Peritendinous Connective Tissue Research Articles

Plantaris Excision Reduces Pain in Midportion Achilles Tendinopathy Even in the Absence of Plantaris Tendinosis.

Background:It is becoming increasingly apparent that the plantaris can contribute to symptoms in at least a subset of patients with midportion Achilles tendinopathy. However, the nature of its involvement remains unclear.Purpose:To determine whether excised plantaris tendons from patients with midportion Achilles tendinopathy display tendinopathic changes and whether the presence of such changes affect clinical outcomes.Study Design:Case series; Level of evidence, 4.Methods:Sixteen plantaris tendons in patients with midportion Achilles tendinopathy recalcitrant to conservative management underwent histological examination for the presence of tendinopathic changes. All patients had imaging to confirm the presence of the plantaris tendon adherent to or invaginated into the focal area of Achilles tendinosis. Visual analog scale (VAS) and Foot and Ankle Outcome Score (FAOS) results were recorded pre- and postoperatively.Results:Sixteen patients (mean age, 26.2 years; range, 18-47 years) underwent surgery, with a mean follow-up of 14 months (range, 6-20 months). The plantaris tendon was histologically normal in 13 of 16 cases (81%). Inflammatory changes in the loose peritendinous connective tissue surrounding the plantaris tendon were evident in all cases. There was significant improvement in mean VAS scores (P < .05) and all domains of the FAOS postoperatively (P < .05).Conclusion:The absence of any tendinopathic changes in the excised plantaris of 13 patients who clinically improved suggests plantaris involvement with Achilles tendinopathy may not yet be fully understood and supports the concept that this may be a compressive or a frictional phenomenon rather than purely tendinopathic.

Exercise-dependent IGF-I, IGFBPs, and type I collagen changes in human peritendinous connective tissue determined by microdialysis

Microdialysis studies indicate that mechanical loading of human tendon during exercise elevates type I collagen production in tendon. However, the possibility that the insertion of microdialysis fibers per se may increase the local collagen production due to trauma has not been explored. Insulin-like growth factor I (IGF-I) and its binding proteins (IGFBPs), which are known to stimulate collagen production in animal tendons, may regulate the translation of mechanical loading to collagen synthesis. Systemic and tissue levels of IGF-I, IGFBP, and type I collagen metabolism markers [procollagen I COOH-terminal propeptide (PICP) and COOH-terminal telopeptide of type I collagen] were measured by microdialysis in peritendinous tissue of the human Achilles tendon in an exercise group (performing a 36-km run, n = 6) and a control group (no intervention, n = 6). An increase in local PICP concentration was seen in both groups after 72 h and stayed elevated in the exercise group at 96 h (P < 0.05). IGFBP-1 in both serum and dialysate increased in the exercise group immediately after exercise (P < 0.05), whereas IGFBP-3 decreased systemically (P < 0.05). Elevation of local IGFBP-4 was observed in both the control and exercise groups after 48 h (P < 0.05). Total IGF-I did not change in locally or systemically in either group. Our results indicate an increased local production of PICP in human peritendinous tissue in response to prolonged mechanical loading with part of the increase due to trauma from the sampling technique. Care must therefore be emphasized to minimize the numbers of insertions with microdialysis. We demonstrated an elevation of IGFBP-1 both systemically and peritendinously in response to prolonged acute exercise. The local increased collagen synthesis was preceded by an elevation of local concentration of IGFBP-4, suggesting that IGFBP-4 may have a key role in the IGF-axis effect on the human collagen synthesis in vivo.

Eccentric rehabilitation exercise increases peritendinous type I collagen synthesis in humans with Achilles tendinosis

It has been shown that 12 weeks of eccentric heavy resistance training can reduce pain in runners suffering from chronic Achilles tendinosis, but the mechanism behind the effectiveness of this treatment is unknown. The present study investigates the local effect of an eccentric training regime on elite soccer players suffering from chronic Achilles tendinosis on the turnover of the peritendinous connective tissue. Twelve elite male soccer players, of whom six suffered from unilateral tendinosis and six were healthy controls, participated in this study. All participants performed 12 weeks of heavy-resistance eccentric training apart from their regular training and soccer activity. Before and after the training period the tissue concentration of indicators of collagen turnover was measured by the use of the microdialysis technique. After training, collagen synthesis was increased in the initially injured tendon (n=6; carboxyterminal propeptide of type I collagen (PICP): pre 3.9+/-2.5 microg/L to post 19.7+/-5.4 microg/L, P<0.05). The collagen synthesis was unchanged in healthy tendons in response to training (n=6; PICP: pre 8.3+/-5.2 microg/L to post 11.5+/-5.0 microg/L, P>0.05). Collagen degradation, measured as carboxyterminal telopeptide region of type I collagen (ICTP), was not affected by training neither in the injured nor in the healthy tendons. The clinical effect of the 12 weeks of eccentric training was determined by using a standardized loading procedure of the Achilles tendons showing a decrease in pain in all the chronic injured tendons (VAS before 44+/-9, after 13+/-9; P<0.05), and all subjects were back playing soccer following the eccentric training regime. The present study demonstrates that chronically injured Achilles tendons respond to 12 weeks of eccentric training by increasing collagen synthesis rate. In contrast, the collagen metabolism in healthy control tendons seems not to be affected by eccentric training. These findings could indicate a relation between collagen metabolism and recovery from injury in human tendons.

