Obtaining Correct Ankle Alignment Using Intraoperative External Fixation for Ankle Arthrodesis.

Ankle arthrodesis remains an important treatment option for patients with ankle arthritis. Many methods have been described; however, no consensus has been reached regarding the best technique to achieve both successful fusion and a good position for optimal foot mechanics. Furthermore, as arthroplasty has become more popular, preservation of the fibula to allow for future arthroplasty has become critical. The present report describes an innovative technique in which temporary external fixation at operative fixation is used, along with internal fixation, to achieve both an optimal foot position and high fusion rates, while maintaining the integrity of the fibula. Seventeen patients were identified who met the criteria for inclusion. Their medical records, including pre- and postoperative radiographs, were reviewed retrospectively. Preoperative and postoperative coronal and sagittal alignment was determined. All patients achieved successful fusion, although 1 (5.9%) patient experienced delayed union. The average tibial/talar ratio preoperatively was 21% (range 8% to 33%), demonstrating anterior subluxation. Postoperatively, this ratio improved to 33% (range 26% to 40%), approximating the normal anatomic ratio. Of the 17 patients, 5 (29.4%) had preoperative varus or valgus alignment of the talas >5°. All 5 cases were successfully corrected to within 2° of normal anatomic alignment. This technique allows the surgeon to achieve good visualization of the joint for preparation and to obtain the optimal position of the foot at arthrodesis without compromising the lateral column significance of the fibula. All patients obtained fusion, and minimal complications were associated with the use of this technique.

Inter- and intra-rater reliability of patellofemoral kinematic and contact area quantification by fast spin echo MRI and correlation with cartilage health by quantitative T1ρ MRI.

BACKGROUND: Patellar maltracking is a leading cause of patellofemoral pain syndrome (PFPS). The aim of this study was to determine the inter- and intra-rater reliability of a semi-automated program for magnetic resonance imaging (MRI) based patellofemoral kinematics. METHODS: Sixteen subjects (10 with PFPS [mean age 32.3; SD 5.2; eight females] and six controls without PFPS 19 [mean age 28.6; SD 2.8; three females]) participated in the study. One set of T2-weighted, fat-saturated fast spin-echo (FSE) MRIs were acquired from each subject in full extension and 30° of knee flexion. MRI including axial T1ρ relaxation time mapping sequences was also performed on each knee. Following image acquisitions, regions of interest for kinematic MRI, and patellar and trochlear cartilage were segmented and quantified with in-house designed spline- based MATLAB semi-automated software. RESULTS: Intraclass Correlations Coefficients (ICC) of calculated kinematic parameters were good to excellent, ICC > 0.8 in patellar flexion, rotation, tilt, and translation (anterior -posterior, medial -lateral, and superior -inferior), and contact area translation. Only patellar tilt in the flexed position and motion from extended to flexed state was significantly different between PFPS and control patients (p=0.002 and p=0.006, respectively). No significant correlations were identified between patellofemoral kinematics and contact area with T1ρ relaxation times. CONCLUSIONS: A semi-automated, spline-based kinematic MRI technique for patellofemoral kinematic and contact area quantification is highly reproducible with the potential to help better understand the role of patellofemoral maltracking in PFPS and other knee disorders. LEVEL OF EVIDENCE: Level IV.

Revision surgery for lumbar pseudarthrosis.

