Effect of taping on the shoulders of Australian football players.

BACKGROUND: Taping of the shoulder is common in many sports, particularly Australian football, a contact sport that often involves marking (catching) the ball overhead and has a high incidence of shoulder instability. HYPOTHESIS: Taping of the shoulder reduces glenohumeral joint laxity and improves proprioception without impairing function. STUDY DESIGN: Crossover study design. METHODS: 33 male players aged 18-31 years were recruited from a local Australian football club. The dominant shoulder of each player was tested with and without taping in a randomised fashion by an examiner blinded to the presence or absence of taping. The tests were (1) inferior glenohumeral joint laxity (the Orthopaedic Research Institute laxometer), (2) shoulder joint position sense accuracy using an optical tracking system, and (3) handballing accuracy. RESULTS: The methods for testing laxity and joint position sense had good intraobserver reliability and sensitivity. All subjects tolerated the taping and testing. Glenohumeral joint laxity (p=0.75), joint position sense (p=0.56) and handballing accuracy (p=0.6) were not changed by taping. CONCLUSIONS: Taping of the shoulder joint in uninjured and non-symptomatic Australian football players in a pattern that attempted not to restrict their range of overhead movement did not significantly affect the accuracy of joint position sense, inferior laxity or handball accuracy. CLINICAL RELEVANCE: These data suggest that taping of the shoulder is unlikely to decrease the incidence of injury-specifically dislocation-of the shoulder in Australian football players.

Randomised, double-blind, placebo-controlled clinical trial of a new topical glyceryl trinitrate patch for chronic lateral epicondylosis.

OBJECTIVE: This study aimed to determine whether a new glyceryl trinitrate patch preparation is effective in treating chronic lateral epicondylosis. DESIGN: Randomised double-blind controlled clinical trial. SETTING: Private practice PATIENTS: 154 adult patients with chronic lateral epicondylosis were recruited, with 136 patients completing the trial. INTERVENTIONS: 8 weeks of glyceryl trinitrate patch application (dosages of 72 mg/24 h, 1.44 mg/24 h, and 3.6 mg/24 h), or placebo patch application. MAIN OUTCOME MEASURES: Subjective global assessment of change in elbow symptoms, patient-rated tennis elbow evaluation, visual analogue pain at rest, visual analogue pain with activity, visual analogue pain intensity, grip strength, and strength testing using the Orthopaedic Research Institute-Tennis Elbow Testing System. RESULTS: At 8 weeks there was a significant decrease in elbow pain with activity in the glyceryl trinitrate 0.72 mg/24 h group compared with placebo (p = 0.04). There were no other significant differences. CONCLUSIONS: Continuous 1.25 mg/24 h topical glyceryl trinitrate treatment, when combined with daily exercise rehabilitation, has previously demonstrated efficacy in treating chronic lateral epicondylosis. There was significantly decreased elbow pain with activity at 8 weeks in the glyceryl trinitrate 0.72 mg/24 h group (p = 0.04). This short-term dose-ranging study did not demonstrate a treatment effect of a new topical glyceryl trinitrate patch in dosages of 1.44 mg/24 h or 3.6 mg/24 h, which conflicts with previous studies on topical glyceryl trinitrate treatment. TRIAL REGISTRATION NUMBER: NCT00447928.

The effectiveness of arthroscopic stabilisation for failed open shoulder instability surgery.

We identified ten patients who underwent arthroscopic revision of anterior shoulder stabilisation between 1999 and 2005. Their results were compared with 15 patients, matched for age and gender, who had a primary arthroscopic stabilisation during the same period. At a mean follow-up of 37 and 36 months, respectively, the scores for pain and shoulder function improved significantly between the pre-operative and follow-up visits in both groups (p = 0.002), with no significant difference between them (p = 0.4). The UCLA and Rowe shoulder scores improved significantly (p = 0.004 and p = 0.002, respectively), with no statistically significant differences between groups (p = 0.6). Kaplan-Meier analysis for time to recurrent instability showed no differences between the groups (p = 0.2). These results suggest that arthroscopic revision anterior shoulder stabilisation is as reliable as primary arthroscopic stabilisation for patients who have had previous open surgery for recurrent anterior instability.

Reliability of a new shoulder laxometer to assess inferior glenohumeral joint translation.

