Greenness, air pollution, and mortality risk: A U.S. cohort study of cancer patients and survivors.

BACKGROUND: Several studies suggest that living in areas of high surrounding greenness may be associated with a lower cardiopulmonary mortality risk. However, associations of greenness with specific causes of death in cancer patients and survivors has not been examined and it is unknown whether this relationship is affected by area levels of fine particulate matter air pollution (PM2.5). This study evaluated associations between greenness and PM2.5 on causes of death in a large, U.S.-based cohort of cancer patients and survivors. METHODS: Surveillance, Epidemiology and End Results (SEER) data were used to generate a cohort of 5,529,005 cancer patients and survivors from 2000 to 2016. Census-tract Normalized Difference Vegetation Index (NDVI) during May-October from 2003 to 2016 was population-weighted to act as a county-level greenness measure. County-level PM2.5 exposure was estimated from annual concentrations averaged from 1999 to 2015. Cox Proportional Hazards models were used to estimate the association between greenness, PM2.5, and cause-specific mortality while controlling for age, sex, race, and other individual and county level variables. FINDINGS: An IQR increase in greenness was associated with a decrease in cancer mortality for cancer patients (Hazard ratio of 0.94, 95% CI: 0.93-0.95), but not for cardiopulmonary mortality (0.98, 95% CI: 0.96-1.00). Inversely, an increase in 10 µg/m3 PM2.5 was associated with increased cardiopulmonary mortality (1.24, 95% CI: 1.19-1.29), but not cancer mortality (0.99, 95% CI: 0.97-1.00). Hazard ratios were robust to inclusion of PM2.5 in models with greenness and vice versa. Although exposure estimates were constant over most stratifications, greenness seemed to benefit individuals diagnosed with high survivability cancers (0.92, 95% CI: 0.90-0.95) more than those with low survivability cancers (0.98. 95% CI: 0.96-0.99). INTERPRETATION: Higher levels of greenness are associated with lower cancer mortality in cancer patients. The evidence suggests minimal confounding between greenness and PM2.5 exposures and risk of mortality.

Fine Particulate Matter Air Pollution and Mortality Risk Among US Cancer Patients and Survivors.

Background: Exposure to fine particulate matter (PM2.5) air pollution has been linked to increased risk of mortality, especially cardiopulmonary and lung cancer mortality. It is unknown if cancer patients and survivors are especially vulnerable to PM2.5 air pollution exposure. This study evaluates PM2.5 exposure and risk for cancer and cardiopulmonary mortality in cohorts of US cancer patients and survivors. Methods: A primary cohort of 5 591 168 of cancer patients and a 5-year survivor cohort of 2 318 068 was constructed using Surveillance, Epidemiology, and End Results Program data from 2000 to 2016, linked with county-level estimates of long-term average concentrations of PM2.5. Cox proportional hazards models were used to estimate PM2.5-mortality hazard ratios controlling for age-sex-race combinations and individual and county-level covariables. Results: Of those who died, 26% died of noncancer causes, mostly from cardiopulmonary disease. Minimal PM2.5-mortality associations were observed for all-cause mortality (hazard ratio [HR] = 1.01, 95% confidence interval [CI] = 1.00 to 1.03) per 10 µg/m3 increase in PM2.5. Substantial adverse PM2.5-mortality associations were observed for cardiovascular (HR = 1.32, 95% CI = 1.26 to 1.39), chronic obstructive pulmonary disease (HR = 1.10, 95% CI = 1.01 to 1.20), influenza and pneumonia (HR = 1.55, 95% CI = 1.33 to 1.80), and cardiopulmonary mortality combined (HR = 1.25, 95% CI = 1.21 to 1.30). PM2.5-cardiopulmonary mortality hazard ratio was higher for cancer patients who received chemotherapy or radiation treatments. Conclusions: Air pollution is adversely associated with cardiopulmonary mortality for cancer patients and survivors, especially those who received chemotherapy or radiation treatment. Given ubiquitous and involuntary air pollution exposures and large numbers of cancer patients and survivors, these results are of substantial clinical and public health importance.

Shape of BMI-Mortality Risk Associations: Reverse Causality and Heterogeneity in a Representative Cohort of US Adults.

