. Now I have reached the ideal weight within 3 months
following a strict diabetes diet together with a 30 or 45 minute exercise
daily and Glucophage 850 twice a day.
Now I am off medication but still on dieting and exercise.
My fasting blood Sugar level is stable at around 5.6 - 5.8 every morning
and stays so after 3 hours of meals. The 2-hour level is usually higher,
but it does not go higher than 9.0 mml/L, and it always comes down to 5.6
- 5.8 after 3 hours or sometimes 4.
I mentioned all that so that I can say that a 45 minute exercise
daily (treadmill) with some aerobics, is much more effective in reducing
the blood sugar level than a
30 minute one. I hope this will help others. But it could also be an
individual case.
Dear Sir,
We read with interest the Review Article "Rotator cuff tendinopathy: A review", by Lewis, doi:10.1136/bjsm.2008.052175.
This manuscript may have been submitted before the publication of our investigations. Nevertheless, we would like to call your attention to the fact that we have performed several studies on the aetiology, histopathology and management of rotator cuff tendinopathy.
We investig...
I have Type 2 diabetes. I'm 53 years old. My blood sugar level was 22 mml/L and I was obese. Now I have reached the ideal weight within 3 months following a strict diabetes diet together with a 30 or 45 minute exercise daily and Glucophage 850 twice a day. Now I am off medication but still on dieting and exercise. My fasting blood Sugar level is stable at around 5.6 - 5.8 every morning and stays so after 3 hours of meals. T...
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