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Biomedical subjects

M D Markel

Publications and source records attributed to M D Markel.

At least 19 recordsLinked to original sources
PubMed2006

Comparison of mechanical debridement and radiofrequency energy for chondroplasty in an in vivo equine model of partial thickness cartilage injury.

OBJECTIVE: The purpose of this study was to develop a long-term model of cartilage injury that could be used to compare the effects of radiofrequency energy (RFE) and mechanical debridement as a treatment. METHODS: Partial thickness fibrillation of patellar cartilage was created in 16 mature ponies. Three months after the initial surgery all injured patellae were randomly selected to receive one of the four treatments (n = 8/treatment): (1) control, (2) mechanical debridement with a motorized shaver, (3) TAC-CII RFE probe, and (4) CoVac 50 RFE probe. The ponies were euthanized 22 months after treatment. Macroscopic appearance of the cartilage surface was scored, vital cell staining was used to determine chondrocyte viability and light microscopy was used to grade the morphometric changes within the cartilage. Mechanical properties (aggregate modulus, Poisson's ratio and permeability) also were determined and compared to normal uninjured cartilage. RESULTS: There were no differences in the cartilage surface scores among the treatment groups and control samples (P > 0.05). The maximum depth of cell death and the percentage of dead area in control and mechanical debridement groups were significantly less than those in both RFE groups. There were no significant differences in maximum depth and the percentage of dead area between the two RFE treatment groups. Histologic scores demonstrated better cartilage morphology for the control and mechanical debridement groups than those of RFE groups. However, even with full thickness chondrocyte death, the matrix in the RFE treated sections was still retained and the mechanical properties of the treated cartilage did not differ from the mechanical debridement group. CONCLUSION: RFE caused greater chondrocyte death and more severe morphological changes compared to untreated degenerative cartilage and mechanical debridement in this model.

Animals↗
PubMed2005

Role of endochondral ossification of articular cartilage and functional adaptation of the subchondral plate in the development of fatigue microcracking of joints.

The mechanisms that regulate functional adaptation of the articular ends of long bones are poorly understood. However, endochondral ossification of articular cartilage and modeling/remodeling of the subchondral plate and epiphyseal trabeculae are important components of the adaptive response. We performed a histologic study of the distal end of the third metacarpal/metatarsal bone of Thoroughbreds after bones were bulk-stained in basic fuchsin and calcified sections were prepared. The Thoroughbred racehorse is a model of an extreme athlete which experiences particularly high cyclic strains in distal limb bones. The following variables were quantified: microcrack boundary density in calcified cartilage (N.Cr/B.Bd); blood vessel boundary density in calcified cartilage (N.Ve/B.Bd); calcified cartilage width (Cl.Cg.Wi); duplication of the tidemark; and bone volume fraction of the subchondral plate (B.Ar/T.Ar). Measurements were made in five joint regions (lateral condyle and condylar groove; sagittal ridge; medial condylar and condylar groove). N.Cr/B.Bd was site-specific and was increased in the condylar groove region; this is the joint region from which parasagittal articular fatigue (condylar) fractures are typically propagated. Formation of resorption spaces in the subchondral plate was co-localized with microcracking. N.Ve/B.Bd was also site-specific. In the sagittal ridge region, N.Ve/B.Bd was increased, Cl.Cg.Wi was decreased, and B.Ar/T.Ar was decreased, when compared with the other joint regions. Multiple tidemarks were seen in all joint regions. Cumulative athletic activity was associated with a significant decrease in B.Ar/T.Ar in the condylar groove regions. N.Cr/B.Bd was positively correlated with B.Ar/T.Ar (P < 0.05, r(s) = 0.29) and N.Ve/B.Bd was negatively correlated with B.Ar/T.Ar (P < 0.005, r2 = 0.14) and Cl.Cg.Wi (P < 0.05, r2 = 0.07). We conclude that endochondral ossification of articular cartilage and modeling/remodeling of the subchondral plate promote initiation and propagation of site-specific fatigue microcracking of the joint surface, respectively, in this model. Microcracking of articular calcified cartilage likely represents mechanical failure of the joint surface. Propagation of microcracks into the subchondral plate is a critical factor in the pathogenesis of articular condylar fatigue (stress) fracture. Functional adaptation of the joint likely protects hyaline cartilage from injury in the short-term but may promote joint degeneration and osteoarthritis with ongoing athleticism.

