Evaluation of the PROMIS Upper Extremity Against Validated Patient-Reported Outcomes in Patients With Early Carpometacarpal Osteoarthritis.

PURPOSE: Internal consistency, construct, and criterion validity of the Patient-Reported Outcomes Measurement Information System (PROMIS) upper extremity (UE) v1.2 were evaluated in patients with early-stage carpometacarpal (CMC) osteoarthritis (OA). We hypothesized that in patients with early CMC OA, PROMIS UE scores would: (1) be lower than those in asymptomatic controls; (2) correlate with established patient-reported outcomes; (3) correlate with pinch and grip strengths; and (4) not correlate with radiographic disease progression. METHODS: Patients with early CMC OA (modified Eaton stage 0 or 1) and matched asymptomatic control patients completed the PROMIS UE, Australian and Canadian Osteoarthritis Hand Index, and Patient-Rated Wrist-Hand Evaluation at 2 time points. The PROMIS UE's internal consistency was evaluated by Cronbach's alpha, construct validity by Spearman correlation coefficients among the patient-reported outcome measures, and criterion validity using measures of strength. A floor or ceiling effect was indicated if more than 15% of patients achieved the lowest or highest possible score. RESULTS: The PROMIS UE had high internal consistency. Patients with early CMC OA had a lower score than healthy controls (average, 42 vs 54, respectively). We observed moderate to high correlations between the PROMIS UEv1.2, Australian and Canadian Osteoarthritis Hand Index, and Patient-Rated Wrist-Hand Evaluation and good criterion validity when compared to key pinch and grip strengths. The PROMIS UE did not correlate to radiographic disease severity. CONCLUSIONS: The PROMIS UE had a high correlation with Australian and Canadian Osteoarthritis Hand Index and a moderate correlation with Patient-Rated Wrist-Hand Evaluation. The PROMIS UE had high internal consistency and good criterion validity. CLINICAL RELEVANCE: The PROMIS UE is a valid assessment for disability in patients with early CMC OA and can serve as a clinical adjunct to an outcome assessment.

Total Wrist Arthroplasty Alignment and Its Potential Association with Clinical Outcomes.

Purpose There is a lack of quantitative research that describes the alignment and, more importantly, the effects of malalignment on total wrist arthroplasty (TWA). The main goal of this pilot study was to assess the alignment of TWA components in radiographic images and compare them with measures computed by three-dimensional analysis. Using these measures, we then determined if malalignment is associated with range of motion (ROM) or clinical outcomes (PRWHE, PROMIS, QuickDash, and grip strength). Methods Six osteoarthritic patients with a single type of TWA were recruited. Radiographic images, computed tomography images, and clinical outcomes of the wrists were recorded. Using posteroanterior and lateral radiographs, alignment measurements were defined for the radial and carpal components. Radiographic measurements were validated with models reconstructed from computed tomography images using Bland-Altman analysis. Biplanar videoradiography (<1mm and <1 degree accuracy) was used to capture and compute ROM of the TWA components. Linear regression assessed the associations between alignment and outcomes. Results Radiographic measures had a 95% limit-of-agreement (mean difference ± 1.96 × SD) of 3 degrees and 3mm with three-dimensional values, except for the measures of the carpal component in the lateral view. In our small cohort, wrist flexion-extension and radial-ulnar deviation were correlated with volar-dorsal tilt and volar-dorsal offset of the radial component and demonstrated a ROM increase of 3.7 and 1.6 degrees per degree increase in volar tilt, and 10.8 and 4.2 degrees per every millimeter increase in volar offset. The carpal component's higher volar tilt was also associated with improvements in patient-reported pain. Conclusions We determined metrics describing the alignment of TWA, and found the volar tilt and volar offset of the radial component could potentially influence the replaced wrist's ROM. Clinical Relevance TWA component alignment can be measured reliably in radiographs, and may be associated with clinical outcomes. Future studies must evaluate its role in a larger cohort.

Biomechanics of the Distal Radioulnar Joint During In Vivo Forearm Pronosupination.