OBJECTIVE: This study tested the reliability of the ORI laxometer, a newly developed non-invasive device for testing inferior translation of the humeral head in humans. DESIGN: The instrument was designed to measure displacement between the top of the acromion and the head of the humerus when loaded in a similar fashion to the sulcus sign. PARTICIPANTS AND INTERVENTIONS: Sixteen healthy subjects (32 shoulders) were measured for inferior glenohumeral joint laxity. One observer used the laxometer in 16 subjects on three separate occasions for the intra-observer trial. Three observers measured the inferior shoulder laxity of six subjects on one occasion in the inter-observer trial. Asymptomatic and unstable shoulders were also compared in 12 subjects with shoulder instability. MAIN OUTCOME MEASUREMENTS: Translation in the glenohumeral joint RESULTS: The range of inferior translation of glenohumeral joint in these subjects was between 0.01 mm and 6.5 mm with a mean of 1.5 mm. The intraclass correlation coefficient (ICC) for inter-observer reliability was 0.74. For intra-observer reliability the ICC was 0.76. These results are considered to be good to excellent. There was no advantage gained by using data from all five cycles of testing compared with three cycles. In patients with shoulder instability, laxometer measurements were significantly greater in their unstable shoulders than in their normal shoulders. CONCLUSIONS: The laxometer is easy to use, painless and gives objective measures for inferior glenohumeral laxity, with good intra- and inter-observer reliabilities. The ORI laxometer may be useful for assessing and monitoring global glenohumeral joint laxity which usually involves inferior laxity.

A sensitive stain for aluminum in undecalcified cancellous bone.

Aluminum is known to accumulate with age in bone and other tissues of humans, even in the absence of renal disease. Our study aimed to develop a histological staining method sufficiently sensitive to detect aluminum in plastic sections of undecalcified bone biopsies from healthy volunteers as well as from patients with renal and non-renal bone diseases. We used quantitative histomorphometry to measure the percentage of trabecular surface stained by aluminum and found that our new method was approximately 50% more sensitive for detecting aluminum than the Acid Solochrome Azurine (ASA) method which in turn was significantly more sensitive than the Aluminon method. Aluminon is widely used in pathology laboratories for diagnostic purposes despite concerns in the literature about Aluminon's limited sensitivity for aluminum. Our histomorphometric results showed that the newly developed method stained approximately 10% of the trabecular surface in bone sections from healthy controls, 38% from renal patients, 26% from patients with vitamin D deficiency, and 29% from patients with osteoporosis. Histomorphometric measurements of aluminum-stained trabecular surfaces in sections stained with ASA were consistent with those obtained in Walton-stained sections but proportionately lower. Moreover, the Walton and ASA methods stained aluminum at similar locations in adjacent bone sections. As the ASA and Walton methods are considerably more sensitive for bone aluminum than the Aluminon method, we recommend that either of them should be used in place of the Aluminon method for routine diagnostic purposes.

Adductor strain and hip range of movement in male professional soccer players.

PURPOSE: To determine whether hip range of movement (ROM) can predict the occurrence of adductor strain among male professional soccer players. METHODS: 120 subjects were prospectively selected from 6 professional soccer clubs in Australia. Internal rotation, external rotation, and ROM of the hip were measured using a goniometer before and during the course of a soccer season (2003-2004). When adductor strain occurred, further assessments of the hip were performed. Injured subjects' hip ROMs were measured again at the end of the season. RESULTS: Eight of the 120 subjects had 9 adductor strains (one bilateral). There was a correlation between preseason decreased hip ROM and occurrence of adductor strain. The mean preseason hip ROM was 44.7 degrees in the injured group and 53.7 degrees in the uninjured group. Once the subjects were able to resume playing soccer, their hip ROM increased to near pre-injury levels. CONCLUSION: Decreased hip ROM may be considered an aetiological factor in the occurrence of adductor strain in male professional soccer players.

Microarray analysis of the tendinopathic rat supraspinatus tendon: glutamate signaling and its potential role in tendon degeneration.

Degenerative tendon injury or "tendinopathy" is one of the most common disorders of the musculoskeletal system. We used a rat model (Soslowsky LJ, Thomopoulos S, Tun S, Flanagan CL, Keefer CC, Mastaw J, and Carpenter JE. J Shoulder Elbow Surg 9: 79-84, 2000) to identify novel gene expression in the exercised-induced degenerated supraspinatus tendon by microarray and real-time PCR analyses. We identified several novel groups of differentially expressed genes, including those involved in apoptosis and related stress responses, and also genes that appear to be involved in glutamate signaling in tendon tissue, similar to recent findings by us in a microarray study of healing in the transected Achilles tendon of the rat (24). Until recently this kind of cellular communication was thought only to exist in cells of the central nervous system (CNS), where it is vital for CNS function. We further show that glutamate appears to induce a proapoptotic response in cultured tendon cells, similar to the "excitotoxic" response of cells in the CNS that become overstimulated. This may prove to be at least a partial cause of degeneration in overused tendon tissue and allow the development of treatments or "prehibilitation" regimens for tendinopathy based on currently used non-toxic glutamate antagonists.