Adaptation, Physiological↗
PubMed2005

Up-regulation of site-specific remodeling without accumulation of microcracking and loss of osteocytes.

Functional adaptation of bone normally protects the skeleton from fracture during daily activity. Accumulation of microcracking and loss of osteocytes have been implicated in the regulation and initiation of targeted (reparative) remodeling of bone and, in certain situations, the development of fatigue or stress fracture. We performed a histologic study of the dorsal cortex of the mid-diaphysis of the third metacarpal (Mc-III) bone of Thoroughbred racehorses after bones were bulk-stained in basic fuchsin and transverse calcified sections were prepared. The Thoroughbred racehorse is an extreme athlete whose Mc-III bone experiences particularly high cyclic strains during training and racing. A group of non-athletic horses was also included in the experiment. The following variables were quantified: activation frequency (Ac.f); bone formation rate (BFR); resorption space density (Rs.N/T.Ar); microcrack density (Cr.Dn); microcrack mean length (Cr.Le); microcrack surface density (Cr.S.Dn); osteocyte density (Ot.N/T.Ar; Ot.N/B.Ar); and bone volume fraction (B.Ar/T.Ar). Ac.f and BFR were estimated using a mathematical algorithm. Using confocal microscopy, bones were examined for fine microcracks, diffuse matrix injury, and disruption of the osteocyte syncytium. Low values for Cr.Dn (#/mm2) were found in both groups (0.022+/-0.008 and 0.013+/-0.006 for racing Thoroughbreds and non-athletic horses, respectively). There was no significant relationship between Cr.Dn and Ot.N/T.Ar; Ot.N/B.Ar, B.Ar/T.Ar, and Ot.N/T.Ar; Ot.N/B.Ar, and remodeling (Ac.f, Rs.N/T.Ar) and Ot.N/T.Ar; Ot.N/B.Ar. Intense remodeling of the Mc-III dorsal cortex was found in the racing Thoroughbreds (Ac.f 12.8+/-7.4 #/mm2/year; BFR 31.5+/-15.6%; Rs.N/T.Ar 0.19+/-0.09 #/mm2) and was significantly increased compared with non-athletic horses. Overall, remodeling was weakly correlated with Cr.Dn (r2=0.15, P<0.05). Subtle matrix injury, not detectable by bright-field microscopy, was particularly evident adjacent to resorption spaces in Thoroughbred bone. In non-athletic horses, disruption of the dendritic cell processes of osteocytes associated with cement lines and interstitial fragments was more evident. Taken together, these findings suggest that site-specific (targeted) induction of remodeling during functional adaptation of bone in a high-strain skeletal site is not dependent on accumulation of microcracking or loss of osteocytes. We hypothesize that athleticism can directly influence bone turnover in this extreme athlete through pathways that do not involve classical linear microcracks.

Age Factors↗
PubMed2004

Response of the osteocyte syncytium adjacent to and distant from linear microcracks during adaptation to cyclic fatigue loading.

