The purpose of this study was to determine the functional changes due to the Graston Therapeutic Technique (GTT) in an animal model. This study attempted to verify the biomechanical changes associated with the Graston Therapeutic Technique (GTT) in order to possibly apply it to humans as a major physical therapy modality. Eighteen adult, male Sprague-Dawley rats were assigned randomly to three groups. The groups were classified as follows: (a) no injured plus GTT treatment, (b) injured minus GTT treatment, (c) injured plus GTT treatment. The GTT therapy began after one week following injury to allow for optimum inflammation and scar formation. The animals receiving GTT had six treatments over the course of two weeks. Running tests were performed on a treadmill at a velocity of 22 cm/s prior to induction of injury, one week following injury, two weeks following injury, and three weeksfollowing injury in the experimental groups. Variables analyzed were knee and ankle range of motion (ROM), stride length (SL), and stride frequency (SF). Significance of effect between experimental groups were determined by repeated measures one-way ANOVA, Scheffe's post hoc test, and Newman-Keuls post hoc test. The stride length and stride frequency results of the present study appeared to indicate that the Graston Therapeutic Technique (GTT) had an effect on changes in the stride length and stride frequency after injury. Statistical analysis between observations for the GTT plus groups indicated a significant difference in the swing phase of knee ROM. The results of this study also indicated that the Graston Therapeutic Technique may have had an influence on knee joint range of motion. / School of Physical Education

M.Tech.

Augmented Soft Tissue Mobilization, a massage therapy which uses a solid instrument rather than human fingers to treat musculoskeletal injuries, has been successful in treating tendinitis. Davidson et al. studied the functional and morphological affects of ASTM on collagenase induced Achilles tendinitis in Sprague-Dawley rats. Morphological observations showed a significant increase in the number and activation of fibroblasts in the ASTM treated Groups. The authors suggested that the physical force of ASTM may promote tendon healing via increased fibroblast recruitment. An important, but unexplained, question is how ASTM would affect the fibroblasts of native, noncollagenase injured, tendons. Studies have shown that mechanical forces can alter cellular functions. The purpose of this study was to examine the morphological changes in native Sprague-Dawley rat Achilles tendons after ASTM therapy using different application pressures.Three animal Groups were randomly established: A) control Group with no ASTM; B) light ASTM with 1 Newton of pressure; and C) heavy ASTM with 3 Newtons of pressure. Upon completion of the therapy, the Achilles tendons of each Group were examined with light and electron microscopy techniques to assess fibroblast number, tendon morphology, and the presence of type I and type III collagen. Fibroblast counts from each Group were compared using a two-way ANOVA, multiple regression, and curvilinear regression analysis. Morphological differences were shown between the three Groups, especially between the non force Group and the two force Groups. The ASTM Group treated with one Newton demonstrated the greatest mean fibroblast count (165.1+/-55.8&160.7+/-49.8). Electron microscopy revealed the presence of activated fibroblasts in the tendons of the two force Groups, ASTM Groups. Polarizing microscopy showed a dramatic increase in the amount of Type III collagen in the two force Groups compared to the non force Group.Ball State UniversityMuncie, IN 47306

Augmented Soft Tissue Mobilization (ASTM) is a new noninvasive technique utilized to treat chronic musculoskeletal injuries. The purpose of this study was to trace the morphological events in collagenase injured rat Achilles tendons during ASTM treatment and to observe passive occurrence of post treatment remodeling in tendons. Twelve groups of rats were divided into the following categories, A) control, B) sham surgery, C) ASTM only, D) ASTM/sham , E) tendinitis, F) ASTM/tendinitis 1 week, G) ASTM/tendinits 2 weeks H) ASTM/tendinits 3 weeks I) ASTM/tendinits 4 weeks, J) Post ASTM 5 weeks, K) Post ASTM 10 weeks, L) Post ASTM 15 weeks. One week after the last designated treatment, the Achilles tendons were harvested and then prepared for light microscopy, electron microscopy, and bifringence polarizing microscopy. An increase in fibroblast activation and proliferation was noted with the tendinitis, ASTM/tendinitis, and post groups. Ossification occurred in the core of the Achilles tendon in all of the ASTM groups. The presence of inflammatory cells was observed in the tendons and longitudinal remodeling of the collagen fibers did not occur. / Department of Biology

Indiana University-Purdue University Indianapolis (IUPUI) / Tendinopathy is a common degenerative pathology that is characterized by activity related pain, focal tendon tenderness, intratendinous imaging changes, and typically results in changes in the histological, mechanical, and molecular properties of the tendon. Tendinopathy is difficult to study in humans, which has contributed to limited knowledge of the pathology, and thus a lack of appropriate treatment options. However, most believe that the pathology is degenerative as a result of a combination of both extrinsic and intrinsic factors. In order to gain understanding of this pathology, animal models are required. Because each tendon is naturally exposed to different conditions, a universal model is not feasible; therefore, an appropriate animal model must be established for each tendon susceptible to degenerative changes. While acceptable models have been developed for several tendons, a reliable model for the Achilles tendon remains elusive. The purpose of this dissertation was to develop an animal model of Achilles tendinopathy by investigating the individual and combined effects of an intrinsic and extrinsic factor on the rodent Achilles tendon. Rats selectively bred for high capacity running and Sprague Dawley rats underwent uphill treadmill running (an extrinsic factor) to mechanically overload the Achilles tendon or served as cage controls. Collagenase (intrinsic factor) was injected into one Achilles tendon in each animal to intrinsically break down the tendon. There were no interactions between uphill running and collagenase injection, indicating that the influence of the two factors was independent. Uphill treadmill running alone failed to produce any pathological changes in the histological or mechanical characteristics of the Achilles tendon, but did modify molecular activity. Intratendinous collagenase injection had negative effects on the histological, mechanical, and molecular properties of the tendon. The results of this dissertation demonstrated that the combined introduction of uphill treadmill running and collagenase injection did not lead to degenerative changes consistent with human Achilles tendinopathy. Intratendiouns collagenase injection negatively influenced the tendon; however, these changes were generally transient and not influenced by mechanical overload. Future studies should consider combinations of other intrinsic and extrinsic factors in an effort to develop an animal model that replicates human Achilles tendinopathy.