Overexpression of nitric oxide synthases in tendon overuse.

Tendon disorders with a chronic nature, including the rotator cuff, are extremely common, and represent a major clinical problem. Mechanical overload has been proposed as an important etiologic factor in tendinopathies. Nitric oxide (NO), a free radical produced by nitric oxide synthases (NOSs), is a potent regulator and stimulator of biological processes including tendon degeneration and healing. It is also involved in response to mechanical stimuli in different tissues. In an animal model of acutely injured tendon healing temporal and differential expression of NOS isoforms has been demonstrated, suggesting that different patterns of NOSs expression may have different biological functions. Therefore, we hypothesized that tendon overuse may result in a differential upregulation of NOSs, particularly iNOS. An animal model of supraspinatus tendon overuse was utilized, which consisted of treadmill running. A group of animals of the same strain and age subjected to normal cage activity were used as controls. Following a 4-week exercise protocol supraspinatus tendons were harvested, RNA was extracted, and subjected to competitive reverse transcription and polymerase chain reaction (RT-PCR) to determine the expression levels of inducible-, endothelial-, and neuronal-NOS isoforms (i-, e-, and nNOS). The mRNA expression of all three NOS isoforms increased in the supraspinatus tendons as a result of overuse exercise. iNOS and eNOS mRNA expression increased fourfold (p < 0.01), and there was an increase, but statistically not significant, in nNOS mRNA expression in the overused tendons when compared with the controls. This study is the first to show that NOS isoforms are upregulated in rotator cuff tendon as a result of chronic overuse, and suggests the involvement of nitric oxide in the response of tendon tissue to increased mechanical stress.

Microarray analysis of healing rat Achilles tendon: evidence for glutamate signaling mechanisms and embryonic gene expression in healing tendon tissue.

Tendon healing is a complex process consisting of a large number of intricate pathways roughly divided into the phases of inflammation, proliferation, and remodeling. Although these processes have been extensively studied at a variety of levels in recent years, there is still much that remains unknown. This study used microarray analyses to investigate the process at a genetic level in healing rat Achilles tendon at 1, 7, and 21 days postinjury, roughly representing the inflammation, proliferation, and remodeling phases. An interesting temporal expression profile was demonstrated, identifying both known and novel genes and pathways involved in the progression of tendon healing. Both inflammatory response and pro-proliferative genes were shown to be significantly upregulated from 24 h postinjury through to 21 days. Day 7 showed the largest increase in genetic activity, particularly with the expression of collagens and other extracellular matrix genes. Interestingly, there was also evidence of central nervous system-like glutamate-based signaling machinery present in tendon cells, as has recently been shown in bone. This type of signaling mechanism has not previously been shown to exist in tendon. Another novel finding from these analyses is that there appears to be several genes upregulated during healing which have exclusively or primarily been characterized as key modulators of proliferation and patterning during embryonic development. This may suggest that similar pathways are employed in wound healing as in the tightly regulated progression of growth and development in the embryo. These results could be of use in designing novel gene-based therapies to increase the efficacy and efficiency of tendon healing.

Nitric oxide synthase isoforms during fracture healing.

We have shown previously that nitric oxide (NO) has regulatory effects on fracture healing. Our aim here was to investigate the temporal expression patterns of the three NO synthase (NOS) isoforms that are responsible for the generation of NO by semiquantitative competitive polymerase chain reaction (PCR) and immunoblot analysis after femoral fractures in rats. We found that 4 days after fracture, there were increases in the levels of messenger RNA (mRNA) for all three NOS isoforms, with peaks for the inducible NOS (iNOS; 35-fold increase, p < 0.05) at day 4, the endothelial NOS (eNOS; 5-fold increase, p < 0.05) at day 7, and the neuronal NOS (bNOS; 16-fold increase, p < 0.05) at day 21. At a protein level, the time course expression of NOS isoforms was consistent with the results of those at the mRNA level. In addition, we have previously reported a 2.5-fold increase in NOS activity detected by [3H]arginine to [3H]citrulline conversion at day 15 compared with that at day 4 after fracture. The findings that the expression of NOS isoforms during fracture healing is type specific and time dependent are important and may have clinical applications in the regulation of bone repair by NOS inhibitors or stimulators at different stages after injury.

