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Matthew J Silva

Publications and source records attributed to Matthew J Silva.

At least 37 records · Page 2Linked to original sources
PubMed2004

Morphological and mechanical properties of caudal vertebrae in the SAMP6 mouse model of senile osteoporosis.

The senescence-accelerated mouse, strain P6 (SAMP6), is a model of senile osteoporosis with relatively low bone mineral density (BMD), low rates of bone formation and reduced long-bone bending strength. Seeking to extend previous descriptions of the SAMP6 skeletal phenotype, we assessed the morphological and mechanical properties of vertebrae from SAM mice at 4 and 12 months of age. We hypothesized that, relative to SAMR1 controls, vertebrae from SAMP6 mice have: (1) less trabecular bone, (2) increased endosteal and periosteal bone size and (3) decreased whole-bone strength. Caudal vertebrae from adult female mice (SAMR1 and SAMP6; 4 and 12 months; n = 10-11 per group) were evaluated by micro-computed tomography and mechanical compression testing. SAMP6 vertebrae had 33% less trabecular bone volume in cephalad and caudal end regions than SAMR1 (P < 0.001) due to significant reductions in both trabecular number (P = 0.002) and thickness (P < 0.001). In contrast to previous findings in SAMP6 long bones, SAMP6 vertebrae showed no evidence of increased overall bone dimensions compared to SAMR1, and in fact had smaller total bone area (TA) and endosteal area (EA) at 12 months of age. Whereas SAMR1 vertebrae showed signs of age-related expansion from 4 to 12 months, SAMP6 vertebral dimensions did not change with age. Mechanical properties of SAMP6 vertebrae were not significantly different than SAMR1 vertebrae (stiffness, yield force, ultimate force, displacement at ultimate force, energy to ultimate force; P > 0.05), another finding in contrast to previous results in SAMP6 long bones. In summary, reduced vertebral trabecular bone volume is another feature of the SAMP6 mice with relevance to senile osteoporosis. However, age-related bone expansion and reduced whole-bone strength were not evident in SAMP6 vertebrae, indicating that while the SAMP6 mouse has many features relevant to senile osteoporosis in humans, not all features are observed or detectable at all skeletal sites.

Animals↗
PubMed2004

Nanoindentation and whole-bone bending estimates of material properties in bones from the senescence accelerated mouse SAMP6.

The senescence accelerated mouse, strain P6 (SAMP6) has been described as a model of senile osteoporosis. Recent results from whole-bone bending tests indicate that, despite having increased moments of inertia, SAMP6 long bones are weak and brittle compared to SAMR1 controls. In the current study we determined material properties of cortical bone from SAMP6 and SAMR1 femora and tibiae by two methods-nanoindentation and whole-bone bending tests combined with simple beam theory. We hypothesized that: (1) SAMP6 mice have reduced cortical bone material properties compared to SAMR1 controls; and (2) modulus estimated from whole-bone bending tests correlates well with modulus determined by nanoindentation. Results from nanoindentation indicated that modulus and hardness are approximately 10% higher in SAMP6 mice compared to SAMR1 controls (p<0.001), a finding consistent with slightly higher mineralization in SAMP6 bones. Despite their superior elastic and hardness properties, the bending failure properties of SAMP6 bones were markedly inferior--ultimate stress and toughness were reduced by 40% and 60%, respectively (p<0.001). Comparisons between the two testing methods for determining modulus showed poor agreement. Modulus estimated from whole-bone bending tests was not correlated with modulus determined by nanoindentation (p=0.054; r2=0.03) and the absolute values differed by a factor of five between the two methods (bending [wet], 6GPa; nanoindentation [dry], 31GPa). Moreover, relative differences between groups were inconsistent between the two methods. We conclude: (1) cortical bone from the SAMP6 mouse has increased modulus and hardness but poor material strength and toughness, which underscores the relevance of the SAMP6 mouse for studies of skeletal fragility, and (2) values of elastic modulus of bone tissue estimated using simple beam theory and bending tests of mouse femora and tibiae are inaccurate and should be interpreted with caution.

Aging↗
PubMed2004

Tendon injury response: assessment of biomechanical properties, tissue morphology and viability following flexor digitorum profundus tendon transection.

