| Abstract |
The rotator cuff is the dynamic stabilizer of the glunohumeral joint. It is a complex of
tendons, which covers the shoulder joint and it is inserted at the humerus. The
supraspinatus, the infraspinatus, the teres minor, the subscapularis and the long head
of biceps tendon construct the rotator cuff.
Rotator cuff tears are extremely common. Cadaver studies in the elderly estimate the
prevalence of rotator cuff tears to be from 20-35%. The prevalence of full thickness
tears is 30% and the rest 70% represent partial tears.
Rotator cuff tears, as well as, the preceding degenerative disorder are the most
frequently causes of dysfunction and pain in the shoulder in patients above 40 years
old. Rotator cuff tears commonly accompanies with pain when they are associated
with long head of biceps (LHB) lesions. It is also known that spontaneously or
surgical resection of the LHB leads to pain relief. Based on these observations we
could easily assume that the LHB is responsible for the pain in these patients rather
than the rotator cuff tear itself. Some authors believe that a possible explanation could
be a repeatedly tendon injury due to an ongoing subacromial impingement of the
LHB. Others suggest that the nervous system contributes to the development of the
clinical picture.
Recently, the term tendinosis has been introduced in order to describe the
degenerative changes, which happen in the tendon when the mechanical stress
exceeds the normal tolerance of the tissue. In that case the tendon fails to develop the
appropriate healing process. The chronic tendon disorders (tendinosis) have not been
fully understood. The term tendonitis has been used to describe them. However,
histopahological studies did not succeed to reveal the presence of inflammatory cells,
which illustrate the acute inflammatory conditions. Therefore, tendinosis appears to
be a degenerative process that is characterized by the presence of dense populations of
fibroblasts, disorganized extracellular matrix and vascular hyperplasia.
In order to investigate the pathogenesis of tendinosis we divided our research into two
directions: 1) We have tried to clarify why tendinosis is painful given the absence of
acute inflammatory cells; 2) and to examine the causes which prevent tendon healing.
For this purpose we studied the potential role of the nervous system as well as the role
of apoptosis in the long head of the biceps tendon.
The nervous system plays a major in the pathogenesis of the so- called ‘’ Neurogenic
Inflammation’’. Neuropeptides such as substance P (SP) and calcitonin gene-related
peptide (CGRP), besides transmitting the pain they participate in vasodilation, plasma
extravagation and cytokines release. Furthermore there is evidence that sympathetic
fibers contribute to the above regulatory system. Imbalances between vasoconstrictor
(TH) and vasodilator (SP, CGRP) mediators may lead to abnormal perfusion,
nutritional deficiency, ischemia and hypoxic degeneration
The nervous system could be involved in the pathophysiology of LHB tendinosis as a
result of the action of the cell adhesion molecules. The cell adhesion molecules are
extremely important to maintain the architecture of the nervous system. Additionally,
a recent study report that cell adhesion molecule L1 CAM is involved in the
mechanisms oh neuropathic pain.
Regarding the impaired healing capacity, which characterizes tendinosis, many
authors believe that apoptosis represent the heart of the problem. Apoptosis, or
programmed cell death is an extremely significant physiological process. It is an
important component of embryogenesis and organogenesis. It is also vital in the
maintenance of homeostasis in many adult tissue through the control of cell
population. Apoptosis is highly regulated by biochemical pathways, which
consequence to intracellular events (mitochondria alterations, nuclear fragmentation)
eventually leading to cell death.
Using immunohistochemical techniques in paraffin and frozen sections as well as
Western Blots techniques we investigated the sensory and sympathetic innervation
and the expression of the L1 CAM in LHB. Finally we tried to evaluate the
involvement of apoptosis in LHB tendinosis. We used neurofilament (NF) antibody as
a general marker, calcitonin gene-related peptide (CGRP) and substance P (SP), for
the sensory fibers and tyrosine hydroxylase (TH) to detect the sympathetic nerve
fibers. Bad, Bax and Bcl2 antibodies were used to assess the apoptosis. L1 CAM
antibody was used to detect the expression of this specific protein. We used tissue
(LHB) harvested from cadavers as well as from patients undergoing LHB tenotomy.
Neurofilament, SP, CGRP and TH antibodies revealed a rich innervation, which was
more common at the proximal insertion to the bone than at the distal tendomuscular
junction. The staining patterns with all antibodies appeared identical showing a thin
interconnected network of nerve fibers.
Using L1 CAM antibody we revealed the expression of L1 CAM in human tendons.
To our knowledge this the first report of L1 CAM expression in human tendons.
We also investigated apoptosis in LHB by using Bad, Bax and Bcl2 antibodies.
Unfortunately we were not able to detect excessive apoptosis in degenerative LHB
tissue compared with the control croup.
In summary, the findings of this study are:
1) The LHB contains a large network of sensory sympathetic nerve fibers, which
is not associated with blood vessels, as it has been described in previous
studies.
2) The distribution of this innervation is heterogeneous, since it is present rather
in the bone insertion side of the tendon.
3) The L1 CAM protein is expressed in the human tendons.
4) We failed to reveal that excessive apoptosis is present in LHB disorders.
Theses results may attributes to factors, which may play a certain role such as
patients’ age.
In conclusion: Our findings may give a possible explanation for the role of LHB in the
pathogenesis of shoulder pain in patients with concomitant impingement syndrome or
rotator cuff tear.
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Νεύρωση του ώμου : προσδιορισμός των λεπτών νευρικών δομών του τενόντιου πετάλου των στροφέων με μεθόδους ανοσοφθορισμού και ανοσοϊστοχημείας και ερμηνεία της ανάπτυξης κλινικών συμπτωμάτων