BACKGROUND CONTEXT: Revision surgery for pseudarthrosis after a lumbar spinal fusion has unpredictable functional results. PURPOSE: The aim of this study was to determine the clinical outcomes of revision surgery to fuse the pseudarthrosis site based on the two most common diagnoses (degenerative disc disease [DDD] vs. spondylolisthesis). STUDY DESIGN: Patients who had a revision surgery between 1995 and 2004 for lumbar pseudarthrosis after short segment lumbar spinal fusion were identified through the institution's Spine Center surgery database. A retrospective chart review of clinical, hospital, and anesthesia records was then performed. PATIENT SAMPLE: Sixty-six patients were included in the study (28 patients with DDD and 38 patients with spondylolisthesis). Inclusion criteria were a surgical diagnosis of pseudarthrosis with a prior fusion of one or two motion segments, minimum 24 months of follow-up, and a diagnosis of either symptomatic DDD or spondylolisthesis as the primary indication for the index fusion surgery. OUTCOME MEASURES: The Oswestry disability index (ODI) and a self-assessment questionnaire were used to evaluate clinical outcomes. METHODS: A retrospective chart and radiographic review was performed. Statistical analysis was done using Student t test for ODI scores and chi-square test for discrete variables from the outcome questionnaires. RESULTS: Follow-up radiographs were available for 64 patients (97%), and a fusion rate of 100% was found in both groups for the radiographs examined. The mean postoperative ODI score was 53.3 (30-84.4) for DDD patients and 37.2 (2.5-76) for the spondylolisthesis group (p<.01). Only 50% of the patients in the DDD group felt that their overall well-being had improved since the surgery. In the spondylolisthesis group, 64% of patients stated that their overall well-being had improved since their revision surgery. CONCLUSIONS: The clinical outcomes after revision surgery for pseudarthrosis are worse in patients with DDD compared with spondylolisthesis despite successful repair of nonunion. Risks and benefits should be well discussed with the patients before deciding on surgical treatment for the management of pseudarthrosis, especially in patients with previous short-segment fusions done for DDD.

T1ρ imaging demonstrates early changes in the lateral patella in patients with patellofemoral pain and maltracking.

BACKGROUND: Patellofemoral pain (PFP) is a common condition and often presents without evidence of arthritis on radiographs. Magnetic resonance imaging (MRI) has shown good correlation between T1ρ and T2 relaxation times and changes in the cartilage matrix, but as of yet, there are limited data in the literature utilizing these modalities to evaluate the patellofemoral joint. HYPOTHESIS: Patients with PFP and patellar tilt will show longer T1ρ relaxation times in the lateral facets of their patella but no difference in T2 values. STUDY DESIGN: Cross-sectional study; Level of evidence, 3. METHODS: A total of 20 patients aged 18 to 45 years with anterior knee pain, patellar tilt, and no evidence of osteoarthritis were identified and consented to undergo MRI including axial T1ρ and T2 relaxation time mapping sequences. Knee cartilage was segmented on spoiled gradient recalled acquisition in steady state (SPGR) images using a spline-based algorithm. These results were then compared with those of 10 age-matched controls. RESULTS: The mean T1ρ values of the lateral facets were significantly elevated in patients with PFP compared with controls (46.33 ± 4.92 ms vs. 42.32 ± 3.67 ms, respectively; P = .031), while no significant difference was observed in the medial facets (42.20 ± 5.55 ms vs. 41.42 ± 4.09 ms, respectively; P = .69). Significantly higher mean T1ρ values were noted in the lateral facets of the patients with PFP (46.33 ms) compared with the medial facets (42.20 ms) (P = .0001), while no significant differences in T1ρ values were observed between the medial and lateral facets of the controls (P = .502). No significant differences were noted in T2 relaxation times. A high correlation was noted between the mean T1ρ values of the whole patella of patients with PFP and the degree of patellar tilt (r = 0.72). CONCLUSION: There were significantly higher T1ρ values in the lateral facets of patients with PFP and patellar tilt that were not seen in control patients. These higher values approach the numbers seen in patients with early osteoarthritis.

Chondrocyte-intrinsic Smad3 represses Runx2-inducible matrix metalloproteinase 13 expression to maintain articular cartilage and prevent osteoarthritis.