OBJECTIVE: This study examines BMI-mortality associations and evaluates strategies intended to limit reverse causality. Heterogeneity in BMI-mortality risk associations across subgroups and causes of death is explored. METHODS: A cohort of 654,382 adults from the US National Health Interview Survey was constructed. Associations between unit BMI levels and mortality were estimated using Cox proportional hazards models, including and excluding the first 5 years of follow-up, with and without controls for smoking or preexisting conditions, and including and excluding ever-smokers and individuals with preexisting conditions. Stratified analyses by individual characteristics were performed. RESULTS: Addressing reverse causality led to reduced risk of mortality among those with low BMI levels (<18 kg/m2 ). Excluding ever-smokers and individuals with preexisting conditions further led to increased risk among those with high BMI levels (between 33 kg/m2 and >40 kg/m2 ) and lowered the estimated nadir risk from 27 kg/m2 to 23 kg/m2 . After excluding ever-smokers and individuals with preexisting conditions, limiting the analysis to >5 years of follow-up produced no substantive changes. Heterogeneous results were observed across individual characteristics, particularly age and causes of death. CONCLUSIONS: The exclusion of smokers and individuals with preexisting conditions alters the BMI-mortality risk association and results in a somewhat lower range of BMI with minimum mortality risk.

Fine Particulate Matter Exposure and Cancer Incidence: Analysis of SEER Cancer Registry Data from 1992-2016.

BACKGROUND: Previous research has identified an association between fine particulate matter (PM2.5) air pollution and lung cancer. Most of the evidence for this association, however, is based on research using lung cancer mortality, not incidence. Research that examines potential associations between PM2.5 and incidence of non-lung cancers is limited. OBJECTIVES: The primary purpose of this study was to evaluate the association between the incidence of cancer and exposure to PM2.5 using >8.5 million cases of cancer incidences from U.S. registries. Secondary objectives include evaluating the sensitivity of the associations to model selection, spatial control, and latency period as well as estimating the exposure-response relationship for several cancer types. METHODS: Surveillance, Epidemiology, and End Results (SEER) program data were used to calculate incidence rates for various cancer types in 607 U.S. counties. County-level PM2.5 concentrations were estimated using integrated empirical geographic regression models. Flexible semi-nonparametric regression models were used to estimate associations between PM2.5 and cancer incidence for selected cancers while controlling for important county-level covariates. Primary time-independent models using average incidence rates from 1992-2016 and average PM2.5 from 1988-2015 were estimated. In addition, time-varying models using annual incidence rates from 2002-2011 and lagged moving averages of annual estimates for PM2.5 were also estimated. RESULTS: The incidences of all cancer and lung cancer were consistently associated with PM2.5. The incident rate ratios (IRRs), per 10-µg/m3 increase in PM2.5, for all and lung cancer were 1.09 (95% CI: 1.03, 1.14) and 1.19 (95% CI: 1.09, 1.30), respectively. Less robust associations were observed with oral, rectal, liver, skin, breast, and kidney cancers. DISCUSSION: Exposure to PM2.5 air pollution contributes to lung cancer incidence and is potentially associated with non-lung cancer incidence. https://doi.org/10.1289/EHP7246.

Cancer mortality risk, fine particulate air pollution, and smoking in a large, representative cohort of US adults.

PURPOSE: Air pollution and smoking are associated with various types of mortality, including cancer. The current study utilizes a publicly accessible, nationally representative cohort to explore relationships between fine particulate matter (PM2.5) exposure, smoking, and cancer mortality. METHODS: National Health Interview Survey and mortality follow-up data were combined to create a study population of 635,539 individuals surveyed from 1987 to 2014. A sub-cohort of 341,665 never-smokers from the full cohort was also created. Individuals were assigned modeled PM2.5 exposure based on average exposure from 1999 to 2015 at residential census tract. Cox Proportional Hazard models were utilized to estimate hazard ratios for cancer-specific mortality controlling for age, sex, race, smoking status, body mass, income, education, marital status, rural versus urban, region, and survey year. RESULTS: The risk of all cancer mortality was adversely associated with PM2.5 (per 10 µg/m3 increase) in the full cohort (hazard ratio [HR] 1.15, 95% confidence interval [CI] 1.08-1.22) and the never-smokers' cohort (HR 1.19, 95% CI 1.06-1.33). PM2.5-morality associations were observed specifically for lung, stomach, colorectal, liver, breast, cervix, and bladder, as well as Hodgkin lymphoma, non-Hodgkin lymphoma, and leukemia. The PM2.5-morality association with lung cancer in never-smokers was statistically significant adjusting for multiple comparisons. Cigarette smoking was statistically associated with mortality for many cancer types. CONCLUSIONS: Exposure to PM2.5 air pollution contributes to lung cancer mortality and may be a risk factor for other cancer types. Cigarette smoking has a larger impact on cancer mortality than PM2.5 , but is associated with similar cancer types.