Insertion site injuries of the flexor digitorum profundus (FDP) tendon often present for delayed treatment. Apart from gross observations made at the time of surgery, the changes that occur in the flexor tendon stump during the interval from injury to repair are unknown. These changes may include tendon softening and loss of viability, which may contribute to the poor outcomes observed clinically and experimentally. Thirty-eight FDP tendons from 23 adult dogs were transected sharply from their insertions on the distal phalanges and were not repaired. Dogs were allowed full weight bearing and were euthanized 7 or 21 days after injury. Biomechanical testing indicated that the resistance of injured tendons to pullout of a Kessler-type suture was not different from control tendons at 7 days and was increased at 21 days by 25% (p<0.05). Morphologically, at 7 and 21 days the cut surface had a smooth appearance and the end of the injured tendon was increased in thickness by 30% and 50%, respectively (p<0.05). Histologically, we observed increased cellularity and dramatic fibroblast proliferation within the injured tendon stump; there was no evidence of decreased cell viability. We conclude that during the interval from 0 to 21 days after FDP insertion-site injury, tendons cells are viable, proliferative and synthesizing new matrix. This leads to increased tendon size and enhanced resistance to suture pullout. These findings offer a scientific rationale supporting the clinical practice of surgical re-attachment within the first 3 weeks after injury.

Animals↗
PubMed2004

Lack of OH in nanocrystalline apatite as a function of degree of atomic order: implications for bone and biomaterials.

Using laser Raman microprobe spectroscopy, we have characterized the degree of hydroxylation and the state of atomic order of several natural and synthetic calcium phosphate phases, including apatite of biological (human bone, heated human bone, mouse bone, human and boar dentin, and human and boar enamel), geological, and synthetic origin. Common belief holds that all the studied phases are hydroxylapatite, i.e., an OH-containing mineral with the composition Ca10(PO4)6(OH)2. We observe, however, that OH-incorporation into the apatite crystal lattice is reduced for nanocrystalline samples. Among the biological samples, no OH-band was detected in the Raman spectrum of bone (the most nanocrystalline biological apatite), whereas a weak OH-band occurs in dentin and a strong OH-band in tooth enamel. We agree with others, who used NMR, IR spectroscopy, and inelastic neutron scattering, that-contrary to the general medical nomenclature-bone apatite is not hydroxylated and therefore not hydroxylapatite. Crystallographically, this observation is unexpected; it therefore remains unclear what atom(s) occupy the OH-site and how charge balance is maintained within the crystal. For non-bone apatites that do show an OH-band in their Raman spectra, there is a strong correlation between the concentration of hydroxyl groups (based on the ratio of the areas of the 3572 deltacm(-1) OH-peak to the 960 deltacm(-1) P-O phosphate peak) and the crystallographic degree of atomic order (based on the relative width of the 960 deltacm(-1) P-O phosphate peak) of the samples. We hypothesize that the body biochemically imposes a specific state of atomic order and crystallinity (and, thus, concentration of hydroxyl) on its different apatite precipitates (bone, dentin, enamel) in order to enhance their ability to carry out tissue-specific functions.

Animals↗
PubMed2004

Cartilage tolerates single impact loads of as much as half the joint fracture threshold.

We hypothesized that one mechanical insult could affect cellular proliferation, matrix turnover, and the structural integrity of cartilage, and that these effects would be dose dependent and time dependent. One impact load of low impact (14.4 MPa +/- 2.1 MPa), medium impact (22.8 MPa +/- 5.8 MPa), or high impact (55.5 MPa +/- 12.6 MPa) was administered to the posterior aspect of the medial femoral condyle of New Zealand White rabbits using a previously validated pendulum device. Animals were euthanized at 2, 6, and 12 weeks after impact, and the impacted and sham (contralateral limb) cartilage were harvested. Each specimen was assessed by light microscopy and by immunohistochemical methods. Although impacted specimens had greater loss of proteoglycan staining than sham cartilage, these changes were neither dose dependent nor time dependent. No structural damage, enzymatic proteoglycan or collagen breakdown, or cellular proliferation was identified in the different impact groups. Articular cartilage is a resilient tissue, particularly in situ, and can tolerate single impact loads of as much as 45% of the joint fracture threshold without considerable disruption or degradation.

Animals↗
PubMed2003

Bone loss following tendon laceration, repair and passive mobilization.

