Poor bone quality is a major factor in skeletal fragility in elderly individuals. The molecular mechanisms that establish and maintain bone quality, independent of bone mass, are unknown but are thought to be primarily determined by osteocytes. We hypothesize that the age-related decline in bone quality results from the suppression of osteocyte perilacunar/canalicular remodeling (PLR), which maintains bone material properties. We examined bones from young and aged mice with osteocyte-intrinsic repression of TGFβ signaling (TβRIIocy-/-) that suppresses PLR. The control aged bone displayed decreased TGFβ signaling and PLR, but aging did not worsen the existing PLR suppression in male TβRIIocy-/- bone. This relationship impacted the behavior of collagen material at the nanoscale and tissue scale in macromechanical tests. The effects of age on bone mass, density, and mineral material behavior were independent of osteocytic TGFβ. We determined that the decline in bone quality with age arises from the loss of osteocyte function and the loss of TGFβ-dependent maintenance of collagen integrity.

Abstract Poor bone quality (BQ) is a major factor in skeletal fragility in the elderly. Molecular mechanisms establishing and maintaining BQ, independent of bone mass, are unknown but are thought to be primarily determined by osteocytes. We hypothesize that the age-related decline in BQ results from suppression of osteocyte perilacunar/canalicular remodeling (PLR), which maintains bone material properties. We examined bones from young and aged mice with an osteocyte-intrinsic repression of TGFβ signaling (TβRIIocy-/-) that suppresses PLR. Control-aged bone displayed decreased TGFβ signaling and PLR, but aging male TβRIIocy-/- bone did not worsen existing PLR suppression. This epistatic relationship impacted collagen material behavior at the nano and tissue scale in macromechanical tests. The effects of age on bone mass, density, and mineral material behavior were independent of osteocytic TGFβ. We determine that the decline of BQ with age arises from lost osteocyte function and maintenance of collagen integrity in a TGFβ-dependent fashion.

Mechanical stimuli are required for the proper development of the musculoskeletal system. Removal of muscle forces during fetal or early post-natal timepoints impairs the formation of bone, tendon, and their attachment (the enthesis). The goal of the current study was to examine the capacity of the shoulder to recover after a short duration of neonatal rotator cuff paralysis, a condition mimicking the clinical condition neonatal brachial plexus palsy. We asked if reapplication of muscle load to a transiently paralyzed muscle would allow for full recovery of tissue properties. CD-1 mice were injected with botulinum toxin A to paralyze the supraspinatus muscle from birth through 2 weeks and subsequently allowed to recover. The biomechanics of the enthesis was determined using tensile testing and the morphology of the shoulder joint was determined using microcomputed tomography and histology. A recovery period of at least 10 weeks was required to achieve control properties, demonstrating a limited capacity of the shoulder to recover after only two weeks of muscle paralysis. Although care must be taken when extrapolating results from an animal model to the human condition, the results of the current study imply that treatment of neonatal brachial plexus palsy should be aggressive, as even short periods of paralysis could lead to long-term deficiencies in enthesis biomechanics and shoulder morphology.

Purpose To compare the tensile properties of a 3-0, 4-strand flexor tendon repair with a 4-0, 4-strand repair and a 4-0, 8-strand repair. Methods Following evaluation of the intrinsic material properties of the 2 core suture calibers most commonly used in tendon repair (3-0 and 4-0), we tested the mechanical properties of 40 cadaver flexor digitorum profundus tendons after zone II repair with 1 of 3 techniques: a 3-0, 4-strand core repair, a 4-0, 8-strand repair, or a 4-0, 4-strand repair. We compared results across suture caliber for the 2 sutures and across tendon repair methods. Results Maximum load to failure of 3-0 polyfilament caprolactam suture was 49% greater than that of 4-0 polyfilament caprolactam suture. The cross-sectional area of 3-0 polyfilament caprolactam was 42% greater than that of 4-0 polyfilament caprolactam. The 4-0, 8-strand repair produced greater maximum load to failure when compared with the 2 4-strand techniques. Load at 2-mm gap, stiffness, and work to yield were significantly greater in the 4-0, 8-strand repair than in the 3-0, 4-strand repair. Conclusions In an ex vivo model, an 8-strand repair using 4-0 suture was 43% stronger than a 4-strand repair using 3-0 suture, despite the finding that 3-0 polyfilament caprolactam was 49% stronger than 4-0 polyfilament caprolactam. These results suggest that, although larger-caliber suture has superior tensile properties, the number of core suture strands across a repair site has an important effect on time zero, ex vivo flexor tendon repair strength. Clinical relevance Surgeons should consider using techniques that prioritize multistrand core suture repair over an increase in suture caliber. (Copyright (C) 2014 by the American Society for Surgery of the Hand. All rights reserved.)

There is little consensus regarding whether the number of core suture strands or the caliber of the core suture has a greater impact on time 0 tensile properties. Our hypothesis was that a 3-0, 4-strand repair would have similar tensile properties as a 4-0, 8-strand repair.

To improve the functional outcomes of intrasynovial tendon suture, prior experiments evaluated individual technical modifications used in the repair process. Few studies, however, have assessed the combinatorial effects of those suture modifications in an integrated biomechanical manner, including a sample size sufficient to make definitive observations on repair technique. Two hundred fifty-six flexor tendon repairs were performed in human cadavera, and biomechanical properties were determined. The effects of five factors for flexor tendon repair were tested: core suture caliber (4-0 or 3-0), number of sutures crossing the repair site (four- or eight-strand), core suture purchase (0.75 or 1.2 cm), peripheral suture caliber (6-0 or 5-0), and peripheral suture purchase (superficial or 2 mm). Significant factors affecting the properties of the repair were the number of core suture strands and the peripheral suture purchase. The least significant factors were core suture purchase and peripheral suture caliber. The choice of core suture caliber affected the properties of repair marginally. Based on these results, we recommend that surgeons continue to focus on multi-strand repair methods, as the properties of eight-strand repairs were far better than those of four-strand repairs. To resist gap formation and enhance repair strength, a peripheral suture with 2 mm purchase is also recommended. Finally, since core suture caliber affected some biomechanical properties, including the failure mode, a 3-0 suture could be considered, provided that future in vivo studies can confirm that gliding properties are not adversely influenced.

Tendon-to-bone healing is typically poor, with a high rate of repair-site rupture. Bone loss after tendon-to-bone repair may contribute to poor outcomes. Therefore, we hypothesized that the local application of the osteogenic growth factor bone morphogenetic protein 2 (BMP-2) would promote bone formation, leading to improved repair-site mechanical properties. Intrasynovial canine flexor tendons were injured in Zone 1 and repaired into bone tunnels in the distal phalanx. BMP-2 was delivered to the repair site using either a calcium phosphate matrix (CPM) or a collagen sponge (COL) carrier. Each animal also received carrier alone in an adjacent repair to serve as an internal control. Repairs were evaluated at 21 days using biomechanical, radiographic, and histologic assays. Although an increase in osteoid formation was noted histologically, no significant increases in bone mineral density occurred. When excluding functional failures (i.e., ruptured and gapped repairs), mechanical properties were not different when comparing BMP-2/CPM groups with carrier controls. A significantly higher percentage of BMP-2 treated specimens had a maximum force <20?N compared to carrier controls. While tendon-to-bone healing can be enhanced by addressing the bone loss that typically occurs after surgical repair, the delivery of BMP-2 using the concentrations and methods of the current study did not improve mechanical properties over carrier alone. The anticipated anabolic effect of BMP-2 was insufficient in the short time frame of this study to counter the post-repair loss of bone. (c) 2012 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 30:17021709, 2012