Fine particulate air pollution and human mortality: 25+ years of cohort studies.

Much of the key epidemiological evidence that long-term exposure to fine particulate matter air pollution (PM2.5) contributes to increased risk of mortality comes from survival studies of cohorts of individuals. Although the first two of these studies, published in the mid-1990s, were highly controversial, much has changed in the last 25 + years. The objectives of this paper are to succinctly compile and summarize the findings of these cohort studies using meta-analytic tools and to address several of the key controversies. Independent reanalysis and substantial extended analysis of the original cohort studies have been conducted and many additional studies using a wide variety of cohorts, including cohorts constructed from public data and leveraging natural experiments have been published. Meta-analytic estimates of the mean of the distribution of effects from cohort studies that are currently available, provide substantial evidence of adverse air pollution associations with all-cause, cardiopulmonary, and lung cancer mortality.

Air pollution and mortality in a large, representative U.S. cohort: multiple-pollutant analyses, and spatial and temporal decompositions.

BACKGROUND: Cohort studies have documented associations between fine particulate matter air pollution (PM2.5) and mortality risk. However, there remains uncertainty regarding the contribution of co-pollutants and the stability of pollution-mortality associations in models that include multiple air pollutants. Furthermore, it is unclear whether the PM2.5-mortality relationship varies spatially, when exposures are decomposed according to scale of spatial variability, or temporally, when effect estimates are allowed to change between years. METHODS: A cohort of 635,539 individuals was compiled using public National Health Interview Survey (NHIS) data from 1987 to 2014 and linked with mortality follow-up through 2015. Modelled air pollution exposure estimates for PM2.5, other criteria air pollutants, and spatial decompositions (< 1 km, 1-10 km, 10-100 km, > 100 km) of PM2.5 were assigned at the census-tract level. The NHIS samples were also divided into yearly cohorts for temporally-decomposed analyses. Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) in regression models that included up to six criteria pollutants; four spatial decompositions of PM2.5; and two- and five-year lagged mean PM2.5 exposures in the temporally-decomposed cohorts. Meta-analytic fixed-effect estimates were calculated using results from temporally-decomposed analyses and compared with time-independent results using 17- and 28-year exposure windows. RESULTS: In multiple-pollutant analyses, PM2.5 demonstrated the most robust pollutant-mortality association. Coarse fraction particulate matter (PM2.5-10) and sulfur dioxide (SO2) were also associated with excess mortality risk. The PM2.5-mortality association was observed across all four spatial scales of PM2.5, with higher but less precisely estimated HRs observed for local (< 1 km) and neighborhood (1-10 km) variations. In temporally-decomposed analyses, the PM2.5-mortality HRs were stable across yearly cohorts. The meta-analytic HR using two-year lagged PM2.5 equaled 1.10 (95% CI 1.07, 1.13) per 10 µg/m3. Comparable results were observed in time-independent analyses using a 17-year (HR 1.13, CI 1.09, 1.16) or 28-year (HR 1.09, CI 1.07, 1.12) exposure window. CONCLUSIONS: Long-term exposures to PM2.5, PM2.5-10, and SO2 were associated with increased risk of all-cause and cardiopulmonary mortality. Each spatial decomposition of PM2.5 was associated with mortality risk, and PM2.5-mortality associations were consistent over time.

Expression of Signaling Molecules Involved in Embryonic Development of the Insertion Site Is Inadequate for Reformation of the Native Enthesis: Evaluation in a Novel Murine ACL Reconstruction Model.