Little is known about the localized changes in bone mass that occur following tendon or ligament injury. Interruption of normal load transfer at the insertion site will presumably lead to a localized loss of bone, although few data exist to support this claim. To test this hypothesis, we transected the canine flexor digitorum profundus (FDP) tendon from its insertion, and either repaired it using a trans-osseous suture technique or left it unrepaired (laceration only). Post-operatively, forelimbs in the repair group were cast immobilized except for 10 min of daily passive mobilization rehabilitation, whereas in the laceration only group dogs were allowed full weight bearing. At 5-42 days post-injury, we assessed bone mineral density (BMD) using pQCT and osteoclast surface by histomorphometry. We measured significant bone loss in the distal phalanx after combined FDP tendon laceration, repair, and post-operative passive mobilization, with BMD decreases of 20%, 40%, and 41% at 10, 21, and 42 days (p<0.01). Moreover, we observed that passive mobilization and tendon laceration each contributed independently to the observed bone loss. At 42 days, BMD was reduced by 21% in bones that were not injured but were subjected to the post-operative passive mobilization protocol, while BMD was reduced by 28% in bones subjected to tendon laceration and full weight bearing (p<0.01). In both the passive mobilization and laceration specimens, we counted significantly increased osteoclasts after only 7-10 days, and these increases persisted through 42 days (p<0.05). We conclude that rapid and sustained bone resorption leads to significant bone loss in the 6-week period following flexor tendon injury and repair. This bone loss may impact healing by impeding the restoration of a strong tendon-bone interface.

Animals↗
PubMed2003

Neovascularization of the flexor digitorum profundus tendon after avulsion injury: an in vivo canine study.

PURPOSE: The changes in matrix material properties and intrinsic vascularization that have been noted in intrasynovial tendon stumps after avulsion injury may be of considerable clinical relevance with regard to the results of surgical repair. Our objective was to determine both the time course and the source of neovascularization of the tendon stump in an in vivo canine model of flexor digitorum profundus (FDP) avulsion after a clinically relevant delay in diagnosis. METHOD: The FDP tendon was released from bone directly by sharp dissection and the vinculum brevis profundus was lacerated, simulating an avulsion injury with interruption of the vascular supply to the tendon stump. After death at 7 and 21 days, tendon vascularity was evaluated with India ink injection and clearing using a modified Spalteholtz technique. RESULTS: All 7-day specimens showed an absence of vascularity compared with the controls. In all 21-day specimens a direct vascular supply originated from local fibrovascular adhesions contacted the stump on its surface and blood vessels penetrated the tendon stump circumferentially. Progressive vascularization of the avulsed tendon stump occurred between 7 and 21 days after injury, originating from fibrovascular adhesions to the surrounding synovial sheath. CONCLUSIONS: Whereas previous studies of intrasynovial flexor tendon laceration and repair have shown a progressive proximal to distal neovascularization of the FDP during the early postoperative period, longitudinal proximal to distal growth from the proximal blood supply of the FDP was not observed toward the unrepaired tendon stump.

Animals↗
PubMed2003

Two-portal repair of canine flexor tendon insertion site injuries: histologic and immunohistochemical characterization of healing during the early postoperative period.

PURPOSE: In vivo animal studies have indicated that the complex structure of the tendon-bone interface may not be restored after repair even under optimal conditions. Controversy exists about the histologic findings in the early postoperative period after tendon reattachment to bone; this may have impact on biomechanical properties. The objective was to study the histologic structure and immunohistochemical staining of the tendon-bone interface in a large model of digital flexor tendon-bone repair. The hypothesis was that the tendon-bone interface matures and assumes a progressively more anatomic histologic and immunohistochemical appearance during the first 6 weeks after repair. METHODS: Twenty-four canine flexor digitorum profundus tendons were released from their insertion by sharp dissection and repaired to bone. The forelimb was immobilized after surgery and 10 minutes of daily passive motion rehabilitation was performed. Dogs were killed at 10, 21, and 42 days after surgery. Hematoxylin-eosin and immunohistochemical staining for types I, II, and II collagen were performed. RESULTS: Although at both 10 and 21 days after surgery substantial inflammation was seen at the tendon-bone repair site, this had decreased markedly by 42 days. Although direct apposition of tendon to bone was seen at 42 days, the mature tendon-bone insertion site was not recreated by this time. Staining for types I and III collagen was diffuse throughout the tendon-bone insertion throughout the interval examined. CONCLUSION: These findings suggest that at 6 weeks after surgery the intact tendon-bone repair site shows minimal histologic and molecular similarity when compared with unoperated specimens.

