A review of the treatment methods for cartilage defects.

The purpose of this article is to provide a broad review of the literature related to the treatment of cartilage defects and degenerated cartilage in animals with some inferences to the treatment in humans. Methods range from the insertion of osteochondral tissue or cells to the application of radio frequency or insertion of scaffolds and growth factors alone or in combination. Debridement, microfracture, radio frequency, and chondrocyte implantation are all methods normally utilized when treating smaller articular cartilage defects. Scaffolds and mosaicplasty are examples of methods to treat larger defects. This review will cover all major treatment methods currently used to treat articular cartilage defects.

Exercise-induced metacarpophalangeal joint adaptation in the Thoroughbred racehorse.

Repetitive bone injury and development of stress fracture is a common problem in humans and animals. The Thoroughbred racehorse is a model in which adaptive failure and associated development of stress fracture is common. We performed a histologic study of the distal end of the third metacarpal bone in two groups of horses: young Thoroughbreds that were actively racing (n = 10) and a group of non-athletic horses (n = 8). The purpose of this study was to determine whether development of articular microcracks was associated with specific alterations to subchondral plate osteocytes. Morphometric measurements were made in five regions of the joint surface: lateral condyle, lateral condylar groove, sagittal ridge, medial condylar groove, and medial condyle. The following variables were quantified: hyaline cartilage width; calcified cartilage width; the number of tidemarks; microcrack density at the articular surface; blood vessel density entering articular cartilage; the presence of atypical bone matrix in the subchondral plate; bone volume fraction; and osteocyte density. Adaptation of articular cartilage was similar in both groups of horses. Vascularization of articular cartilage was increased in the group of non-athletic horses. Microcracks, which typically had an oblique orientation to the joint surface, were co-localized with blood vessels, and resorption spaces. Microcracking was increased in the condylar grooves of athletic horses compared with the other joint regions and was also increased compared with the condylar groove regions of non-athletic horses. Coalescence of microcracks also led to development of an intracortical articular condylar stress fracture in some joints and targeted remodeling of affected subchondral plate. The subchondral plate of the condyles in athletic horses was sclerotic, and contained atypically stained bone matrix with increased numbers of osteocytes with atypical morphology. However, osteocyte numbers were not significantly different between groups. We conclude that differences in site-specific microdamage accumulation and associated targeted remodeling between athletic and non-athletic horses are much greater than differences in subchondral osteocyte morphology. However, the presence of atypical subchondral bone matrix in athletic horses was associated with extensive osteocyte loss. Although osteocyte mechanotransduction is considered important for functional adaptation, in this model, adaptation is likely regulated by multiple mechanotransduction pathways.

Comparison of radiofrequency treatment and mechanical debridement of fibrillated cartilage in an equine model.

OBJECTIVE: To compare a radiofrequency energy (RFE) prototype probe to mechanical debridement (MD) and a commercially available RFE system used for chondroplasty in the treatment of an experimentally created partial thickness cartilage lesion in horses. The study design was experimental, randomized complete block, n=8, using fifteen mature ponies. METHODS: Grade 2 to 3 cartilage lesions were prepared in both patellae. After 10 months duration, the injuries were used to study the effects of MD, a commercially available bipolar RFE device (CoVac 50; ArthroCare Corporation) and a prototype monopolar RFE device (Smith & Nephew Endoscopy). Six months after treatment the patellae were examined for chondrocyte viability and cartilage structure. RESULTS: Mean depth of cell death was significantly different among groups (controls, MD

The effects of radiofrequency energy probe speed and application force on chondrocyte viability.

OBJECTIVE: To determine the thermal effects of monopolar radiofrequency energy (mRFE) on bovine articular cartilage when it was moved at different speeds and using varying application forces. METHODS: Thirty-six fresh osteochondral sections divided into two groups (18 sections/group) were used in this study. The first group was tested at three speed rates of mRFE probe (1 mm/sec, 5 mm/sec and 10 mm/sec) at a constant force (50 g) applied to the probe tip. In the second group, three application forces of the probe tip were tested (25 g, 50 g and 75 g) at a constant speed (5 mm/sec) (n = 6/test). All tests were performed using a custom-built jig to control the mRFE (Vulcan EAS) probe during a 20-mm pass on each section. After treatment, viability of osteochondral sections was determined by confocal laser microscopy (CLM) combined with vital cell staining. RESULTS: There were not any significant differences in cartilage thickness of tested osteochondral sections among the different speeds or forces. During the mRFE probe treatments at different speeds, CLM demonstrated that probe application at the speed of 1 mm/sec caused significantly greater chondrocyte death than at the speeds of 5 and 10 mm/sec, whereas there were no significant differences in chondrocyte death among the variable application forces (p > 0.05). DISCUSSION: This in vitro study demonstrated that RFE thermal penetration correlated most closely with probe application speed than application force for this mRFE probe. CLINICAL RELEVANCE: Improper use of mRFE may cause thermal injury on articular cartilage.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

An in vitro biomechanical comparison of two interlocking-nail systems for fixation of ostectomized equine third metacarpal bones.