BACKGROUND: Since healing of anterior cruciate ligament (ACL) grafts occurs by formation of a fibrovascular scar-tissue interface rather than by reformation of the native fibrocartilage transition zone, the purpose of our study was to examine expression of various signaling molecules and transcription factors that are known to be involved in embryologic insertion-site development following ACL reconstruction. We also aimed to characterize a murine model of ACL reconstruction to allow future study of the molecular mechanisms of healing. METHODS: Seventy-nine mice underwent reconstruction of the ACL with autograft. Healing was assessed using histology in 12 mice and quantitative real-time polymerase chain reaction (qRT-PCR) gene-expression analysis in 3 mice at 1 week postoperatively (Group-1 mice) and by biomechanical analysis in 7, histological analysis in 7, immunohistochemical analysis in 5, microcomputed tomography analysis in 5, and qRT-PCR analyses in 8 at 2 weeks (Group-2 mice) and 4 weeks (Group-3 mice) postoperatively. Fifteen additional mice did not undergo surgery and were used for biomechanical (7 mice), qRT-PCR (3 mice), and immunohistochemical (5 mice) analyses to obtain baseline data for the native ACL. RESULTS: Histological analysis demonstrated healing by formation of fibrovascular tissue at the tendon-bone interface. Immunohistochemical analysis showed a positive expression of proteins in the Indian hedgehog, Wnt, and parathyroid hormone-related protein (PTHrP) pathways. There was minimal Sox-9 expression. Gene-expression analysis showed an initial increase in markers of tissue repair and turnover, followed by a subsequent decline. Mean failure force and stiffness of the native ACL were 5.60 N and 3.44 N/mm, respectively. Mean failure force and stiffness were 1.29 N and 2.28 N/mm, respectively, in Group 2 and were 1.79 N and 2.59 N/mm, respectively, in Group 3, with 12 of 14 failures in these study groups occurring by tunnel pull-out. CONCLUSIONS: The spatial and temporal pattern of expression of signaling molecules that direct embryologic insertion-site formation was not adequate to restore the structure and composition of the native insertion site. CLINICAL RELEVANCE: Development of a murine model to study ACL reconstruction will allow the use of transgenic animals to investigate the cellular, molecular, and biomechanical aspects of tendon-to-bone healing following ACL reconstruction, ultimately suggesting methods to improve healing in patients.

Outcomes of Patellofemoral Osteochondral Lesions Treated With Structural Grafts in Patients Older Than 40 Years.

Background Chondral lesions in the patellofemoral compartment represent a difficult entity to treat among active patients, with no clear consensus on the optimal treatment strategy. The purpose of this study was to review the functional outcomes of patients >40 years old with primary patellofemoral osteochondral lesions who underwent a cartilage restoration procedure with a structural graft. Methods Following institutional review board approval, 35 patients >40 years treated for patellofemoral chondral or osteochondral injuries were retrospectively identified. Seventeen (47%) had prior surgery (mean 1.4 procedures, range 1-4). Average follow-up was 3.6 ± 1.6 years. Average patient age was 51.5 years (range 40-72 years); 54% were male. Twenty-six (74%) had isolated trochlear lesions, 7 had isolated patellar lesions (20%), while 2 (6%) had bipolar lesions. Twenty patients (57%) were treated with synthetic biphasic scaffold plugs (SS), 9 (26%) with fresh osteochondral allograft (OCA) and 6 (17%) with osteochondral autograft transfer (OAT). Outcomes were measured with validated measures: Activity of Daily Living Score (ADL), International Knee Documentation Committee (IKDC) Subjective Evaluation form, and Marx Activity Scale (MAS). Results The average lesion size for the entire cohort was 3.1 ± 1.7 cm2. Average defect size was 2.6 ± 1.7 cm2 for the SS group, 4.3±1.5 cm2 for the OCA group, and 2.9 ± 0.8 cm2 for the OAT group ( P > 0.051). Outcome scores for the entire population demonstrated significant improvement in ADL ( P = 0.002) and IKDC scores ( P = 0.004) between baseline and final follow-up, while MAS scores were maintained ( P = 0.51). Conclusion Structural grafts are a viable treatment option for symptomatic focal osteochondral lesions of the patellofemoral joint in patients 40 years and older, with anticipated improvements in pain and function and maintenance of preoperative activity levels.

Outcomes following Structural Grafting of Distal Femoral Osteochondral Injuries in Patients Aged 40 Years and Older.