Cyclic loading induces fatigue in bone and initiates a complex, functionally adaptive response. We investigated the effect of a single period of fatigue on the histologic structure and biomechanical properties of bone. The ulnae of 40 rats were subjected to cyclic fatigue (-6000 microepsilon) unilaterally until 40% loss of stiffness developed, followed by 14 days of adaptation. The contralateral ulna served as a treatment control (n = 20 rats), and a baseline loaded/non-loaded group (n = 20 rats/group) was included. Bones from 10 rats/group were examined histologically and the remaining bones (10 rats/group) were tested mechanically. The following measurements were collected: volumetric bone mineral density (vBMD); ultimate force (Fu); stiffness (S); energy-to-failure (U); cortical area (Ct.Ar); microcrack density (Cr.Dn); microcrack mean length (Cr.Le); microcrack surface density (Cr.S.Dn); osteocyte density (Ot.N/T.Ar and Ot.N/TV); bone volume fraction (B.Ar/T.Ar); resorption space density (Rs.N/Ct.Ar); and maximum and minimum area moments of inertia (IMAX and IMIN). Using confocal microscopy, the bones were examined for diffuse matrix injury, canalicular disruption, and osteocyte disruption. The adapted bones had increased B.Ar, IMAX, and IMIN in the mid-diaphysis. Fatigue loading decreased structural properties and induced linear microcracking. At 14 days, adaptation restored structural properties and microcracking was partially repaired. There was a significant nonlinear relationship between Ot.N/T.Ar and B.Ar/T.Ar during adaptation. Disruption of osteocytes was observed adjacent to microcracks immediately after fatigue loading, and this did not change after the period of adaptation. In fatigue-loaded bone distant from microcracks, diffuse matrix injury and canalicular disruption were often co-localized and were increased in the lateral (tension) cortex. These changes were partially reversed after adaptation. Loss of canalicular staining and the presence of blind-ends in regions with matrix injury were suggestive of rupture of dendritic cell processes. Taken together, these data support the general hypothesis that the osteocyte syncytium can respond to cyclic loading and influence targeted remodeling during functional adaptation. Changes in the appearance of the osteocyte syncytium were found in fatigue-loaded bone with and without linear microcracks. We hypothesize that the number of dendritic cell processes that experience load-related disruption may determine osteocyte metabolic responses to loading and influence targeted remodeling.

Adaptation, Physiological↗
PubMed2003

Degradation of bone structural properties by accumulation and coalescence of microcracks.

Failure of bone adaptation to protect the skeleton from fatigue fracture is common, and site-specific accumulation and coalescence of microcracking in regions of high strain during cyclic loading is considered a key factor that decreases the resistance of whole bones to fracture. We investigated the effect of cyclic fatigue loading on the monotonic structural properties of the rat ulna during accumulation and coalescence of microcracks. Cyclic end-loading of the ulna was performed at 4 Hz ex vivo at an initial peak strain of -6000 muepsilon to 20% loss of stiffness (n = 7) or 40% loss of stiffness (n = 7) bilaterally. A 0% loss of stiffness monotonically loaded control group (n = 7) was also included. Volumetric bone mineral density (vBMD), ultimate strength (F(u)), stiffness (S), and energy-to-failure (U) were determined in one ulna and in the contralateral ulna vBMD, cortical bone area (B.Ar), maximum and minimum second moments of inertia (I(MAX) and I(MIN)), microcrack density (Cr.Dn), microcrack mean length (Cr.Le), and microcrack surface density (Cr.S.Dn) were determined. In two additional groups of rats, cyclic end-loading of the ulna was also performed ex vivo unilaterally to 20% loss of stiffness (n = 10) and 40% loss of stiffness (n = 10) and then vBMD, F(u), S, U, B.Ar, I(MAX), and I(MIN) were determined bilaterally. Fatigue loading had incremental degradative effects on ulna structural properties. This decreased resistance to fracture was associated with accumulation and coalescence of branching arrays of microcracks within the cortex of the ulna. Microcracking was most prominent in the middiaphysis and corresponded to the region of the bone that fractured during monotonic structural testing. Fatigue loading influenced the relationship between bone cross-sectional geometry and vBMD and ulna structural properties. At 40% loss of stiffness, F(u), S, and U were all significantly correlated with cross-sectional bone geometry and vBMD, whereas this was not the case at 20% loss of stiffness and with the 0% loss of stiffness monotonic control ulnae. We also found a biologically significant individual animal effect. Larger ulnae required a higher number of load cycles for fatigue to develop, retained higher strength, and accumulated a greater amount of microcracking at the end of the cyclic fatigue testing. Small increases in bone size and density can substantially improve the resistance of whole bones to fracture as microcracking accumulates and coalesces during cyclic fatigue loading.

Animals↗
PubMed2002

Elevation of a collagenase generated type II collagen neoepitope and proteoglycan epitopes in synovial fluid following induction of joint instability in the dog.