OBJECTIVE: To compare the mechanical properties of 2 interlocking-nail systems for fixation of ostectomized equine third metacarpi (MC3): (1) a standard interlocking nail with 2 parallel screws proximal and distal to a 1-cm ostectomy; and (2) a modified interlocking nail with 2 screws proximal and distal to a 1-cm ostectomy with the screws offset by 30 degrees. ANIMAL OR SAMPLE POPULATION: Twelve pairs of adult equine forelimbs intact from the midradius distally. METHODS: Twelve pairs of equine MC3 were divided into 2 test groups (6 pairs each): torsion and caudocranial 4-point bending. Standard interlocking nails (6-hole, 13-mm diameter, 230-mm length) were placed in 1 randomly selected bone from each pair. Modified interlocking nails (6-hole, 13-mm, 230-mm length, screw holes offset by 30 degrees) were placed in the contralateral bone from each pair. All bones had 1-cm mid-diaphyseal ostectomies. Six construct pairs were tested in caudocranial 4-point bending to determine stiffness and failure properties. The remaining 6 construct pairs were tested in torsion to determine torsional stiffness and yield load. Mean values for each fixation method were compared using a paired t test within each group. Significance was set at P <.05. RESULTS: Mean (+/-SEM) values for the MC3-standard interlocking-nail composite and the MC3-modified interlocking-nail composite, respectively, in 4-point bending were: composite rigidity, 3,119 +/- 334.5 Nm/rad (newton. meter/radian) and 3,185 +/- 401.2 Nm/rad; yield bending moment, 205.0 +/- 18.46 Nm and 186.7 +/- 6.17 Nm; and failure bending moment, 366.4 +/- 21.82 Nm and 378.1 +/- 20.41 Nm. There were no significant differences in the biomechanical values for bending between the 2 fixation methods. In torsion, mean (+/-SEM) values for the MC3-standard interlocking-nail composite and the MC3-modified interlocking-nail composite were: composite rigidity, 135.5 +/- 7.128 Nm/rad and 112.5 +/- 7.432 Nm/rad; gap stiffness, 207.6 +/- 10.57 Nm/rad and 181.7 +/- 12.89 Nm/rad; and yield load, 123.3 +/- 2.563 Nm and 107.5 +/- 8.353 Nm, respectively. Composite rigidity and gap stiffness for standard interlocking-nail fixations were significantly higher than the modified interlocking-nail fixation technique in torsion. Yield load had a tendency to be higher for the standard interlocking-nail fixation (P =.15). CONCLUSIONS: No significant differences in biomechanical properties were identified between a standard interlocking nail and one with the screw holes offset by 30 degrees in caudocranial 4-point bending. The standard interlocking nail was superior to the modified interlocking nail in torsional gap stiffness and composite rigidity. The torsional yield load also tended to be higher for the standard interlocking nail. CLINICAL RELEVANCE: The standard interlocking nail with parallel screw holes is superior to a modified interlocking nail with the screw holes offset by 30 degrees in ostectomized equine MC3 bones in vitro when tested in torsion.

Arthrodesis of the equine proximal interphalangeal joint: a biomechanical comparison of three 4.5-mm and two 5.5-mm cortical screws.

OBJECTIVE: To compare the biomechanical characteristics and mode of failure of 2 parallel-screw techniques for proximal interphalangeal joint arthrodesis in horses. STUDY DESIGN: Randomized block design, blocking for horse (1-5), method of screw fixation (three 4.5-mm vs two 5.5-mm), side (left limb vs right limb), and end (front limb vs hind limb). Constructs were loaded to failure in 3-point bending in a dorsal-to-palmar (plantar) direction. SAMPLE POPULATION: Twenty limbs (10 limb pairs) from 5 equine cadavers. METHODS: A combined aiming device was used to facilitate consistent screw placement. Three parallel 4.5-mm cortical screws were placed in lag fashion in 1 limb of a pair, and 2 parallel 5.5-mm cortical screws were placed in lag fashion in the contralateral limb. Arthrodesis constructs were tested in 3-point bending in a dorsal-to-palmar (plantar) direction using a materials-testing machine. Loading rate was 19 mm/s. Maximal bending moment at failure and composite stiffness were obtained from bending moment-angular deformation curves. Data were analyzed using ANOVA and chi(2) analysis. RESULTS: There were no significant differences in bending moment (P >.05, power = 0.8 @ delta = 19%) or composite stiffness (P >.05, power = 0.8 @ delta = 19%) between the 2 fixation techniques. Higher maximal bending moment was found in front limbs than hind limbs, and front limbs with two 5.5-mm screws than hind limbs with two 5.5-mm screws. In all cases, constructs completely failed. A greater number of 4.5-mm cortical screws failed than 5.5-mm cortical screws. CONCLUSIONS-In pastern arthrodesis constructs loaded in 3-point bending, end (front limb vs hind limb) affected maximal bending moment at failure of constructs. There was no significant effect of horse, treatment, or side on maximal bending moment or stiffness. Two 5.5-mm cortical screws should provide a surgically simpler pastern arthrodesis than three 4.5-mm cortical screws while maintaining similar biomechanical characteristics. CLINICAL RELEVANCE: Three 4.5-mm screws or two 5.5-mm screws will provide similar biomechanical characteristics in bending when performing equine pastern arthrodesis.