Background Ulnar variance (UV) and center of rotation (COR) location at the level of the distal radioulnar joint (DRUJ) change with forearm rotation. Nevertheless, these parameters have not been assessed dynamically during active in vivo pronosupination. This assessment could help us to improve our diagnosis and treatment strategies. Questions/purposes We sought to (1) mathematically model the UV change, and (2) determine the dynamic COR's location during active pronosupination. Methods We used biplanar videoradiography to study DRUJ during in vivo pronation and supination in nine healthy subjects. UV was defined as the proximal-distal distance of ulnar fovea with respect to the radial sigmoid notch, and COR was calculated using helical axis of motion parameters. The continuous change of UV was evaluated using a generalized linear regression model. Results A second-degree polynomial with R 2 of 0.85 was able to model the UV changes. Maximum negative UV occurred at 38.0 degrees supination and maximum positive UV occurred at maximum pronation. At maximum pronation, the COR was located 0.5 ± 1.8 mm ulnarly and 0.6 ± 0.8 mm volarly from the center of the ulnar fovea, while at maximum supination, the COR was located 0.2 ± 0.6 mm radially and 2.0 ± 0.5 mm volarly. Conclusion Changes in UV and volar translation of the COR are nonlinear at the DRUJ during pronosupination. Clinical Relevance Understanding the dynamic nature of UV as a function of pronosupination can help guide accurate evaluation and treatment of wrist pathology where the UV is an important consideration. The dynamic behavior of COR might be useful in designing DRUJ replacement implants to match the anatomical motion.

Targeted Ptpn11 deletion in mice reveals the essential role of SHP2 in osteoblast differentiation and skeletal homeostasis.

The maturation and function of osteoblasts (OBs) rely heavily on the reversible phosphorylation of signaling proteins. To date, most of the work in OBs has focused on phosphorylation by tyrosyl kinases, but little has been revealed about dephosphorylation by protein tyrosine phosphatases (PTPases). SHP2 (encoded by PTPN11) is a ubiquitously expressed PTPase. PTPN11 mutations are associated with both bone and cartilage manifestations in patients with Noonan syndrome (NS) and metachondromatosis (MC), although the underlying mechanisms remain elusive. Here, we report that SHP2 deletion in bone gamma-carboxyglutamate protein-expressing (Bglap+) bone cells leads to massive osteopenia in both trabecular and cortical bones due to the failure of bone cell maturation and enhanced osteoclast activity, and its deletion in Bglap+ chondrocytes results in the onset of enchondroma and osteochondroma in aged mice with increased tubular bone length. Mechanistically, SHP2 was found to be required for osteoblastic differentiation by promoting RUNX2/OSTERIX signaling and for the suppression of osteoclastogenesis by inhibiting STAT3-mediated RANKL production by osteoblasts and osteocytes. These findings are likely to explain the compromised skeletal system in NS and MC patients and to inform the development of novel therapeutics to combat skeletal disorders.

SHP2 regulates the development of intestinal epithelium by modifying OSTERIX+ crypt stem cell self-renewal and proliferation.

The protein tyrosine phosphatase SHP2, encoded by PTPN11, is ubiquitously expressed and essential for the development and/or maintenance of multiple tissues and organs. SHP2 is involved in gastrointestinal (GI) epithelium development and homeostasis, but the underlying mechanisms remain elusive. While studying SHP2's role in skeletal development, we made osteoblast-specific SHP2 deficient mice using Osterix (Osx)-Cre as a driver to excise Ptpn11 floxed alleles. Phenotypic characterization of these SHP2 mutants unexpectedly revealed a critical role of SHP2 in GI biology. Mice lacking SHP2 in Osx+ cells developed a fatal GI pathology with dramatic villus hypoplasia. OSTERIX, an OB-specific zinc finger-containing transcription factor is for the first time found to be expressed in GI crypt cells, and SHP2 expression in the crypt Osx+ cells is critical for self-renewal and proliferation. Further, immunostaining revealed the colocalization of OSTERIX with OLFM4 and LGR5, two bona fide GI stem cell markers, at the crypt cells. Furthermore, OSTERIX expression is found to be associated with GI malignancies. Knockdown of SHP2 expression had no apparent influence on the relative numbers of enterocytes, goblet cells or Paneth cells. Given SHP2's key regulatory role in OB differentiation, our studies suggest that OSTERIX and SHP2 are indispensable for gut homeostasis, analogous to SOX9's dual role as a master regulator of cartilage and an important regulator of crypt stem cell biology. Our findings also provide a foundation for new avenues of inquiry into GI stem cell biology and of OSTERIX's therapeutic and diagnostic potential.