Animals↗
PubMed2002

SHIP-deficient mice are severely osteoporotic due to increased numbers of hyper-resorptive osteoclasts.

The hematopoietic-restricted protein Src homology 2-containing inositol-5-phosphatase (SHIP) blunts phosphatidylinositol-3-kinase-initiated signaling by dephosphorylating its major substrate, phosphatidylinositol-3,4,5-trisphosphate. As SHIP(-/-) mice contain increased numbers of osteoclast precursors, that is, macrophages, we examined bones from these animals and found that osteoclast number is increased two-fold. This increased number is due to the prolonged life span of these cells and to hypersensitivity of precursors to macrophage colony-stimulating factor (M-CSF) and receptor activator of nuclear factor-kappa B ligand (RANKL). Similar to pagetic osteoclasts, SHIP(-/-) osteoclasts are enlarged, containing upwards of 100 nuclei, and exhibit enhanced resorptive activity. Moreover, as in Paget disease, serum levels of interleukin-6 are markedly increased in SHIP(-/-) mice. Consistent with accelerated resorptive activity, 3D trabecular volume fraction, trabecular thickness, number and connectivity density of SHIP(-/-) long bones are reduced, resulting in a 22% loss of bone-mineral density and a 49% decrease in fracture energy. Thus, SHIP negatively regulates osteoclast formation and function and the absence of this enzyme results in severe osteoporosis.

Animals↗
PubMed2002

Recent progress in flexor tendon healing.

Although advances in the treatment of flexor tendon injuries have led to improved clinical outcomes during the past several decades, a subset of patients continue to experience a loss of function. Using a canine model of sharp transection of the flexor digitorum profundus tendon followed by repair and rehabilitation using clinically relevant techniques, we have examined the influence of multistrand suture and postoperative rehabilitation variables on digital function and tendon strength. Our findings highlight the critical role of repair technique in providing a stiff and strong repair and indicate that continued refinement of suture techniques is warranted in order to minimize repair-site elongation (gap). Gap formation continues to occur at a high frequency, and the formation of gaps greater than 3 mm delays the accrual of repair-site strength that occurs with time. Furthermore, our results indicate that passive-motion rehabilitation that produces a moderate amount of tendon excursion (2 mm) at low levels of tendon force (5 N) is sufficient to inhibit adhesion formation and to promote healing. Increases in excursion or force beyond these levels do not accelerate the healing process. These findings suggest that we are approaching the limit of the extent to which we can modulate healing by manipulating rehabilitation variables such as tendon excursion and force. Future advances will probably require manipulation of the biological factors that promote healing.

Animals↗
PubMed2002

The rigidity of repaired flexor tendons increases following ex vivo cyclic loading.

Transected flexor tendons are typically treated by suture repair followed by rehabilitation that generates repetitive tendon loading. Recent results in an in vivo canine model indicate that during the first 10 days after injury and repair, there is an increase in the rigidity of the tendon repair site. Our objective was to determine whether or not ex vivo cyclic loading of repaired flexor tendons causes a similar increase in repair-site rigidity. We simulated 10 days of rehabilitation by applying 6000 loading cycles to repaired canine flexor tendons ex vivo at force levels generated during passive motion rehabilitation; we then evaluated their tensile mechanical properties. High-force (peak force, 17 N) cyclic loading increased repair-site rigidity by 100% and decreased repair-site strain by 50%, whereas low-force (5 N) loading did not change the properties of the repair site. This mechanical conditioning effect may explain, in part, the changes in tensile properties observed after only 10 days of healing in vivo. Mechanical conditioning of repaired flexor tendons by repetitive forces applied during rehabilitation may lead to increases in repair-site rigidity and decreases in strain, thereby altering the mechanical loading environment of tissues and cells at the repair site.

Animals↗
PubMed2002

The insertion site of the canine flexor digitorum profundus tendon heals slowly following injury and suture repair.

