We have used Fourier transform infrared spectroscopy (FTIR) to characterise the chemical and structural composition of the tendons of the rotator cuff and to identify structural differences among anatomically distinct tears. Such information may help to identify biomarkers of tears and to provide insight into the rates of healing of different sizes of tear. The infrared spectra of 81 partial, small, medium, large and massive tears were measured using FTIR and compared with 11 uninjured control tendons. All the spectra were classified using standard techniques of multivariate analysis.

FTIR readily differentiates between normal and torn tendons, and different sizes of tear. We identified the key discriminating molecules and spectra altered in torn tendons to be carbohydrates/phospholipids (1030 cm⁻¹ to 1200 cm⁻¹), collagen (1300 cm⁻¹ to 1700 cm⁻¹ and 3000 cm⁻¹ to 3350 cm⁻¹) and lipids (2800 cm⁻¹ to 3000 cm⁻¹).

Our study has shown that FTIR spectroscopy can identify tears of the rotator cuff of varying size based upon distinguishable chemical and structural features. The onset of a tear is mainly associated with altered structural arrangements of collagen, with changes in lipids and carbohydrates. The approach described is rapid and has the potential to be used peri-operatively to determine the quality of the tendon and the extent of the disease, thus guiding surgical repair.

The aim of this study was to investigate genetic influences on the development and progression of tears of the rotator cuff. From a group of siblings of patients with a tear of the rotator cuff and of controls studied five years earlier, we determined the prevalence of tears of the rotator cuff with and without associated symptoms using ultrasound and the Oxford Shoulder Score.

In the five years since the previous assessment, three of 62 (4.8%) of the sibling group and one of the 68 (1.5%) controls had undergone shoulder surgery. These subjects were excluded from the follow-up.

Full-thickness tears were found in 39 of 62 (62.9%) siblings and in 15 of 68 (22.1%) controls (p = 0.0001). The relative risk of full-thickness tears in siblings as opposed to controls was 2.85 (95% confidence interval (CI) 1.75 to 4.64), compared to 2.42 (95% CI 1.77 to 3.31) five years earlier. Full-thickness tears associated with pain were found in 30 of 39 (76.9%) tears in the siblings and in eight of 15 (53.3%) tears in the controls (p = 0.045). The relative risk of pain associated with a full-thickness tear in the siblings as opposed to the controls was 1.44 (95% CI 2.04 to 8.28) (p = 0.045).

In the siblings group ten of 62 (16.1%) had progressed in terms of tear size or development compared to one of 68 (1.5%) in the control group which had increased in size.

Full-thickness rotator cuff tears in siblings are significantly more likely to progress over a period of five years than in a control population. This implies that genetic factors have a role, not only in the development but also in the progression of full-thickness tears of the rotator cuff.

We have conducted a prospective study to assess the mid-term clinical results following arthroscopic repair of the rotator cuff. Patients were evaluated using the Constant score, subjective satisfaction levels and post-operative ultrasound scans.

Of 115 consecutive patients who underwent arthroscopic repair of the rotator cuff at our institution, 102 were available for follow-up. The mean period of follow-up was for 35.8 months (24 to 73). The mean age of the patients was 57.3 years (23 to 78). There were 18 small (≤ 1 cm in diameter), 44 medium (1 cm to 3 cm in diameter), 34 large (3 cm to 5 cm in diameter) and six massive (> 5 cm in diameter) tears. There was a statistically significant increase in the size of the tear with increasing age (p = 0.0048).

The mean pre-operative Constant score was 41.4 points (95% confidence interval, 37.9 to 44.9), which improved to 84.5 (95% confidence interval, 82.2 to 86.9). A significant inverse association (p = 0.0074), was observed between the size of the tear and the post-operative Constant score, with patients having smaller tears attaining higher Constant scores after repair. Post-operatively, 80 patients (78.4%) were able to resume their occupations and 84 (82.4%) returned to their pre-injury leisure activities. Only eight (7.8%) of 102 patients were not satisfied with the outcome.