Osteochondral lesions of the distal femur represent a challenging clinical entity, particularly in patients > 40 years of age. Microfracture has demonstrated inferior results in this population with clinical deterioration beyond 1 to 2 years postoperatively. Limited evidence exists to support alternative cartilage restoration procedures. The purpose of this study was to report functional outcomes and activity levels following cartilage restoration procedures in patients > 40 years with symptomatic distal femoral osteochondral lesions. From 2000 to 2012, 61 patients with distal femoral osteochondral injuries were retrospectively identified. Mean follow-up was 3.6 ± 1.4 years; mean age was 51.6 years (range 40-71); 59% were male. Of 61 patients, 35 patients (57%) were treated with synthetic scaffold (SS) plugs (off-label), 14 (23%) with osteochondral allograft (OCA), and 12 (20%) with autologous osteochondral transfer (AOT). Validated outcome measures including activity of daily living (ADL) score, International Knee Documentation Committee (IKDC) subjective evaluation form, and Marx activity scale (MAS) were used. The average lesion size was 3.8 ± 2.1 cm2. Lesion size was significantly greater in the OCA group (5.8 ± 1.8 cm2), compared with the SS (3.2 ± 1.9 cm2) and AOT group (3.3 ± 1.8 cm2, p ≤ 0.0024). Collectively, outcome scores for the entire population demonstrated significant improvement in ADL (61.36 ± 17.76-76.81 ± 17.2, p < 0.0001) and IKDC scores (40.28 ± 13.28-61.84 ± 20.83, p < 0.001) from baseline to final follow-up, with no significant change in MAS (4.19 ± 5.13-2.59 ± 3.92, p = 0.07). Similarly, subgroup analysis identified that all treatment groups (SS, OCA, and AOT) demonstrated significant improvement in ADL and IKDC scores from preoperative to final postoperative visit (p ≤ 0.0361). MAS scores were maintained in the OCA and AOT groups (p ≥ 0.1704), but significantly decreased in the SS group (4.3 ± 5.2-2.7 ± 4.11, p = 0.0163). Ten patients (16.3%) required revision surgery at a mean of 4.4 years (range 0.3-13.4 years). Cartilage restoration procedures using structural grafts are successful in patients 40 years and older, with improved pain and functional outcome scores compared with preoperative baseline scores. OCA and AOT should primarily be used, given recent concerns with SS implants.

Restriction of Postoperative Joint Loading in a Murine Model of Anterior Cruciate Ligament Reconstruction: Botulinum Toxin Paralysis and External Fixation.

Control of knee motion in small animal models is necessary to study the effect of mechanical load on the healing process. This can be especially challenging in mice, which are being increasingly used for various orthopedic reconstruction models. We explored the feasibility of botulinum toxin (Botox; Allergan, Dublin, Ireland) paralysis and a newly designed external fixator to restrict motion of the knee in mice undergoing anterior cruciate ligament (ACL) reconstruction. Nineteen C57BL/6 mice were allocated to two groups: (1) Botox group (n = 9) and (2) external fixator group (n = 10). Mice in Botox group received two different doses of Botox: 0.25 unit (n = 3) and 0.5 unit (n = 6). Injection was performed 72 hours prior to ACL reconstruction into the quadriceps, hamstring, and calf muscles of the right hind leg. Mice in external fixator group received an external fixator following ACL reconstruction. Mice were monitored for survival, tolerance, and achievement of complete knee immobilization. All mice were meant for sacrifice on day 14 postoperatively. No perceptible change in gait was observed with 0.25 unit of Botox. All mice that received 0.5 unit of Botox had complete hind limb paralysis documented by footprint analysis 2 days after injection but failed to tolerate anesthesia and were euthanized 24 hours after operation due to their critical condition. In contrast, the external fixator was well tolerated and effectively immobilized the limb. There was a single occurrence of intraoperative technical error in the external fixator group that led to euthanasia. No mechanical failure or complication was observed. Botox paralysis was not a viable option for postoperative restriction of motion and joint loading in mice. However, external fixation was an effective method for complete knee immobilization and can be used in murine models requiring postoperative control of knee loading. This study introduces a robust research tool to allow control of postoperative joint loading in animal models such as ACL reconstruction, permitting study of the effects of mechanical load on the biologic aspects of tendon-to-bone healing.

Orthopaedic Residents Improve Confidence and Knot-Tying Speed With a Skills Course.

PURPOSE: To determine the effect of a knot-tying module, within an arthroscopic training course, on resident speed, resident confidence, and biomechanical quality of arthroscopically tied knots. METHODS: Sixty-four participants (8 postgraduate year [PGY]-3 and 8 PGY-4 orthopaedic residents annually for 4 years) were enrolled in a 5-day training course, which included a daily knot-tying module. Self-assessed confidence was obtained by pre-course (day 1) and post-course (day 5) questionnaire. Each participant tied 5 sequential knots using an arthroscopic knot-tying station. Time per knot was recorded in seconds. Knots were later preloaded, cycled, and tested for peak load to failure and displacement change. Mean peak load to failure, displacement change, speed, and confidence were compared before and after training. RESULTS: The mean time to complete 5 knots was significantly faster after training (12.8 minutes before the course [day 1] v 9.39 minutes after the course [day 5]) (P < .0001). Confidence improved from pre-course (mean, 3.3) to post-course (mean, 7.8) questionnaires (P < .0001). No statistically significant difference was found between peak force for pre-course (mean, 136 N) and post-course (mean, 138 N) knots (P = .076). No statistically significant difference was detected in mean displacement change (mean, 3.51 mm before the course v 3.57 mm after the course) (P = .61). Comparison of PGY-3 and PGY-4 residents was significant only for a higher pre-course confidence in PGY-4 residents (P = .02). CONCLUSIONS: Participation in an arthroscopic knot-tying module improves resident speed and confidence in tying arthroscopic knots. Our data did not show a significant change in peak load to failure or loop security with training. These findings suggest that participation in a knot-tying module improves efficiency regarding arthroscopic knot tying by residents. CLINICAL RELEVANCE: Residents who practice arthroscopic knot tying 5 days per year as part of an arthroscopic training course may be more efficient in the operating room.