Cyclo-oxygenase-2 mediated prostaglandin release regulates blood flow in connective tissue during mechanical loading in humans.

Mechanical loading is known to increase connective tissue blood flow of human tendons and to cause local release of vasodilatory substances. The present study investigated the importance of prostaglandins (PG) formed by cyclo-oxygenase isoforms (COX-1 and 2) for the exercise-related increase in blood flow in connective tissue. Healthy individuals (n = 24, age: 23-31 years) underwent 30 min of intermittent, isometric, plantarflexion with both calf muscles either without (n = 6, Control, C) or with blockade of PG formation, either COX-2 specific (n = 10, Celecoxib 2 x 100 mg day-1 for 3 days prior to the experiment) or COX unspecific (n = 8, indomethacin 100 mg (12 and 1 h pre-experiment) and acetyl salicylic acid 500 mg day-1 for 3 days pre-experiment). Prostaglandin E2 (PGE2) concentration was determined by microdialysis and blood flow by 133Xe washout. In C, interstitial PGE2 rose from (0.8 +/- 0.2 (rest) to 1.4 +/- 0.5 ng ml-1 (exercise), P < 0.05), whereas during unspecific COX inhibition, tissue PGE2 was completely inhibited at rest and during exercise. COX-2 specific blockade did not inhibit tissue PGE2 at rest, but totally abolished the exercise induced increase. Blood flow was similar in the three groups at rest (P > 0.05), whereas the increase in flow with exercise was reduced by 35 and 43 % with COX-2 specific blockade (3.2 +/- 0.7 to 6.1 +/- 1.5 ml (100 g tissue)-1 min-1 or COX unspecific blockade (3.0 +/- 0.8 to 7.6 +/- 1.6), respectively, compared to C (2.7 +/- 0.8 to 10.2 +/- 2.0)(P < 0.05). The findings indicate that COX-2 specific mechanisms are responsible for the exercise-induced increase in prostaglandin synthesis, and that increase in tissue prostaglandin plays an important role for blood flow in peritendinous connective tissue during physical loading in vivo.

Training‐induced changes in peritendinous type I collagen turnover determined by microdialysis in humans

1. Acute exercise is found to increase collagen type I formation locally in peritendinous connective tissue of the Achilles' tendon in humans, as determined from changes in interstitial concentrations of collagen propeptide (PICP) and a collagen degradation product (ICTP) by the use of microdialysis catheters. However, the local collagen type I turnover response to training is unknown. 2. Nineteen young males were studied before and after 4 and 11 weeks of physical training. Microdialysis catheters with a high molecular mass cut-off value (3000 kDa), allowing the determination of PICP and ICTP, were placed in the peritendinous space ventral to the Achilles' tendon, under ultrasound guidance, in both legs. The catheters were perfused with a Ringer-acetate solution containing (3)H-labelled human type IV collagen for in vivo recovery determination (relative recovery: 79 +/- 2 %, mean +/- S.E.M.). 3. The PICP concentration in the peritendinous tissue increased in response to training (from 5 +/- 1 to 35 +/- 5 microg l(-1) (4 weeks), P < 0.05) and remained elevated throughout the training period (28 +/- 6 microg l(-1), 11 weeks). Tissue ICTP only rose transiently with training (from 2.2 +/- 0.1 to 2.8 +/- 0.2 microg l(-1) (4 weeks), P < 0.05, and 2.5 +/- 0.2 microg l(-1) (11 weeks), P > 0.05 vs. basal). Plasma PICP was unchanged whereas plasma ICTP declined by 17 % in response to training. 4. The findings indicate that physical training results in an increased turnover of collagen type I in local connective tissue of the peritendinous Achilles' region. Early in the process both synthesis and degradation are elevated, whereas later, the anabolic processes are dominating causing a net synthesis of type I collagen in tendon-related tissue in humans.

The connective-tissue envelope in revascularisation of patellar tendon grafts

Free patellar tendon grafts used for the intra-articular replacement of ruptured anterior cruciate ligaments (ACL) lack perfusion at the time of implantation. The central core of the graft undergoes a process of ischaemic necrosis which may result in failure. Early reperfusion of the graft may diminish the extent of this process. We assessed the role of peritendinous connective tissue in the revascularisation of the patellar tendon graft from the day of implantation up to 24 days in a murine model using intravital microscopy. The peritendinous connective-tissue envelope of the graft was either completely removed, partially removed or not stripped before implantation into dorsal skinfold chambers of recipient mice. Initial revascularisation of the grafts with preserved peritendinous connective tissues began after two days. The process was delayed by five to six times in completely stripped patellar tendons (p &lt; 0.05). Only grafts with preserved connective tissues showed high viability whereas those which were completely stripped appeared to be subvital. The presence of peritendinous connective tissues accelerates the revascularisation of free patellar tendon grafts.