Nitric oxide modulates fracture healing.

The role of the messenger molecule nitric oxide has not been evaluated in fracture healing. NO is synthesized by three kinds of nitric oxide synthase (NOS): inducible NOS (iNOS), endothelial (eNOS), and neuronal (bNOS). We evaluated the role of these enzymes in a rat femur fracture-healing model. There was no messenger RNA (mRNA) expression, immunoreactivity, or enzymatic activity for NOS in unfractured femoral cortex. After fracture, however, mRNA, protein, and enzymatic activity for iNOS were identified in the healing rat femoral fracture callus, with maximum activity on day 15. The mRNA expression for eNOS and bNOS was induced slightly later than for iNOS, consistent with a temporal increase in calcium-dependent NOS activity that gradually increased up to day 30. mRNA expression for the three NOS isoforms also was found in six of six human fracture callus samples. To study the effect of suppression of NO synthesis on fracture healing, an experimental group of rats was fed an NOS inhibitor, L-nitroso-arginine methyl ester (L-NAME), and the control group was fed its inactive enantiomer, D-nitroso-arginine methyl ester (D-NAME). An 18% (p < or = 0.01) decrease in cross-sectional area and a 45% (p < or = 0.05) decrease in failure load were observed in the NOS-inhibited group on day 24 after fracture. Furthermore, the effect of NO supplementation to fracture healing was studied by delivering NO to the fracture site using carboxybutyl chitosan NONOate locally. On day 17 after fracture, there was a 30% (p < or = 0.05) increase in cross-sectional area in the NO-donor group compared with the NOS inhibition group. These results show for the first time that NO is expressed during fracture healing in rats and in humans, that suppression of NOS impairs fracture healing, and that supplementation of NO can reverse the inhibition of healing produced by NOS inhibitors.

Nitric oxide in arthritis.

Nitric oxide's (NO) involvement in arthritis was first demonstrated when levels of nitrite, a stable endproduct of NO metabolism, were shown to be elevated in serum and synovial fluid samples of rheumatoid and osteoarthritis patients. NO production by chondrocytes, its involvement in various biochemical events of cartilage metabolism, and the in vivo suppression of experimental arthritis by NO synthase inhibitors further implicated NO in arthritis. However, a conclusive role for NO in the pathogenesis of arthritis remains to be defined, in contrast to the NO-cGMP signal transduction pathway of endothelium-mediated vasodilation. It appears that NO has limited modulating effects in cartilage metabolism, with evidence for both protective and deleterious effects. Recent developments that contribute to our understanding of NO's role in arthritis are discussed.

Genotype dependent and cigarette specific effects on endothelial nitric oxide synthase gene expression and enzyme activity.

We explored the interactive effects of endothelial nitric oxide synthase (eNOS) genotypes and cigarette smoking on protein levels and enzyme activity in 33 postpartum placentas. Whilst the eNOS protein levels were lower in the rare allele (0.48+/-0.11, n=9 vs. 1. 05+/-0.10, n=24, P<0.01), the eNOS enzyme activity was about 7-fold higher in the rare allele (4556.2+/-255.4 vs. 621.8+/-180.5 cpm/mg/min, P<0.01). Smokers had lower eNOS protein levels (1.07+/-0. 09 vs. 0.50+/-0.19, P<0.05) in both alleles. It reduced the eNOS activities only in the rare allele (non-smokers: 6143.8+/-251.2, n=5, smokers: 2968.5+/-259.4, n=4, 52% reduction, P<0.01). We conclude that associations between eNOS polymorphism and protein levels and enzyme activities are modifiable by smoking, the effects of smoking are dependent on the eNOS genotypes.

Osteoporosis influences the early period of fracture healing in a rat osteoporotic model.

