Study Design: This is a retrospective study. Objective: The objective of this study was to evaluate lumbar spine synovial cyst recurrence rates of decompression-alone versus decompression/fusion procedures. Background: Improvements in imaging modalities allow for increased diagnosis and surgical treatment of symptomatic spinal juxtafacet synovial cysts. Conservative management may be used as a first-line management strategy, however rarely provides durable, effective relief of symptoms. Surgical treatment of spinal synovial cysts ranges from decompression and cyst excision to decompression with fusion procedures. Decompression procedures alone have a higher risk of recurrence of spinal synovial cysts. Methods: We retrospectively reviewed 87 patients undergoing surgical treatment of lumbar spinal juxtafacet synovial cysts as a single institution over 20 years. Surgical treatment consisted of either decompression versus decompression/fusion procedures. Preoperative symptoms included back pain, radiculopathy, motor deficits, or sensory deficits. The incidence of recurrence of spinal synovial cysts at the same-site or differing sites was compared between 2 categories of surgical treatment. Revision surgical procedure rates were also evaluated. Results: A total of 55 (63%) patients were treated with an index decompression-only procedure for the lumbar spinal synovial cyst compared with 32 (37%) patients treated with an index decompression and fusion procedure. Fifty-eight (68%) of the lumbar spinal cysts occurred at the L4–L5 level. There were 10 (11.5%) spinal synovial cyst recurrences in the decompression-only group, and 0 recurrences in the decompression/fusion group. Revision decompression procedures were performed in 4 of the 10 (4.6%) recurrences, and 6 of 10 (6.9%) recurrences had subsequent decompression and fusion surgery. The mean time to recurrence was 23.9±17.3 months. The mean length of follow-up was 65.1±48.6 months. Both recurrence and nonrecurrence cohorts had significant symptomatic improvement using Odom criteria. Conclusions: Decompression and cyst excision was the more common surgical treatment of lumbar spinal synovial cysts compared with decompression/fusion procedure in our study. The rate of synovial cyst recurrence and revision surgery in patients undergoing index decompression was relatively low and comparable to current literature. Symptomatic improvement of patients undergoing decompression versus decompression/fusion was similar in our study. Although the fusion may be required for the extent of pathology or coexisting instability, decompression and excision of spinal synovial cysts provide durable, effective treatment with a known, appropriate risk of recurrence and subsequent revision surgery.
Gut microbial metabolites are increasingly recognized as determinants of health and disease. However, whether host–microbe crosstalk influences peripheral arteries is not understood. Neointimal hyperplasia, a proliferative and inflammatory response to arterial injury, frequently limits the long‐term benefits of cardiovascular interventions such as angioplasty, stenting, and bypass surgery. Our goal is to assess the effect of butyrate, one of the principal short chain fatty acids produced by microbial fermentation of dietary fiber, on neointimal hyperplasia development after angioplasty. Treatment of male Lewis Inbred rats with oral vancomycin for 4 weeks changed the composition of gut microbes as assessed by 16S rRNA‐based taxonomic profiling and decreased the concentration of circulating butyrate by 69%. In addition, rats treated with oral vancomycin had exacerbated neointimal hyperplasia development after carotid angioplasty. Oral supplementation of butyrate reversed these changes. Butyrate also inhibited vascular smooth muscle cell proliferation, migration, and cell cycle progression in a dose‐dependent manner in vitro. Our results suggest for the first time that gut microbial composition is associated with the severity of arterial remodeling after injury, potentially through an inhibitory effect of butyrate on VSMC.
BackgroundThe microbiome has a functional role in a number of inflammatory processes and disease states. While neointimal hyperplasia development has been linked to inflammation, a direct role of the microbiota in neointimal hyperplasia has not yet been established. Germ-free (GF) mice are an invaluable model for studying causative links between commensal organisms and the host. We hypothesized that GF mice would exhibit altered neointimal hyperplasia following carotid ligation compared to conventionally raised (CONV-R) mice.MethodsTwenty-week-old male C57BL/6 GF mice underwent left carotid ligation under sterile conditions. Maintenance of sterility was assessed by cultivation and 16S rRNA qPCR of stool. Neointimal hyperplasia was assessed by morphometric and histologic analysis of arterial sections after 28 days. Local arterial cell proliferation and inflammation was assessed by immunofluorescence for Ki67 and inflammatory cell markers at five days. Systemic inflammation was assessed by multiplex immunoassays of serum. CONV-R mice treated in the same manner served as the control cohort. GF and CONV-R mice were compared using standard statistical methods.ResultsAll GF mice remained sterile during the entire study period. Twenty-eight days after carotid ligation, CONV-R mice had significantly more neointimal hyperplasia development compared to GF mice, as assessed by intima area, media area, intima+media area, and intima area/(intima+media) area. The collagen content of the neointimal lesions appeared qualitatively similar on Masson’s trichrome staining. There was significantly reduced Ki67 immunoreactivity in the media and adventitia of GF carotid arteries 5 days after ligation. GF mice also had increased arterial infiltration of anti-inflammatory M2 macrophages compared to CONV-R mouse arteries and a reduced proportion of mature neutrophils. GF mice had significantly reduced serum IFN-γ-inducible protein (IP)-10 and MIP-2 5 days after carotid ligation, suggesting a reduced systemic inflammatory response.ConclusionsGF mice have attenuated neointimal hyperplasia development compared to CONV-R mice, which is likely related to altered kinetics of wound healing and acute inflammation. Recognizing the role of commensals in the regulation of arterial remodeling will provide a deeper understanding of the pathophysiology of restenosis and support strategies to treat or reduce restenosis risk by manipulating microbiota.