An Approach to Robotic Testing of the Wrist Using Three-Dimensional Imaging and a Hybrid Testing Methodology.

Robotic technology is increasingly used for sophisticated in vitro testing designed to understand the subtleties of joint biomechanics. Typically, the joint coordinate systems in these studies are established via palpation and digitization of anatomic landmarks. We are interested in wrist mechanics in which overlying soft tissues and indistinct bony features can introduce considerable variation in landmark localization, leading to descriptions of kinematics and kinetics that may not appropriately align with the bony anatomy. In the wrist, testing is often performed using either load or displacement control with standard material testers. However, these control modes either do not consider all six degrees-of-freedom (DOF) or reflect the nonlinear mechanical properties of the wrist joint. The development of an appropriate protocol to investigate complexities of wrist mechanics would potentially advance our understanding of normal, pathological, and artificial wrist function. In this study, we report a novel methodology for using CT imaging to generate anatomically aligned coordinate systems and a new methodology for robotic testing of wrist. The methodology is demonstrated with the testing of 9 intact cadaver specimens in 24 unique directions of wrist motion to a resultant torque of 2.0 N·m. The mean orientation of the major principal axis of range of motion (ROM) envelope was oriented 12.1 ± 2.7 deg toward ulnar flexion, which was significantly different (p < 0.001) from the anatomical flexion/extension axis. The largest wrist ROM was 98 ± 9.3 deg in the direction of ulnar flexion, 15 deg ulnar from pure flexion, consistent with previous studies [1,2]. Interestingly, the radial and ulnar components of the resultant torque were the most dominant across all directions of wrist motion. The results of this study showed that we can efficiently register anatomical coordinate systems from CT imaging space to robotic test space adaptable to any cadaveric joint experiments and demonstrated a combined load-position strategy for robotic testing of wrist.

SHP2 regulates intramembranous ossification by modifying the TGFß and BMP2 signaling pathway.

SHP2 is a ubiquitously expressed protein tyrosine phosphatase, which is involved in many signaling pathways to regulate the skeletal development. In endochondral ossification, SHP2 is known to modify the osteogenic fate of osteochondroprogenitors and to impair the osteoblastic transdifferentiation of hypertrophic chondrocytes. However, how SHP2 regulates osteoblast differentiation in intramembranous ossification remains incompletely understood. To address this question, we generated a mouse model to ablate SHP2 in the Prrx1-expressing mesenchymal progenitors by using "Cre-loxP"-mediated gene excision and examined the development of calvarial bone, in which the main process of bone formation is intramembranous ossification. Phenotypic characterization showed that SHP2 mutants have severe defects in calvarial bone formation. Cell lineage tracing and in situ hybridization data showed less osteoblast differentiation of mesenchymal cells and reduced osteogenic genes expression, respectively. Further mechanistic studies revealed enhanced TGFß and suppressed BMP2 signaling in SHP2 ablated mesenchymal progenitors and their derivatives. Our study uncovered the critical role of SHP2 in osteoblast differentiation through intramembranous ossification and might provide a potential target to treat craniofacial skeleton disorders.

SHP2 Regulates the Osteogenic Fate of Growth Plate Hypertrophic Chondrocytes.