The connective-tissue envelope in revascularisation of patellar tendon grafts.

Free patellar tendon grafts used for the intra-articular replacement of ruptured anterior cruciate ligaments (ACL) lack perfusion at the time of implantation. The central core of the graft undergoes a process of ischaemic necrosis which may result in failure. Early reperfusion of the graft may diminish the extent of this process. We assessed the role of peritendinous connective tissue in the revascularisation of the patellar tendon graft from the day of implantation up to 24 days in a murine model using intravital microscopy. The peritendinous connective-tissue envelope of the graft was either completely removed, partially removed or not stripped before implantation into dorsal skinfold chambers of recipient mice. Initial revascularisation of the grafts with preserved peritendinous connective tissues began after two days. The process was delayed by five to six times in completely stripped patellar tendons (p < 0.05). Only grafts with preserved connective tissues showed high viability whereas those which were completely stripped appeared to be subvital. The presence of peritendinous connective tissues accelerates the revascularisation of free patellar tendon grafts.

Behavior of Tendons During Lower-Leg Lengthening in Dogs Using the Ilizarov Method

Twenty-two dogs were provided with a circular fixator. Lengthening of the right lower leg by 2.5 cm was performed on 18 dogs 5 days after tibial osteotomy using a distraction rate of 0.5 mm, twice per day. Nine dogs with leg lengthening and two dogs of the control group without leg lengthening were sacrificed at the end of the distraction phase of 25 days and the remaining dogs after another 25 days. Post mortem, the tendons of the tibialis anterior, extensor digitorum longus, peroneus longus, and the Achilles tendon were taken from the operated-on right side and the left nonoperated-on control side and were analyzed histologically. The control group showed no histologic changes in the tendons of either side nor in those of the unlengthened left side of the operated-on dogs. Thirty-three tendons (41%) of dogs with leg lengthening were seen to have undergone histomorphological changes. An increase of the peritendinous connective tissue was seen, combined with chronic inflammatory cell infiltration in the tendons and/or the epitendinous tissues, edema, tendon fragmentation, necrosis, scarring of the tendons with dystrophic calcification and/or ossification, and broadening of the tenosynovial sheath. Furthermore, signs of histoneogenesis with growth in the tendons were found. Degenerative changes occurred far more often in the tendons of the ventral side of the lower leg and a slight pes equinus was regularly observed in the lengthened extremity. Therefore, pes equinus prevention and physiotherapy are important in the therapeutic use of lower-leg lengthening to minimize possible stress-induced damage of the ventral tendons.

Fibrous architecture of the dorsal aponeurosis of the thumb.

The extensor apparatus of the thumb displays obvious structural variations in its proximo-distal expanse. Its associated tissue comes in close relation to the dorsal aponeurosis that have varying topographical relationships to the extensor apparatus of the thumb. This region is especially important as the location of pathological and repair processes. In this anatomical study using a modified embedding technique a histological description of the fibrous architecture of the dorsal aponeurosis and the peritendinous connective tissue body of the thumb is presented. The dorsal connective tissue of the thumb forms different layers of collagen lamellae as a peritendinous system around the tendons of the long and short extensor tendons of the thumb. This peritendinous laminar system as the main part of the dorsal aponeurosis is connected with both the capsular and the retinacular ligaments of the thumb. It will be shown that the structural variations of the dorsal aponeurosis and peritendinous connective tissue are an expression of different topographical zones of stress along the lines of a balanced musculofibrous stabilization of the interphalangeal joint of the thumb. The expansions in the peritendinous intercellular space act as defined gliding spaces or clefts of the extensor apparatus.

Cell morphology and collagen types in equine tendon scar

The histological appearance of cells and tissues in the reparative scar tissue which forms in the equine superficial flexor tendon following partial rupture was compared to that of normal tendon. The repair fibroblasts were found to be larger and more basophilic than the tenocytes of normal tendon, to have large vesicular nuclei and to resemble the 'myofibroblasts' described in scar tissue elsewhere. The cell to matrix ratio in scarred zones of tendon was found to be increased and the concentration of collagen in these areas was less than in normal tendon. However, the scar tissue collagen was more readily extractable and contained a different pattern of collagen types. Normal equine tendon was found to be composed almost exclusively of type I collagen whereas the scarred tendon had substantial quantities (20 to 30 per cent) of type III collagen in addition to type I. The presence of type III collagen in the scarred tendon was confirmed by indirect immunofluorescence using antibodies to purified type III collagen. These observations suggest that tendon scar tissue is not derived from proliferating tenocytes but from mesenchymal cells resting in peritendinous connective tissue or blood vessels. As a result of the presence of type III collagen, the scarred tendon is also likely to have less tensile strength than normal tendon.