An in vitro biomechanical comparison of interlocking nail constructs and double plating for fixation of diaphyseal femur fractures in immature horses.

OBJECTIVE: To compare the biomechanical properties of intact immature horse femurs and 3 stabilization methods in ostectomized femurs. ANIMAL OR SAMPLE POPULATION: Eighteen pairs of femurs from immature horses aged 1 to 15 months, and weighing 68 to 236 kg. METHODS: Thirty-four immature horse femurs were randomly assigned to 1 of 5 test groups: 1) interlocking intramedullary nail (IIN) (n = 6); 2) IIN with a cranial dynamic compression plate (I/DCP) (n = 6); 3) 2 dynamic compression plates (2DCP) (n = 8); 4) intact femurs tested to failure in lateromedial (LM) bending (n = 6); and 5) intact femurs tested to failure in caudocranial (CaCr) bending (n = 8). Mid-diaphyseal ostectomies (1 cm) were performed in all fixation constructs. Biomechanical testing consisted of 4 nondestructive tests: CaCr bending, LM bending, compression, and torsion, followed by bending to failure. All groups were tested to failure in LM bending with the exception of 1 group of intact femurs tested to failure in CaCr bending. Stiffness and failure properties were compared among groups. RESULTS: The 2DCP-femur construct had greater structural stiffness in nondestructive bending than the IIN-femur construct in either LM or CaCr bending, and the I/DCP-femur construct in LM bending. Only the I/DCP and 2DCP fixations were similar to intact bone in nondestructive-bending tests. In addition, the 2DCP-femur construct had greater structural and gap torsional stiffness than the I/DCP-femur construct, and greater gap torsional stiffness than the IIN-femur construct. However, all of the fixation methods tested, including the 2DCP-femur construct, had lower structural stiffness in torsional loading compared with intact bone. No significant differences in structural stiffness were found between intact bones and femur constructs tested nondestructively in compression. In resistance to LM bending to failure, the 2DCP-femur construct was superior to the IIN-femur construct, yet similar to the I/DCP-femur construct. Also, evaluation of yield and failure loads revealed no significant differences between intact bone and any of the femur constructs tested to failure in LM bending. CONCLUSIONS: In general, the 2DCP-femur construct provided superior strength and stiffness compared with the IIN and I/DCP-femur constructs under bending and torsion. CLINICAL RELEVANCE: Double plating of diaphyseal comminuted femoral fractures in immature horses may be the best method of repair, because in general, it provides the greatest strength and stiffness in bending and torsion.

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.

Thermal chondroplasty with radiofrequency energy. An in vitro comparison of bipolar and monopolar radiofrequency devices.

The purpose of this study was to examine the in vitro effects of three radiofrequency energy devices (two bipolar devices and one monopolar device) for the performance of thermal chondroplasty. Thirty-two fresh bovine femoral osteochondral sections (approximately 3 x 4 x 5 cm) from eight cows were divided into four groups (three treatment patterns and one sham-operated group with eight specimens per group). The three treatment patterns consisted of 1) radiofrequency energy delivered by a mechanical jig at 1 mm/sec in a contact mode (50 g of pressure), 2) radiofrequency energy delivered by a mechanical jig at 1 mm/sec in a noncontact mode (1 mm between probe tip and articular cartilage surface), and 3) radiofrequency energy smoothing of abraded cartilage during arthroscopic visualization. Thermal smoothing of the abraded cartilage surface was accomplished with all three devices. Significant chondrocyte death, as determined by confocal laser microscopy and cell viability staining, was observed with each device. The bipolar radiofrequency systems penetrated 78% to 92% deeper than the monopolar system. The bipolar systems penetrated to the level of the subchondral bone in all osteochondral sections during arthroscopically guided paintbrush pattern treatment. Radiofrequency energy should not be used for thermal chondroplasty until further work can establish consistent methods for limiting the depth of chondrocyte death while still achieving a smooth articular for thermal chondroplasty until further work can establish consistent methods for limiting the depth of chondrocyte death while still achieving a smooth articular surface.