Transdifferentiation of hypertrophic chondrocytes into bone-forming osteoblasts has been reported, yet the underlying molecular mechanism remains incompletely understood. SHP2 is an ubiquitously expressed cytoplasmic protein tyrosine phosphatase. SHP2 loss-of-function mutations in chondroid cells are linked to metachondromatosis in humans and mice, suggesting a crucial role for SHP2 in the skeleton. However, the specific role of SHP2 in skeletal cells has not been elucidated. To approach this question, we ablated SHP2 in collagen 2α1(Col2α1)-Cre- and collagen 10α1(Col10α1)-Cre-expressing cells, predominantly proliferating and hypertrophic chondrocytes, using "Cre-loxP"-mediated gene excision. Mice lacking SHP2 in Col2α1-Cre-expressing cells die at mid-gestation. Postnatal SHP2 ablation in the same cell population caused dwarfism, chondrodysplasia and exostoses. In contrast, mice in which SHP2 was ablated in the Col10α1-Cre-expressing cells appeared normal but were osteopenic. Further mechanistic studies revealed that SHP2 exerted its influence partly by regulating the abundance of SOX9 in chondrocytes. Elevated and sustained SOX9 in SHP2-deficient hypertrophic chondrocytes impaired their differentiation to osteoblasts and impaired endochondral ossification. Our study uncovered an important role of SHP2 in bone development and cartilage homeostasis by influencing the osteogenic differentiation of hypertrophic chondrocytes and provided insight into the pathogenesis and potential treatment of skeletal diseases, such as osteopenia and osteoporosis.

SHP2 regulates osteoclastogenesis by promoting preosteoclast fusion.

Genes that regulate osteoclast (OC) development and function in both physiologic and disease conditions remain incompletely understood. Shp2 (the Src homology-2 domain containing protein tyrosine phosphatase 2), a ubiquitously expressed cytoplasmic protein tyrosine phosphatase, is implicated in regulating M-CSF and receptor activator of nuclear factor-κB ligand (RANKL)-evoked signaling; its role in osteoclastogenesis and bone homeostasis, however, remains unknown. Using a tissue-specific gene knockout approach, we inactivated Shp2 expression in murine OCs. Shp2 mutant mice are phenotypically osteopetrotic, featuring a marked increase of bone volume (BV)/total volume (TV) (+42.8%), trabeculae number (Tb.N) (+84.1%), structure model index (+119%), and a decrease of trabecular thickness (Tb.Th) (-34.1%) and trabecular spacing (Tb.Sp) (-41.0%). Biochemical analyses demonstrate that Shp2 is required for RANKL-induced formation of giant multinucleated OCs by up-regulating the expression of nuclear factor of activated T cells, cytoplasmic 1 (Nfatc1), a master transcription factor that is indispensable for terminal OC differentiation. Shp2 deletion, however, has minimal effect on M-CSF-dependent survival and proliferation of OC precursors. Instead, its deficiency aborts the fusion of OC precursors and formation of multinucleated OCs and decreases bone matrix resorption. Moreover, pharmacological intervention of Shp2 is sufficient to prevent preosteoclast fusion in vitro. These findings uncover a novel mechanism through which Shp2 regulates osteoclastogenesis by promoting preosteoclast fusion. Shp2 or its signaling partners could potentially serve as pharmacological targets to regulate the population of OCs locally and/or systematically, and thus treat OC-related diseases, such as periprosthetic osteolysis and osteoporosis.

In Vivo kinematics of the trapeziometacarpal joint during thumb extension-flexion and abduction-adduction.

PURPOSE: The primary aim of this study was to determine whether the in vivo kinematics of the trapeziometacarpal (TMC) joint differ as a function of age and sex during thumb extension-flexion (Ex-Fl) and abduction-adduction (Ab-Ad) motions. METHODS: The hands and wrists of 44 subjects (10 men and 11 women with ages 18-35 y and 10 men and 13 women with ages 40-75 y) with no symptoms or signs of TMC joint pathology were imaged with computed tomography during thumb extension, flexion, abduction, and adduction. The kinematics of the TMC joint were computed and compared across direction, age, and sex. RESULTS: We found no significant effects of age or sex, after normalizing for size, in any of the kinematic parameters. The Ex-Fl and Ab-Ad rotation axes did not intersect, and both were oriented obliquely to the saddle-shaped anatomy of the TMC articulation. The Ex-Fl axis was located in the trapezium and the Ab-Ad axis was located in the metacarpal. Metacarpal translation and internal rotation occurred primarily during Ex-Fl. CONCLUSIONS: Our findings indicate that normal TMC joint kinematics are similar in males and females, regardless of age, and that the primary rotation axes are nonorthogonal and nonintersecting. In contrast to previous studies, we found Ex-Fl and Ab-Ad to be coupled with internal-external rotation and translation. Specifically, internal rotation and ulnar translation were coupled with flexion, indicating a potential stabilizing screw-home mechanism. CLINICAL RELEVANCE: The treatment of TMC pathology and arthroplasty design require a detailed and accurate understanding of TMC function. This study confirms the complexity of TMC kinematics and describes metacarpal translation coupled with internal rotation during Ex-Fl, which may explain some of the limitations of current treatment strategies and should help improve implant designs.