Treatment of injuries of the flexor digitorum profundus (FDP) tendon insertion site has changed little during the past 50 years, in part because there are no reports describing flexor tendon insertion site healing. Our objective was to assess the effects of repair technique and post-operative time on tendon-bone healing using a canine model of injury and repair. We transected 48 FDP tendons from 24 dogs at their insertions and repaired them using either a four- or eight-strand suture technique. We assessed the mechanical properties of the repaired tendon-bone construct, tendon collagen biochemistry, and distal phalanx bone mineral density (BMD) at 0, 10, 21 and 42 days. Suture method had no significant effect on any outcome (p > 0.05). In particular, use of an eight-strand double modified Kessler technique did not result in increased stiffness or strength compared to a four-strand technique. With time, the repair site became stiffer, as demonstrated by a 230% increase in rigidity and a 50% decrease in strain from 0 to 42 days. However, from 0 to 42 days the ultimate force of the insertion site did not increase. This lack of increase in ultimate force was consistent with decreases in collagen content, non-reducible crosslinks and distal phalanx BMD. Taken together, our results indicate that the canine FDP tendon heals slowly after it is injured at its insertion site and sutured onto the distal phalanx. While these findings may be limited to the particular repair method we used, they demonstrate a need for devising new treatment strategies to improve healing of flexor tendon insertion site injuries.

Animals↗
PubMed2002

In vivo fatigue loading of the rat ulna induces both bone formation and resorption and leads to time-related changes in bone mechanical properties and density.

Fatigue loading triggers bone resorption and is associated with stress fractures. Neither the osteogenic response nor the changes in bone mechanical properties following in vivo fatigue loading have been quantified. To further characterize the skeletal response to fatigue loading, we assessed bone formation, mechanical properties, density and resorption in the ulnae of 72 adult rats subjected to a single bout of in vivo loading followed by 0, 6, 12 or 18 days of recovery. Axial, compressive loading (peak force 13.3 N, 2 Hz) was applied to the right forelimb until the ulna was fatigued to a pre-determined level. The left forelimb served as a contralateral control. The primary osteogenic response to fatigue loading was woven bone formation that occurred on the periosteal surface of the ulnar diaphysis and was significantly greater in loaded limbs versus controls at 6, 12 and 18 days (p <.0.05). Ultimate force of the ulna in three-point bending decreased by 50% and stiffness decreased by 70% on day 0 (p < 0.01 vs. control), indicative of acute fatigue damage. By day 12, ultimate force and stiffness had returned to control levels (p > 0.05) and by day 18 had increased 20% beyond controls (p < 0.01). Bone cross-sectional area, moment of inertia, and mineral content increased with recovery time (p < 0.01), consistent with the increases in woven bone formation and mechanical properties. Intracortical resorption space density and osteoclast density also increased with recovery time (p < 0.05), indicating activation of intracortical remodeling. In summary, our findings demonstrate the remarkable ability of the adult skeleton to rapidly form periosteal woven bone and thereby offset the negative structural effects of acute fatigue damage and subsequent intracortical resorption.

Animals↗
PubMed2002

Vascular anatomy of the human flexor digitorum profundus tendon insertion.

The vascular anatomy of the flexor digitorum profundus (FDP) tendon insertion is described by using a vascular injection and modified Spalteholtz tissue clearing protocol in 36 human cadaver digits. A consistent dense palmar and dorsal vascular supply to the tendon at its insertion into the distal phalanx was observed based on sources from both the distal phalanx and the vinculum brevis profundus. Multiple palmar-dorsal vascular interconnections were seen between these spatially distinct vascular networks, a finding not observed previously in studies of the vascular anatomy of tendon or ligament insertions. Additionally a well-defined dorsal zone of hypovascularity was identified subjacent to the volar plate of the distal interphalangeal joint, within 1 cm of the tendon insertion. Recognition of the vascular supply to the FDP insertion at the distal phalanx permits further evaluation of the vascular, histologic, and cellular events after FDP tendon avulsion and improves the understanding of the biologic response mechanisms involved in bone-tendon healing.

Fingers↗
PubMed2002

A method for delivering variable impact stresses to the articular cartilage of rabbit knees.