CLINICAL RELEVANCE: Measurement of markers of cartilage pathology in synovial fluid may provide clinical rheumatologists and osteoarthritis (OA) researchers important information for early diagnosis of OA as well as a method for monitoring disease progression and response to treatment. This study demonstrates the value of this approach in an established model of OA (cranial cruciate ligament rupture) at a point distant enough from the original surgical manipulation so as to have little to no effect on the marker concentrations. OBJECTIVE: The objective of this study was to determine whether measurement of markers of cartilage collagen cleavage and proteoglycan turnover in synovial fluid from a canine model could be used to detect cartilage changes following the onset of joint instability during the development of OA. DESIGN: A model of joint instability that develops OA was created in 18 mature dogs using monopolar radiofrequency energy (MRFE). MRFE was arthroscopically applied to one cranial cruciate ligament (CCL) while the contralateral CCL was sham treated. The treated CCLs ruptured approximately 8 weeks (55 +/- 1.6 days) after MRFE treatment. Synovial fluid was collected at time zero prior to MRFE treatment, 4 weeks after MRFE treatment, and at 4, 8, and 16 weeks after CCL rupture. Synovial fluid concentrations of the neoepitope COL2-3/4C long (type II collagen cleavage by collagenase) and epitopes 3B3(-) (proteoglycan aggrecan sulfation) and 846 (associated with aggrecan synthesis) were analyzed. RESULTS: Compared to sham treated joints, the synovial fluid concentrations of COL2-3/4C long and 3B3(-) were significantly increased 2.2 fold and 2.9 fold, respectively, in joints with MRFE treated CCLs following CCL rupture. Concentrations of the 846 epitope in synovial fluid showed a trend toward an increase, which was not significant, after CCL rupture. CONCLUSIONS: Concentrations of the collagenase-cleaved type II collagen neoepitope and 3B3(-) epitope in synovial fluid were significantly increased by 4 weeks and remained elevated for at least 16 weeks after CCL rupture. This suggests that in dogs the COL2-3/4C long neoepitope and 3B3(-) epitope are sensitive markers for changes in joint cartilage turnover in joints that are developing OA.

Animals↗
PubMed2001

The effect of recombinant human bone morphogenetic protein-2 on femoral reconstruction with an intercalary allograft in a dog model.

This study compared the effect of augmentation of allograft host bone junctions with recombinant human bone morphogenetic protein-2 (rhBMP-2) on an absorbable collagen sponge (ACS), autogenous cancellous bone graft (CBG), and a collagen sponge alone in a canine intercalary femoral defect model repaired with a frozen allograft. Outcome assessment included serial radiographs, dual energy X-ray absorptiometry scans, and gait analyses, and mechanical testing and histology of post-mortem specimens. The distal junction healed more quickly and completely with rhBMP-2 than ACS alone based on qualitative radiography and histologic evaluations. The primary tissue in the unhealed gaps in the ACS group was fibrous connective tissue. The proximal allograft host bone junction had complete bone union in the three treatment groups. There was significantly greater new bone callus formation at both junctions with rhBMP-2 than with CBG or ACS alone that resulted in increased bone density around the allograft host bone junctions. All dogs shifted their weight from the treated leg to the contralateral pelvic limb immediately after surgery. Weight bearing forces were redistributed equally between the pelvic limbs at 12 weeks after surgery with rhBMP-2, at 16 weeks after surgery with CBG, and at 24 weeks after surgery with ACS alone. Bending and compressive stiffnesses of the whole treated femora were equal to the contralateral control femora in all treatment groups, whereas torsional rigidities of the whole treated femora for the CBG and ACS groups were significantly less than the control. Both the proximal and distal junctions the treated with rhBMP-2 had torsional stiffnesses and strengths equal to intact control bones. Ultimate failure torques of the proximal junctions of the CBG group and of both junctions of the ACS group were significantly less than the BMP-treated bones. Augmentation of the allograft host bone junctions with rhBMP-2 on an ACS gave results for all parameters measured that equaled or exceeded autogenous graft in this canine intercalary femoral defect model.

Animals↗
PubMed2001

Effect of bipolar radiofrequency energy on human articular cartilage. Comparison of confocal laser microscopy and light microscopy.