OBJECTIVE: To identify mechanisms by which Smad3 maintains articular cartilage and prevents osteoarthritis. METHODS: A combination of in vivo and in vitro approaches was used to test the hypothesis that Smad3 represses Runx2-inducible gene expression to prevent articular cartilage degeneration. Col2-Cre;Smad3(fl/fl) mice allowed study of the chondrocyte-intrinsic role of Smad3 independently of its role in the perichondrium or other tissues. Primary articular cartilage chondrocytes from Smad3(fl/fl) mice and ATDC5 chondroprogenitor cells were used to evaluate Smad3 and Runx2 regulation of matrix metalloproteinase 13 (MMP-13) messenger RNA (mRNA) and protein expression. RESULTS: Chondrocyte-specific reduction of Smad3 caused progressive articular cartilage degeneration due to imbalanced cartilage matrix synthesis and degradation. In addition to reduced type II collagen mRNA expression, articular cartilage from Col2-Cre;Smad3(fl/fl) mice was severely deficient in type II collagen and aggrecan protein due to excessive MMP-13-mediated proteolysis of these key cartilage matrix constituents. Normally, transforming growth factor ß (TGFß) signals through Smad3 to confer a rapid and dynamic repression of Runx2-inducible MMP-13 expression. However, we found that in the absence of Smad3, TGFß signals through p38 and Runx2 to induce MMP-13 expression. CONCLUSION: Our findings elucidate a mechanism by which Smad3 mutations in humans and mice cause cartilage degeneration and osteoarthritis. Specifically, Smad3 maintains the balance between cartilage matrix synthesis and degradation by inducing type II collagen expression and repressing Runx2-inducible MMP-13 expression. Selective activation of TGFß signaling through Smad3, rather than p38, may help to restore the balance between matrix synthesis and proteolysis that is lost in osteoarthritis.

ISSLS prize winner: repeated disc injury causes persistent inflammation.

STUDY DESIGN: An in vivo rat model of disc degeneration with emphasis on characterizing acute and chronic cytokine production. OBJECTIVE: To compare the morphologic and proinflammatory response between a single and triple-stab injury in attempts to establish mechanisms of chronic disc inflammation. SUMMARY OF BACKGROUND DATA: The features that distinguish physiologic (asymptomatic) from pathologic (symptomatic) degeneration are unclear. Epidemiologic evidence suggests that cumulative damage and elevated disc cytokine levels may be linked to increased low back pain rates. Although acute injury stimulates a healing response that includes transient cytokine production, repetitive damage may be necessary to trigger the persistent inflammation suspected to underlie chronic pain. METHODS: Tail discs were exposed surgically and stabbed with a number 11 blade. During the subsequent acute healing phase, triple-stab discs were percutaneously injured with a 23-gauge needle at day 3 and then again at day 6 after the initial blade incision. Cytokine (IL-1 beta, IL-6, IL-8, and TNF-alpha) production was quantified using enzyme linked immunosorbent assay, and, in addition to MAPK signaling pathways (phosphorylated forms of ERK, JNK, and p38), was localized by immunohistochemistry. Disc architecture was evaluated using histology. RESULTS: Both single-stab and triple-stab discs degenerated with time, yet degeneration was more severe with repeated injury where nuclear proteoglycan was replaced by disorganized collagen. Four days after single-stab, there was a transient peak in IL-1 beta and IL-8 production that was localized to the wound track and associated granulation tissue. By contrast, triple-stab induced an activated annular fibroblast phenotype (p38 positive) that caused a prolonged, diffuse inflammatory response with elevated levels of TNF-alpha, IL-1 beta, and IL-8 up to 28 days after injury. Disc inflammation was accompanied by reactive changes in the adjacent vertebral marrow spaces that was initially lytic at day 4, becoming sclerotic by day 56. CONCLUSION: Our results demonstrate that repeated injury during active healing leads to persistent inflammation and enhanced disc degeneration. These data support the premise that damage accumulation and its associated inflammation may distinguish pathologic from physiologic disc degeneration. In the future, this triple-stab model may be useful to evaluate the efficacy of anti-inflammatory low back pain treatments.