Osteoporotic fractures commonly occur in the elderly. Although current therapies are aimed at the prevention and treatment of osteoporotic fractures, studies examing the fracture healing process in osteoporotic bone are limited. We produced an osteoporotic rat model by ovariectomy (ovx) and maintained a low calcium diet (LCD) in order to evaluate the influence of osteoporosis on fracture healing. Callus formation and strength was monitored over a 3 week period by histological and biomechanical assessment. Data collected simultaneously on a group of rats undergoing sham surgery (sx) were used for comparison. A 40% reduction in fracture callus cross-sectional area and a 23% reduction in bone mineral density in the healing femur of the ovx rats was observed on day 21 following fracture as compared with the sx group (p < 0.01). Biomechanical data from the healing femur of the ovx rats revealed a fivefold decrease in the energy required to break the fracture callus, a threefold decrease in peak failure load, a twofold decrease in stiffness and a threefold decrease in stress as compared with the sx group (p < 0.01, respectively). Histomorphological analysis revealed a delay in fracture callus healing with poor development of mature bone in the ovx rats. This study provides physical evidence of altered fracture healing in osteoporotic bone, which may have important implications in evaluating the effects of new treatments for osteoporosis on fracture healing.

Clinical pharmacokinetics of allopurinol.

Allopurinol is a widely used drug in the management of hyperuricaemia. It is rapidly and extensively absorbed following oral administration. The major and active metabolite, oxypurinol, is detected in the circulation within 15 minutes of allopurinol administration. Oxypurinol concentrations are higher than those of the parent drug and accumulation occurs during long term administration. Up to 80% of allopurinol is recovered in the urine within 24 hours, mainly in the form of oxypurinol. Allopurinol is negligibly absorbed after rectal administration. In animals, allopurinol is found in highest concentrations in vascular tissue, blood, liver, intestine and heart. It is negligibly bound to plasma proteins. Oxypurinol is eliminated by the kidney and has a much longer elimination half-life than allopurinol. Oxypurinol accumulates in patients with renal dysfunction; hence allopurinol dosages should be adjusted in such patients. Allopurinol inhibits the metabolism of 6-mercaptopurine and azathioprine, which require dosage modifications. The interaction of allopurinol with oral anticoagulants and phenytoin has not been clearly established in clinical practice.

S-substituted isothioureas are potent inhibitors of nitric oxide biosynthesis in cartilage.

Nitric oxide (NO.) is a multifunctional messenger molecule generated by a family of enzymes, the nitric oxide synthases, and is overproduced in osteoarthritis and rheumatoid arthritis. Chondrocytes are the major native source of NO. in diarthrodial joints. Chondrocytic inducible nitric oxide synthase induced by inflammatory cytokines and bacterial cell wall fragments mediates many of the catabolic events in arthritis. Agents which specifically inhibit chondrocyte inducible NO. synthase, may thus have a role in the management in arthritis. We evaluated a novel class of potential inducible NO. synthase inhibitors, the S-substituted isothioureas, for their ability to inhibit inducible NO. synthase activity in cultured bovine chondrocytes and explants of cartilage from patients with osteoarthritis. Two isothioureas, S-methyl isothiourea and S-(aminoethyl) isothiourea were 2-4 times more potent than NG-monomethyl-L-arginine monoacetate, 5-10 times more potent than aminoguanidine and over 300 times more potent than N omega-nitro-L-arginine and N omega-nitro-L-arginine methyl ester. The rank order of potency of the NO. synthase inhibitors was S-(aminoethyl) isothiourea > S-methyl isothiourea > NG-monomethyl-L-arginine > aminoguanidine > N omega-nitro-L-arginine = N omega-nitro-L-arginine methyl ester. The order of potency was reversed (N omega-nitro-L-arginine methyl ester = N omega-nitro-L-arginine > NG-monomethyl-L-arginine = S-methyl isothiourea > S-(aminoethyl) isothiourea > aminoguanidine) when evaluating the same compounds ability to inhibit constitutive NO. synthase activity in bovine endothelial cells. In comparison to conventional arginine based analogs, the isothioureas represent a more potent and relatively specific class of inhibitors of inducible NO. synthase in cartilage and thus may be beneficial in the management of arthritis.

Achilles tendon healing: a correlation between functional and mechanical performance in the rat.

The pathogenesis and treatment of rupture of the Achilles tendon remain a source of controversy. This study presents the results of a biomechanical, functional, and morphological evaluation of a group of rats that had division and repair of the Achilles tendon. A total of 46 rats were used: 18 for biomechanical testing, 18 for functional evaluation, and 10 for histology. Morphological examination revealed an early inflammatory response with loose connective tissue formation that was replaced gradually by fibroblasts and a collagenous matrix. The functional evaluation (Achilles functional index [AFI]) was made from measurements of the hind pawprints of walking rats. Division and repair of the Achilles tendon produced a significant functional impairment (mean [+/- SEM] AFI = -87 +/- 8; p < 0.001), which gradually improved with healing time. The load to failure for the repaired tendons consistently improved with healing time, in a manner similar to the functional recovery. The average deformation (repair/control) varied considerably and was not related to healing time. The stiffness of the repaired tendons increased with healing time and was 60% of the corresponding control side by day 15. The major finding of this study was a strong correlation between the AFI and the failure load of the healing tendon-bone constructs (250-300 g group, r = 0.97, p < 0.001; 325-375 g group, r = 0.96, p < 0.001).