Ptpn11 deletion in a novel progenitor causes metachondromatosis by inducing hedgehog signalling.

The tyrosine phosphatase SHP2, encoded by PTPN11, is required for the survival, proliferation and differentiation of various cell types. Germline activating mutations in PTPN11 cause Noonan syndrome, whereas somatic PTPN11 mutations cause childhood myeloproliferative disease and contribute to some solid tumours. Recently, heterozygous inactivating mutations in PTPN11 were found in metachondromatosis, a rare inherited disorder featuring multiple exostoses, enchondromas, joint destruction and bony deformities. The detailed pathogenesis of this disorder has remained unclear. Here we use a conditional knockout (floxed) Ptpn11 allele (Ptpn11(fl)) and Cre recombinase transgenic mice to delete Ptpn11 specifically in monocytes, macrophages and osteoclasts (lysozyme M-Cre; LysMCre) or in cathepsin K (Ctsk)-expressing cells, previously thought to be osteoclasts. LysMCre;Ptpn11(fl/fl) mice had mild osteopetrosis. Notably, however, CtskCre;Ptpn11(fl/fl) mice developed features very similar to metachondromatosis. Lineage tracing revealed a novel population of CtskCre-expressing cells in the perichondrial groove of Ranvier that display markers and functional properties consistent with mesenchymal progenitors. Chondroid neoplasms arise from these cells and show decreased extracellular signal-regulated kinase (ERK) pathway activation, increased Indian hedgehog (Ihh) and parathyroid hormone-related protein (Pthrp, also known as Pthlh) expression and excessive proliferation. Shp2-deficient chondroprogenitors had decreased fibroblast growth factor-evoked ERK activation and enhanced Ihh and Pthrp expression, whereas fibroblast growth factor receptor (FGFR) or mitogen-activated protein kinase kinase (MEK) inhibitor treatment of chondroid cells increased Ihh and Pthrp expression. Importantly, smoothened inhibitor treatment ameliorated metachondromatosis features in CtskCre;Ptpn11(fl/fl) mice. Thus, in contrast to its pro-oncogenic role in haematopoietic and epithelial cells, Ptpn11 is a tumour suppressor in cartilage, acting through a FGFR/MEK/ERK-dependent pathway in a novel progenitor cell population to prevent excessive Ihh production.

Locking buttons increase fatigue life of locking plates in a segmental bone defect model.

BACKGROUND: Durability of plate fixation is important in delayed union. Although locking plates result in stronger constructs, it is not known if locking affects the fatigue life of a plate. Two locking screws on either side of the nonunion could decrease working length and increase strain in the plate. However, the reinforcing effect of the locking head on the plate may compensate, so that it is unclear whether locking reduces fatigue life. QUESTIONS/PURPOSES: We determined whether locking screws, compression screws, and locking buttons reduce or increase the fatigue life of a plate. METHODS: We tested fatigue life of four constructs using an eight-hole locking plate in a segmental defect model: (1) all locking screws (Locked; n = 5); (2) all compression screws (Unlocked; n = 5); (3) six compression screws with two locking buttons in the central holes (Button; n = 6); and (4) six compression screws with two open central holes (Open; n = 6). RESULTS: The Button group had the longest fatigue life (1.3 million cycles). There was no difference between the Locked and Unlocked groups. All of the constructs failed by fracture of the plates through a screw hole adjacent to the defect. CONCLUSIONS: Locking screws did not improve fatigue life, however a locking button increased the fatigue life of a locking plate in a segmental bone defect model. CLINICAL RELEVANCE: Locking buttons in holes adjacent to a defect may improve durability, which is important when delayed union is a possibility.