OBJECTIVE: To develop a method by which a single impact force of controlled magnitude and rate could be applied uniformly to an area on the posterior aspect of the medial femoral condyle of adult rabbits. DESIGN: An in-vivo animal model using a pendulum device, designed and manufactured to supply the kinetic energy necessary to apply different impact loads to the posterior aspect of the medial femoral condyle of a rabbit. SETTING: Biomechanical laboratory, University Medical Center. SUBJECTS: A total of thirty-six femoral condyles from 3-kilogram New Zealand White (NZW) rabbits were used during this evaluation. INTERVENTION: An aluminum impactor was made based on the sagittal and coronal radii of curvature of six matched pairs (n = 12) of femurs from three-kilogram NZW rabbits. This impactor was coupled with the pendulum and used to apply different impact loads to both of the medial femoral condyle of the knees of NZW rabbits (n = 24). MAIN OUTCOME MEASUREMENTS: Peak impact force, time to peak impact force, and average contact area between impactor and medial femoral condyle, were measured for each group of animals tested. RESULTS: The pendulum delivered a consistent impact force to the rabbit condyle of 120.0 N (+/-18.1; coefficient of variance, 15 percent) with 400 grams attached to the pendulum arm, at an average time to peak force of 0.021 seconds (+/-0.001, co. var. 4.8 percent). The peak impact force was significantly different for each of the three impact mass groups of animals (p < 0.001). By contrast, time to peak force for each mass group averaged approximately 0.020 seconds and the average contact area was 6.26 mm2 (+/-0.51). Quantitative assessment of the exposed medium pressure-sensitive film confirmed uniform impact force intensity within each specimen. CONCLUSIONS: An in-vivo animal model was developed to deliver a controlled and rapid impact force to a specific area of the weight-bearing surface of the adult rabbit knee. These loads were applied at a rate comparable to the clinical setting of falling onto an outstretched hand, thus simulating a common clinical scenario by which cartilage is often injured. This model can be used in future experiments to investigate mechanism by which posttraumatic arthritis develops after articular injuries.

Animals↗
PubMed2002

Long bones from the senescence accelerated mouse SAMP6 have increased size but reduced whole-bone strength and resistance to fracture.

The senescence accelerated mouse strain P6 (SAMP6) has emerged as a useful model of senile osteoporosis because it has many features of the disease, including low trabecular bone formation and low areal bone density. We further characterized the SAMP6 model of senile osteoporosis by comparing morphological, mechanical, and densitometric properties of femurs and tibias from SAMP6 mice to those of the control strain (SAMR1) at 4 months and 12 months of age. SAMP6 long bones had increased periosteal width and endosteal area (p < 0.05), resulting in an average increase of 30% in moments of inertia (p < 0.05), but no difference in bone area (p > 0.05) compared with control. Despite their increased moments of inertia, long bones from SAMP6 mice were relatively weak and brittle. Ultimate bending moment was reduced by 25%, and both postyield displacement and energy-to-fracture were reduced by 60% compared with SAMR1 controls (p < 0.001). Average cortical ash fraction was increased slightly from 0.74 in SAMR1 to 0.76 in SAMP6 bones (p < 0.05), indicating that increased mineralization may have contributed to the brittleness of SAMP6 bones. The relative differences we observed--increased endosteal and periosteal dimensions, reduced bending strength, increased brittleness, and increased mineralization--are analogous to changes that occur in the aging human skeleton. Moreover, these features were consistently observed in young (4-month) and old (12-month) animals. These findings extend the previous descriptions of the SAMP6 mouse and identify key mechanical features that further validate its relevance as a unique and functionally relevant model of senile osteoporosis.

Aging, Premature↗
PubMedDate not supplied

Effect of hemorrhage on medial collateral ligament healing in a mouse model.

BACKGROUND: Medial collateral ligament injuries heal by a scar response. HYPOTHESIS: Increased hemorrhage at the site of medial collateral ligament injury improves healing. STUDY DESIGN: Controlled laboratory study. METHODS: Ninety-six mice were divided into two groups. Group 1 mice underwent knee medial collateral ligament transection with the opposite knee as a sham-operated control and group 2 animals additionally had 0.25 ml of tail cut blood pipetted to the medial collateral ligament transection site and sham-operated opposite knee. Ligament specimens were harvested at 3, 7, 21, and 28 days. RESULTS: Immunohistochemical analysis demonstrated peak macrophage counts at day 7 in all transected specimens. Macrophage counts were higher in group 2 than in group 1 at all time points, with a statistically significant increase of macrophages noted at day 7. In situ hybridization demonstrated increased collagen gene expression, with peaks at 7 and 28 days after transection. Group 2 animals showed increased gene expression at all time points as compared with group 1, with a statistically significant increase noted at 7 and 28 days. Biomechanical testing demonstrated progressive healing at each time point. At 28 days, the load to failure was 67% that of the sham-operated knee. CONCLUSIONS: This study suggests there is an increased healing response with bleeding at the ligament injury site. CLINICAL RELEVANCE: Identification of the factors involved with increased healing may allow manipulation of the healing response in the clinical setting.

Animals↗