PURPOSE: To evaluate chondrocyte viability using confocal laser microscopy (CLM) following exposure to bipolar radiofrequency energy (bRFE) and to contrast CLM with standard light microscopy (LM) techniques. TYPE OF STUDY: In vitro analysis using chondromalacic human cartilage. METHODS: Twelve fresh chondral specimens were treated with the ArthroCare 2000 bRFE system (ArthroCare, Sunnyvale, CA) coupled with 1 of 2 types of probes and at 3 energy delivery settings (S2, S4, S6). A sham-operated group was treated with no energy delivered. Specimens were analyzed for chondrocyte viability and chondral morphology with CLM using fluorescent vital cell staining and with LM using H&E and safranin-O staining. RESULTS: LM with H&E staining showed smoothing of fine fronds of fibrillated cartilage; thickened fronds were minimally modified. Chondrocyte nuclei were present and not morphologically different than nuclei within sham-operated and adjacent untreated regions. LM with safranin-O staining showed a clear demarcation between treated and untreated regions. CLM, however, showed chondrocyte death: the depth and width of chondrocyte death increased with increasing bRFE settings. CONCLUSIONS: CLM showed that bRFE delivered through the probes investigated created significant chondrocyte death. These changes were not apparent using LM techniques.

Aged↗
PubMed2001

The effects of monopolar radiofrequency energy on intact and lacerated ovine menisci.

PURPOSE: To evaluate the effect of monopolar radiofrequency energy (RFE) on intact and lacerated meniscal tissue. TYPE OF STUDY: In vitro study. Application of monopolar RFE to soft tissue for treatment of various musculoskeletal disorders has been explored recently, although its effect on meniscal tissue has not been critically evaluated. Monopolar RFE denatures and fuses collagen. Given that menisci are composed primarily of type I collagen, we proposed that RFE could be applied to meniscal tears with minimal effect on healthy meniscal tissue. METHODS: Adult sheep menisci were given 1 of 2 treatments (65 degrees C, 15 W or 75 degrees C, 10 W) with a monopolar RFE generator. Specimens were processed for scanning electron microscopy (SEM), transmission electron microscopy (TEM), light microscopy, and confocal laser microscopy. A computer-based area-determination program was used to calculate the treated area in confocal laser images. RESULTS: SEM changes in treated tissue consisted of surface smoothing with collagen fibril fusion. Changes apparent with TEM included tissue homogenization with loss of cross-striations and fusion of collagen fibrils. Histologic changes consisted of fusion and loss of collagen fiber individualization, pyknosis of fibrochondrocyte nuclei, and loss of lacunae surrounding fibrochondrocytes. There were clear demarcations between treated and untreated tissue with both treatments. There were no discernible differences between treatment groups on SEM, TEM, or histologic examination. Confocal laser microscopic evaluations showed distinct treatment areas. The mean area affected ranged from 6.6% for 65 degrees C, 15 W to 8.8% for 75 degrees C, 10 W. CONCLUSIONS: The primary effects of monopolar RFE treatment of menisci in this study were consistent with thermal tissue damage limited to the treatment area. Monopolar RFE treatment of a meniscal laceration may stabilize the tear by fusing collagenous tissue in the surrounding area and prevent propagation along tissue lines. This study presents preliminary in vitro results. Further studies are necessary before clinical applications can be recommended.

Animals↗
PubMed2001

Thermal capsulorrhaphy treatment of shoulder instability: basic science.

Thermal capsulorrhaphy is a new treatment modality for shoulder instability, where the joint capsular tissue is heated and reduced in length by laser or radiofrequency energy to regain joint stability. Experimental studies have shown that (1) joint capsular tissue can be modified significantly (shortened) by thermal energy at the temperature range of 70 degrees to 80 degrees C; (2) thermal energy causes immediate deleterious effects such as loss of the mechanical properties, collagen denaturation, and cell necrosis; (3) thermally treated tissue is repaired actively by a residual population of fibroblasts and vascular cells, with concomitant improvement of mechanical properties; (4) the shrunken tissue stretches with time if the tissue is subjected to physiologic loading immediately after surgery; and (5) leaving viable tissue between treated regions significantly improves the healing process. Therefore, the application of thermal energy to achieve joint stability relies on an initial effect (shrinkage), and to a great extent the tissue's healing response to regain the tissue's mechanical properties. Particularly, induction of active repair and joint capsular thickening with tissue remodeling regulated by functional demand seem to be essential factors for a successful outcome. Thermal treatment causes an initial deleterious effect on the tissue's properties, and overtreatment can lead to severe immediate and permanent tissue damage. In addition, scientific data of newly developed devices are limited, and the information from manufacturers often is unreliable and misleading. Carefully controlled long-term clinical and scientific studies should be done to additionally clarify the advantages and disadvantages of this technique.