In vivo kinematics of the scaphoid, lunate, capitate, and third metacarpal in extreme wrist flexion and extension.

PURPOSE: Insights into the complexity of active in vivo carpal motion have recently been gained using 3-dimensional imaging; however, kinematics during extremes of motion has not been elucidated. The purpose of this study was to determine motion of the carpus during extremes of wrist flexion and extension. METHODS: We obtained computed tomography scans of 12 healthy wrists in neutral grip, extreme loaded flexion, and extreme loaded extension. We obtained 3-dimensional bone surfaces and 6-degree-of-freedom kinematics for the radius and carpals. The flexion and extension rotation from neutral grip to extreme flexion and extreme extension of the scaphoid and lunate was expressed as a percentage of capitate flexion and extension and then compared with previous studies of active wrist flexion and extension. We also tested the hypothesis that the capitate and third metacarpal function as a single rigid body. Finally, we used joint space metrics at the radiocarpal and midcarpal joints to describe arthrokinematics. RESULTS: In extreme flexion, the scaphoid and lunate flexed 70% and 46% of the amount the capitate flexed, respectively. In extreme extension, the scaphoid extended 74% and the lunate extended 42% of the amount the capitates extended, respectively. The third metacarpal extended 4° farther than the capitate in extreme extension. The joint contact area decreased at the radiocarpal joint during extreme flexion. The radioscaphoid joint contact center moved onto the radial styloid and volar ridge of the radius in extreme flexion from a more proximal and ulnar location in neutral. CONCLUSIONS: The contributions of the scaphoid and lunate to capitate rotation were approximately 25% less in extreme extension compared with wrist motion through an active range of motion. More than half the motion of the carpus when the wrist was loaded in extension occurred at the midcarpal joint. CLINICAL RELEVANCE: These findings highlight the difference in kinematics of the carpus at the extremes of wrist motion, which occur during activities and injuries, and give insight into the possible etiologies of the scaphoid fractures, interosseous ligament injuries, and carpometacarpal bossing.

Elongation of the dorsal carpal ligaments: a computational study of in vivo carpal kinematics.

PURPOSE: The dorsal radiocarpal (DRC) and dorsal intercarpal (DIC) ligaments play an important role in scapholunate and lunotriquetral stability. The purpose of this study was to compute changes in ligament elongation as a function of wrist position for the DRC and the scaphoid and trapezoidal insertions of the DIC. METHODS: We developed a computational model that incorporated a digital dataset of ligament origin and insertions, bone surface models, and in vivo 3-dimensional kinematics (n = 28 wrists), as well as an algorithm for computing ligament fiber path. RESULTS: The differences between the maximum length and minimum length of the DRC, DIC scaphoid component, and DIC trapezoidal component over the entire range of motion were 5.1 ± 1.5 mm, 2.7 ± 1.5 mm, and 5.9 ± 2.5 mm, respectively. The DRC elongated as the wrist moved from ulnar extension to radial flexion, and the DIC elongated as the wrist moved from radial deviation to ulnar deviation. CONCLUSIONS: The DRC and DIC lengthened in opposing directions during wrist ulnar and radial deviation. Despite complex carpal bone anatomy and kinematics, computed fiber elongations were found to vary linearly with wrist position. Errors between computed values and model predictions were less than 2.0 mm across all subjects and positions. CLINICAL RELEVANCE: The relationships between ligament elongation and wrist position should further our understanding of ligament function, provide insight into the potential effects of dorsal wrist incisions on specific wrist ranges of motion, and serve as a basis for modeling of the wrist.

Carpal and forearm kinematics during a simulated hammering task.