Background The potential role of the gut microbiome in cardiovascular diseases is increasingly evident. Arterial restenosis attributable to neointimal hyperplasia after cardiovascular procedures such as balloon angioplasty, stenting, and bypass surgery is a common cause of treatment failure, yet whether gut microbiota participate in the development of neointimal hyperplasia remains largely unknown. Methods and Results We performed fecal microbial transplantation from conventionally raised male C57BL/6 mice to age‐, sex‐, and strain‐matched germ‐free mice. Five weeks after inoculation, all mice underwent unilateral carotid ligation. Neointimal hyperplasia development was quantified after 4 weeks. Conventionally raised and germ‐free cohorts served as comparison groups. Conclusions Germ‐free mice have significantly attenuated neointimal hyperplasia development compared with conventionally raised mice. The arterial remodeling response is restored by fecal transplantation. Our results describe a causative role of gut microbiota in contributing to the pathogenesis of neointimal hyperplasia.
Background: Pelvic ring injury outcome studies rely on radiographic assessment. To date, no study investigates the accuracy of radiographic measurement. The aim of this study was to assess the accuracy and interobserver reliability of pelvic ring displacement measurement in an injury model. We hypothesize that current radiographic measurement methods do not accurately quantify the three-dimensional pelvic ring displacement. Methods: Ten orthopaedic traumatologists evaluated 12 pelvic ring injury model displacements using AP, inlet, and outlet radiographs and axial CT images. Observers completed a survey of demographic and treatment approach strategies. Radiographic displacement measurements in axial, coronal, and sagittal planes were analyzed for accuracy using. Absolute displacement measurements were categorized with Matta and Tornetta grading system for Fleiss Kappa inter-reliability correlation evaluation. Results: The mean age of orthopaedic traumatologists was 47.5 years (range 36 to 59) with a mean 15.3 years (range 4 to 27) of pelvic fracture surgery experience. Radiographic measurement of isolated uniplanar of pelvic displacement in axial, sagittal, or coronal plane alone was more accurate than multiplanar pelvic displacements with more than one plane of displacement, 6.6 6 5.7 mm error compared with 9.6 6 6.3 mm error, respectively (P = 0.0035). Measurement accuracy was greater with isolated coronal plane (4 6 3.5 mm error) compared with isolated axial plane (9.9 6 7.1 mm error) or isolated sagittal plane displacement (6.7 6 4 mm error). Interrater reliability for the radiographic displacement measurement by observers showed an overall poor agreement with 0.24. Conclusion: Radiographic displacement measurement in these modeled pelvic ring injuries has notable inaccuracy among various measurement methods. Coronal and sagittal plane radiographic displacement measurements are more accurate compared with axial
angiotensin II, underwent treatment with losartan through an osmotic minipump (30 mg/kg/d  21 days; n ¼ 3-5 per group) with or without induction of AAA by the validated periadventitial calcium chloride model. Systolic blood pressure (SBP) was recorded weekly by tail cuff method and compared with normotensive control BPN/3J mice. At terminal procedure, mice underwent aortic diameter (AoD) measurement by digital microscopy. Changes in blood pressure and AoD were computed as a percentage change from baseline, analyzed by analysis of variance, and are presented as mean 6 standard error of the mean .Results: Before intervention, all BPH/2J mice displayed elevated SBP compared with normotensive BPN/3J mice (180 6 6 mm Hg vs 145 6 4 mm Hg; P < .05). However, BPH/2J mice subsequently undergoing losartan pump implantation showed a significant reduction in SBP by day 7 (153 6 2 mm Hg vs 172 6 3 mm Hg in BPH/2J; P < .05), and this was maintained through day 21 (157 6 4 mm Hg vs 170 6 3 mmHg in BPH/2J; P < .05). As expected, the induction of AAA had no effect on SBP but resulted in significantly increased AoD (69.4% 6 5.2%; P < .05). In BPH/2J mice undergoing AAA induction, concomitant losartan therapy reduced SBP at 7 days (141 6 4 mm Hg vs 181 6 4 mm Hg at baseline; P < .05), and this effect was maintained through day 21. Interestingly, AAA dilation was significantly attenuated in this group (19.73% 6 4.2%; P < .05 vs BPH/2J + AAA).Conclusions: Under conditions of non-angiotensin II-dependent hypertension, losartan maintained antihypertensive efficacy and abrogated AAA growth, suggesting a role for mechanical AT1R activation in aneurysm development. Given the pharmacotherapeutic implications of this association, further investigation into the underlying mechanism linking AT1R and AAA growth is warranted.
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