Animals↗
PubMed2001

Influence of an interdental full pin on stability of an acrylic external fixator for rostral mandibular fractures in dogs.

OBJECTIVE: To determine total stiffness and gap stiffness of an external fixation system in a canine mandibular fracture gap model incorporating a full interdental pin as the only point of rostral fixation in a bilateral type-I external fixator. SAMPLE POPULATION: 10 canine mandibles. PROCEDURE: Bilateral mandibular ostectomies were performed between premolars 3 and 4. A type-I external fixator incorporating a full interdental pin was placed to stabilize a 0.5-cm fracture gap. Four pin configurations (intact mandibular bodies with fixator; ostectomized mandibular bodies and complete fixator; ostectomized mandibular bodies with caudal pins of rostral fragment cut; ostectomized mandibular bodies with all pins of rostral fragment cut) were tested in dorsoventral bending 5 times on each mandible. The full interdental pin remained intact in all configurations. Total stiffness and gap stiffness were determined for each configuration on a materials testing machine. RESULTS: Total stiffness of intact mandibles was significantly greater than that of ostectomized mandibles, regardless of external fixator configuration. However, total stiffness and gap stiffness were not significantly different among different external fixator configurations applied to ostectomized mandibles. CONCLUSION AND CLINICAL RELEVANCE: External fixator configurations with only the full interdental pin engaging the rostral fragment were as stiff as configurations that had 2 or 4 additional pins in the rostral fragment for the applied loads. External fixators for rostral mandibular fractures may be rigidly secured with rostral fragment implants applied extracortically, avoiding iatrogenic trauma to teeth and tooth roots.

Animals↗
PubMed2000

Comparison of three methods of gluteal muscle attachment to an allograft/endoprosthetic composite in a canine model.

This study used radiography, gait analysis, gluteal muscle mass, mechanical testing, and qualitative histology to compare three methods of gluteal muscle attachment to an allograft/endoprosthetic composite of the proximal 25% of the femur in an in vivo canine model. The three methods of gluteal muscle attachment were identical to those used clinically in human patients for hip revision and proximal femoral limb salvage: the host gluteal tendon sutured to the allograft tendon (tendon group), the host greater trochanter with intact gluteal tendons secured to the allograft with a cable-grip system (grip group), and periosteally vascularized proximal femoral bone onlay with intact tendons wrapped around the allograft (wrap group). On the basis of radiographs taken every 2 months, the tendon group had more graft fractures than did the grip or wrap group. Radiographic union of the graft-host bone junction occurred more rapidly and there was less graft resorption in the wrap group than in the other two groups. In all dogs, peak vertical ground-reaction forces in the treated limb decreased immediately after surgery and then slowly increased over the length of the study. The dogs in the wrap group regained normal weight-bearing on the treated limb more quickly than did those in the other groups. The constructs in the tendon group were weaker and less stiff immediately after surgery than were those in the other groups or in intact controls. Histologic analysis confirmed that the wrap technique resulted in complete union of the host bone-allograft junction more often than did the other techniques. The wrap method had the best functional outcome after 9 months when an allograft/endoprosthetic composite was used during total hip arthroplasty in this canine model.

Animals↗
PubMed2000

The mechanism of joint capsule thermal modification in an in-vitro sheep model.

The purpose of this study was to understand the mechanism responsible for joint capsule shrinkage after nonablative laser application in an in-vitro sheep model. Femoropatellar joint capsular tissue specimens harvested from 20 adult sheep were treated with one of three power settings of a holmium:yttrium-aluminum-garnet laser or served as a control. Laser treatment significantly shortened the tissue and decreased tissue stiffness in all three laser groups, whereas failure strength was not altered significantly by laser treatment. Transmission electron microscopic examination showed swollen collagen fibrils and loss of membrane integrity of fibroblasts. A thermometric study revealed nonablative laser energy caused tissue temperature to rise in the range of 64 degrees C to 100 degrees C. Electrophoresis after trypsin digestion of the tissue revealed significant loss of distinct alpha bands of Type I collagen in laser treated samples, whereas alpha bands were present in laser treated tissue without trypsin digestion. The results of this study support the concept that the primary mechanism responsible for the effect of nonablative laser energy is thermal denaturation of collagen in joint capsular tissue associated with unwinding of the triple helical structure of the collagen molecule.