PURPOSE: Hammering is a functional task in which the wrist generally follows a path of motion from a position of combined radial deviation and extension to combined ulnar deviation and flexion, colloquially referred to as a dart thrower's motion. The purpose of this study was to measure wrist and forearm motion and scaphoid and lunate kinematics during a simulated hammering task. We hypothesized that the wrist follows an oblique path from radial extension to ulnar flexion and that there would be minimal radiocarpal motion during the hammering task. METHODS: Thirteen healthy volunteers consented to have their wrist and distal forearm imaged with computed tomography at 5 positions while performing a simulated hammering task. The kinematics of the carpus and distal radioulnar joint were calculated using established markerless bone registration methods. The path of wrist motion was described relative to the sagittal plane. Forearm rotation and radioscaphoid and radiolunate motion were computed as a function of wrist position. RESULTS: All volunteers performed the simulated hammering task using a path of wrist motion from radial extension to ulnar flexion that was oriented an average of 41 degrees +/- 3 degrees from the sagittal plane. These paths did not pass through the anatomic neutral wrist position; rather, they passed through a neutral hammering position, which was offset by 36 degrees +/- 8 degrees in extension. Rotations of the scaphoid and lunate were not minimal but averaged 40% and 41%, respectively, of total wrist motion. The range of forearm pronation-supination during the task averaged 12 degrees +/- 8 degrees . CONCLUSIONS: The simulated hammering task was performed using a wrist motion that followed a coupled path of motion, from extension and radial deviation to flexion and ulnar deviation. Scaphoid and lunate rotations were greatly reduced, but not minimized, compared with rotations during pure wrist flexion/extension. This is likely because an extended wrist position was maintained throughout the entire task studied.

Conformational changes in the carpus during finger trap distraction.

PURPOSE: Wrist distraction is a common treatment maneuver used clinically for the reduction of distal radial fractures and midcarpal dislocations. Wrist distraction is also required during wrist arthroscopy to access the radiocarpal joint and has been used as a test for scapholunate ligament injury. However, the effect of a distraction load on the normal wrist has not been well studied. The purpose of this study was to measure the three-dimensional conformational changes of the carpal bones in the normal wrist as a result of a static distractive load. METHODS: Using computed tomography, the dominant wrists of 14 healthy volunteers were scanned at rest and during application of 98 N of distraction. Load was applied using finger traps, and volunteers were encouraged to relax their forearm muscles and to allow distraction of the wrist. The motions of the bones in the wrist were tracked between the unloaded and loaded trial using markerless bone registration. The average displacement vector of each bone relative to the radius was calculated, as were the interbone distances for 20 bone-bone interactions. Joint separation was estimated at the radiocarpal, midcarpal, and carpometacarpal joints in the direction of loading using the radius, lunate, capitate, and third metacarpal. RESULTS: With loading, the distance between the radius and third metacarpal increased an average of 3.3 mm +/- 3.1 in the direction of loading. This separation was primarily in the axial direction at the radiocarpal (1.0 mm +/- 1.0) and midcarpal (2.0 mm +/- 1.7) joints. There were minimal changes in the transverse direction within the distal row, although the proximal row narrowed by 0.98 mm +/- 0.7. Distraction between the radius and scaphoid (2.5 mm +/- 2.2) was 2.4 times greater than that between the radius and lunate (1.0 mm +/- 1.0). CONCLUSIONS: Carpal distraction has a significant (p < .01) effect on the conformation of the carpus, especially at the radiocarpal and midcarpal joints. In the normal wrist, external traction causes twice as much distraction at the lunocapitate joint than at the radiolunate joint.

An improved method for cable grip fixation of the greater trochanter after trochanteric slide osteotomy.

This study proposes a novel method for reattachment of the trochanteric slide osteotomy. The strength of this new fixation system was compared to established configurations. Fifteen sawbone femurs were used. Our configuration used cables above and below the lesser trochanter with a third cable around the shaft of the femur while passing the loose ends through the inferior hole of the cable grip. Displacement of the trochanter was measured with increasing load. Force required for catastrophic failure was also measured. The 3-cable construct resulted in significantly less displacement with increasing load and required a larger force to cause failure (1 cm and 2 cm). We theorize that our configuration produces a biomechanically stronger construct than previously used methods.

Recombinant human platelet-derived growth factor-BB augmentation of new-bone formation in a rat model of distraction osteogenesis.