Effects of immobilization on Achilles tendon healing in a rat model.

The aim of this study was to evaluate the effects of immobilization and mobilization on the functional and biomechanical recovery of injured Achilles tendons. Male Sprague-Dawley rats were allocated randomly into four groups: (a) sham operation, (b) division only (surgical transection of the Achilles tendon without immobilization), (c) "dummy" external fixation (division of the Achilles tendon and application of Kirschner wires), and (d) rigid external fixation (division of the Achilles tendon and immobilization with Kirschner wires connected by two triangular frames). All procedures were performed on the right lower limb; the left, uninjured, lower limb served as an internal control. Kirschner wires and external fixators were removed on day 12. Functional performance was determined from measurements of hind pawprints of rats walking preoperatively and on postoperative days 1, 3, 5, 7, 9, 11, 13, and 15. On day 15, the animals were killed and biomechanical evaluations were performed on both the injured and the uninjured Achilles tendon constructs. No functional or mechanical deficits were observed in the sham-operation group. Animals subjected to division of the Achilles tendon had an initial functional deficit that returned to near normal by day 15. The application of Kirschner wires was associated with an impairment of the functional performance of the rat as well as of the mechanical properties of the tendon-bone constructs. Immobilization by connection of the Kirschner wires to an external frame had an additional, highly significant (p < 0.001) detrimental effect on the functional and mechanical recovery of Achilles tendon-calcaneal complexes.

Temporal expression of nitric oxide synthase isoforms in healing Achilles tendon.

We investigated the temporal expressions of the three nitric oxide synthase (NOS) isoforms by semi-quantitative polymerase chain reaction (PCR) assays and by immunoblot analysis, following Achilles tendon transection in rats. Four days after injury, there were increases in the steady-state levels of mRNA for all three NOS isoforms, with peaks for the inducible isoform (iNOS) (23-fold increase) at day 4, the endothelial isoform (eNOS) (24-fold increase) at day 7 and the neuronal isoform (bNOS) (seven-fold increase) at day 21. The temporal expression of NOS isoforms at a protein level was consistent with the results at the mRNA level. We have previously shown a five-fold increase in the NOS activity, as detected by 3H-arginine to 3H-citrulline conversion, at day 7 postinjury. These findings indicate that all three NOS isoforms are expressed during tendon healing with differential expression patterns during the various phases of tendon healing. These findings may prove clinically relevant with respect to strategies for regulating tendon healing.

The Achilles Functional Index.

The literature regarding the management of spontaneous rupture of the Achilles tendon is controversial and confusing. The relative infrequency of the condition in any one center prohibits the completion of well-designed clinical studies. Many of the disputes could be addressed and innovations tested if an appropriate animal model were available. We present a method for evaluating Achilles tendon function from measurements of the prints, preserved in bromphenol-blue-impregnated photocopying paper, of the hindfeet of walking rats. The stimulus for this study was derived from de Medinaceli's method for assessing the functional condition of rat sciatic nerves (de Medinaceli L, Freed WJ, Wyatt RJ: An index of the functional condition of rat sciatic nerve based on measurements made from walking tracks. Exp Neurol 77:634-643, 1982). Four variables were measured from these walking tracks, and comparisons between the damaged (experimental) and intact (normal) side were converted to proportional deficits. The relative contribution of each parameter to the overall deficit was determined by multiple linear regression analysis, and the variables were weighted accordingly to obtain an "Achilles Functional Index" (AFI). A sham operation produced no functional deficit, whereas animals subjected to a 0.5-cm midsubstance Achilles tendon defect demonstrated a markedly impaired AFI. Animals with repaired transected Achilles tendons also demonstrated a significant, but less severely impaired AFI. The functional deficit in this repair group returned to control values by postoperative day 15, whereas animals with a defect remained impaired at day 15. Furthermore, an excellent correlation was found between the functional recovery and biomechanical properties (ultimate failure load) of the healing tendon (r = 0.94; p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)