Analysis of Variance↗
PubMed2000

The biologic response to laser thermal modification in an in vivo sheep model.

The purpose of this study was to evaluate the effect of nonablative laser energy on mechanical, histologic, ultrastructural, and biochemical properties of joint capsular tissue in an in vivo sheep model. Femoropatellar joint capsule was treated with the holmium:yttrium-aluminum-garnet laser via an arthroscope, and tissues were harvested immediately after surgery, or at 3, 7, 14, 30, 60, 90, and 180 days after surgery (n = 8/group). Laser treatment caused significant decreases in tissue stiffness from 0 to 7 days after surgery, then stiffness gradually increased after 14 days. Tissue strength was lowest 3 days after laser treatment. Histologic examination revealed immediate collagen hyalinization and cell necrosis, followed by active cellular response characterized by extensive fibroblast migration and capillary sprouting. Tissue appeared to be normal histologically 60 days after surgery; however, collagen fibrils remained uniformly small. This study showed an active tissue response secondary to thermal modification with concomitant recovery of mechanical properties by 30 days after surgery. Whether the shrinkage or joint stability was maintained with time remains to be evaluated. To clarify the advantages and disadvantages of this technique, a carefully controlled clinical trial with long term followup should be performed.

Animals↗
PubMed2000

Effects of monopolar radiofrequency energy on ovine joint capsular mechanical properties.

Radiofrequency energy may provide a relatively noninvasive method to stabilize joints with excessive laxity by thermally shrinking redundant joint capsular tissue. The authors determined the percentage of shrinkage associated with five radiofrequency treatment temperatures and evaluated the effect of this energy on the structural properties of joint capsular tissue in vitro. First, 36 adult sheep femoropatellar joint capsular specimens were treated with one of five treatment temperatures (n = 6 per group) or served as a control to determine tissue shrinkage. An additional 24 specimens were treated with three temperatures that resulted in different shrinkage: 45 degrees C, 65 degrees C, and 85 degrees C. Tissue stiffness, relaxation, and failure strength were determined for each specimen (n = 6 per group). Tissue shrinkage was correlated significantly with treatment temperature. There was a significant decrease in tensile stiffness in the 65 degrees C and 85 degrees C treatment groups. There were no significant differences between stress relaxation before treatment and after treatment. Relaxation properties after treatment were not different from each other or from control values either normalized to pretreatment values or expressed as raw data. Failure strength was not affected significantly at any temperature.

Animals↗
PubMed2000

Comparative effects of laser and radiofrequency energy on joint capsule.

The study compared the effects of laser and monopolar radiofrequency energy on thermal and architectural properties of joint capsular tissue in an in vitro ovine model. Sheep glenohumeral joint capsular specimens were treated with laser (5, 10, 15 W) or radiofrequency energy (55 degrees, 65 degrees, 75 degrees C) (n = six per group). Energy application caused significant tissue shrinkage and decreased surface area in all laser and radiofrequency treatment groups. Tissue thickness significantly increased in all treatment groups except for radiofrequency 55 degrees C. Tissue shrinkage, surface area, and thickness each correlated significantly with the delivered laser energy per tissue area or mean radiofrequency probe temperature. There were no significant differences among laser 10 W, laser 15 W, and radiofrequency 75 degrees C treatment groups for these three architectural parameters. Tissue temperature was elevated significantly in the laser 10 W, laser 15 W, radiofrequency 65 degrees C, and radiofrequency 75 degrees C groups when compared with the control. Tissue temperature changes between the laser 10 W and radiofrequency 75 degrees C groups were similar; however, laser treatment produced a steeper temperature increase accompanying its peak temperature. Despite different mechanisms, laser and radiofrequency energy can achieve similar and predictable tissue modification, which is temperature dependent. Additional in vivo studies must be performed to evaluate the applicability of these techniques to clinical use.

Animals↗