BACKGROUND: Distraction osteogenesis creates a challenging bone-healing environment with protracted demand for cells of the osteoblast lineage. Platelet-derived growth factor-BB (PDGF-BB) is an osteoblast mitogen and chemotaxin that has been shown to accelerate and/or enhance bone-healing in several preclinical studies. The purpose of the present study was to determine whether recombinant human platelet-derived growth factor-BB (rhPDGF-BB) would have a similar effect on regenerate healing after distraction osteogenesis. METHODS: Unilateral 7-mm mid-diaphyseal femoral lengthening procedures were performed in eighty-three male Sprague-Dawley rats that were separated into five experimental groups. During the distraction period (Days 7 to 28), each animal received a weekly 50-microL injection of either sodium acetate buffer, bovine collagen dissolved in sodium acetate buffer, or one of three concentrations of rhPDGF-BB (100, 300, or 1000 microg/mL) into the distraction site. Animals from each group were killed on Days 35, 42, 49, 56, and 63. Healing was assessed with biweekly serial radiographs, micro-computed tomography of the explanted bones, and histologic analysis. RESULTS: rhPDGF-BB treatment significantly increased new-bone formation at the midconsolidation time points (Days 42, 49, and 56) as well as the union rate. On Day 49 regenerate bone volume was significantly greater in each of the three rhPDGF-BB-treated groups than in the controls (p < 0.05, p = 0.0002, and p < 0.05 for the 100, 300, and 1000 microg/mL rhPDGF-BB groups, respectively), whereas on Day 42 regenerate bone volume was significantly greater in the 300 and 1000 microg/mL rhPDGF-BB groups than in the controls (p = 0.0002 and p < 0.05, respectively) and on Day 56 regenerate bone volume was significantly greater in the 100 and 300 microg/mL rhPDGF-BB groups than in the controls (p < 0.05 and p < 0.0001, respectively). The overall union rate was 40.4% (nineteen of forty-seven) in the rhPDGF-BB-treated animals, compared with 4.5% (one of twenty-two) in the controls (p = 0.01). The radiographic and histologic results were consistent with new-bone formation as quantified by micro-computed tomography, although they were less definitive. CONCLUSIONS: The administration of exogenous rhPDGF-BB into the distraction site during diaphyseal distraction enhanced bone-healing in a rat model of distraction osteogenesis as evidenced by both increased regenerate new-bone formation and a higher union rate.

Interfragmentary motion in patients with scaphoid nonunion.

PURPOSE: Scaphoid nonunions are a common complication of scaphoid fractures and frequently progress to degenerative arthritis. This study evaluated the effect of scaphoid nonunion on the in vivo kinematics of the radioscaphocapitate articulation. METHODS: Computed tomography with a markerless registration technique was used to quantify motion of the scaphoid, lunate, and capitate in vivo, in 6 patients with unilateral scaphoid nonunion. The 3-dimensional helical axis of motion rotations of each bone were measured as a function of wrist flexion-extension and compared with those of the uninjured contralateral wrist. Mixed linear modeling was used to compare flexion-extension of the injured scaphoid fragments with those of the uninjured scaphoid, and the lunate of the injured wrist with the lunate of the uninjured wrist. Interfragmentary motion in the injured scaphoid was assessed by calculating rotation of the distal fragment relative to the proximal fragment, as well as the linear displacement between the 2 fragments at the fracture site. RESULTS: Flexion and extension of the distal scaphoid fragment was similar to that of the uninjured scaphoid. Extension of the proximal fragment was significantly decreased by 38%, compared with the uninjured scaphoid. Similarly, extension of the lunate in the injured wrist was significantly decreased, by 40%. Interfragmentary rotation was 33% of wrist motion in flexion and 35% of wrist motion in extension. Maximum interfragmentary displacement was on the order of 1 mm. CONCLUSIONS: Scaphoid nonunions have a dramatic impact on carpal kinematics, partially uncoupling the proximal and distal carpal rows. Although the results of this in vivo study differ from past in vitro studies, the increase in lunocapitate motion we identified is consistent with the current theory that the scaphoid acts as a fundamental link between the proximal and distal carpal rows.