Recurrent tears were detected by ultrasound in 19 (18.6%) patients, and were generally smaller than the original ones. Patients with recurrent tears experienced a mean improvement of 31.6 points (95% confidence interval, 23.6 to 39.6) in their post-operative Constant scores. Those with intact repairs had significantly improved (p < 0.0001) Constant scores (mean improvement 46.3 points, 95% confidence interval, 41.9 to 50.6). Patient satisfaction was high in 94 cases (92%), irrespective of the outcome of the Constant score. Recurrent tears appear to be linked to age-related degeneration.

Arthroscopic repair of the rotator cuff leads to high rates of satisfaction (92%) and good functional results, albeit with a recurrence rate of 18.6% (19 of 102).

We have undertaken an in vivo assessment of the tissue metabolism and cellular activity in torn tendons of the rotator cuff. Cellular oxygen consumption was measured in 13 patients undergoing mini-open repair of small, medium, large and massive full-thickness tears. Measurements were also taken from three control patients who were undergoing open stabilisation of the shoulder with grossly normal tendons. The level of oxygen and nitrous oxide was measured amperometrically using silver needle microelectrodes at the apex of the tear and 1.5 cm from its edge. With nitrous oxide indicating the degree of perfusion, oxygen consumption was calculated at each location to reflect cellular activity. All of the torn tendons had lower levels of cellular activity than the control group. This activity was lower still in the tissue nearest to the edge of the tear with the larger tears showing the lowest activity. This indicated reduced levels of tissue metabolism and infers a reduction in tendon viability. Our findings suggest that surgical repair of torn tendons of the rotator-cuff should include the more proximal, viable tissue, and may help to explain the high rate of re-rupture seen in larger tears

We have studied cellular and vascular changes in different stages of full thickness tears of the rotator cuff. We examined biopsies from the supraspinatus tendon in 40 patients with chronic rotator cuff tears who were undergoing surgery and compared them with biopsies from four uninjured subscapularis tendons. Morphological and immunocytochemical methods using monoclonal antibodies directed against leucocytes, macrophages, mast cells, proliferative and vascular markers were used.

Histological changes indicative of repair and inflammation were most evident in small sized rotator cuff tears with increased fibroblast cellularity and intimal hyperplasia, together with increased expression of leucocyte and vascular markers. These reparative and inflammatory changes diminished as the size of the rotator cuff tear increased. Marked oedema and degeneration was seen in large and massive tears, which more often showed chondroid metaplasia and amyloid deposition. There was no association between the age of the patient and the duration of symptoms. In contrast, large and massive tears showed no increase in the number of inflammatory cells and blood vessels.

Small sized rotator cuff tears retained the greatest potential to heal, showing increased fibroblast cellularity, blood vessel proliferation and the presence of a significant inflammatory component. Tissue from large and massive tears is of such a degenerative nature that it may be a significant cause of re-rupture after surgical repair and could make healing improbable in this group.

We describe 20 patients, aged between 43 and 88 years, with delayed nerve palsy or deepening of an initial palsy caused by arterial injury from low-energy injuries to the shoulder. The onset of palsy ranged from immediately after the injury to four months later. There was progression in all the patients with an initial partial nerve palsy. Pain was severe in 18 patients, in 16 of whom it presented as neurostenalgia and in two as causalgia. Dislocation of the shoulder or fracture of the proximal humerus occurred in 16 patients. There was soft-tissue crushing in two and prolonged unconsciousness from alcoholic intoxication in another two.

Decompression of the plexus and repair of the arterial injury brought swift relief from pain in all the patients. Nerve recovery was generally good, but less so in neglected cases. The interval from injury to the repair of the vessels ranged from immediately afterwards to 120 days.

Delayed onset of nerve palsy or deepening of a nerve lesion is caused by bleeding and/or impending critical ischaemia and is an overwhelming indication for urgent surgery. There is almost always severe neuropathic pain.