From patient care to research: a validation study examining the factors contributing to data quality in a primary care electronic medical record database.

BACKGROUND: Electronic Medical Records (EMRs) are increasingly used in the provision of primary care and have been compiled into databases which can be utilized for surveillance, research and informing practice. The primary purpose of these records is for the provision of individual patient care; validation and examination of underlying limitations is crucial for use for research and data quality improvement. This study examines and describes the validity of chronic disease case definition algorithms and factors affecting data quality in a primary care EMR database. METHODS: A retrospective chart audit of an age stratified random sample was used to validate and examine diagnostic algorithms applied to EMR data from the Manitoba Primary Care Research Network (MaPCReN), part of the Canadian Primary Care Sentinel Surveillance Network (CPCSSN). The presence of diabetes, hypertension, depression, osteoarthritis and chronic obstructive pulmonary disease (COPD) was determined by review of the medical record and compared to algorithm identified cases to identify discrepancies and describe the underlying contributing factors. RESULTS: The algorithm for diabetes had high sensitivity, specificity and positive predictive value (PPV) with all scores being over 90%. Specificities of the algorithms were greater than 90% for all conditions except for hypertension at 79.2%. The largest deficits in algorithm performance included poor PPV for COPD at 36.7% and limited sensitivity for COPD, depression and osteoarthritis at 72.0%, 73.3% and 63.2% respectively. Main sources of discrepancy included missing coding, alternative coding, inappropriate diagnosis detection based on medications used for alternate indications, inappropriate exclusion due to comorbidity and loss of data. CONCLUSIONS: Comparison to medical chart review shows that at MaPCReN the CPCSSN case finding algorithms are valid with a few limitations. This study provides the basis for the validated data to be utilized for research and informs users of its limitations. Analysis of underlying discrepancies provides the ability to improve algorithm performance and facilitate improved data quality.

Subtalar joint axis in patients with symptomatic peritalar subluxation compared to normal controls.

BACKGROUND: The etiology of peritalar subluxation (PTS) is poorly understood and likely mutifactorial. An anatomic predisposition for posterolateral subluxation of the hindfoot has not been previously described or investigated. The aim of the current study was to describe the morphology of the subtalar joint axis (STJA) in patients with symptomatic PTS compared to normal controls. METHODS: We identified patients with symptomatic PTS who had undergone operative correction from hospital records. The angle of the axis of the posterior facet of the subtalar joint was made on simulated weight-bearing CT (SWBCT) scans. A control group of patients who had no foot deformity on standing films was used for comparison. The STJA was defined as the angle between the superior talar dome and the posterior facet of the talus on coronal CT scan. The mean, maximum, and minimum STJAs were calculated for each cut from anterior to posterior across the posterior facet. The trend in progression across the posterior facet was also examined. RESULTS: After exclusions, 22 feet in 20 patients were included in the study group and compared to 20 control subjects. It was seen that patients with PTS had an increased valgus orientation of the subtalar joint. In patients with PTS the STJA began in valgus and progressed to even greater valgus from anterior to posterior across the posterior facet. The STJA in control subjects was seen instead to begin in slight varus and transition to valgus at the junction of the anterior and middle third and then increase in valgus as the joint progressed posteriorly. CONCLUSIONS: The valgus orientation of the coronal plane of the subtalar joint may represent an anatomic contribution to the etiology of PTS. LEVEL OF EVIDENCE: Level III, comparative series.

Observed changes in radiographic measurements of the first ray after frontal and transverse plane rotation of the hallux: does the hallux drive the metatarsal in a bunion deformity?

It is well known that the pathologic positions of the hallux and the first metatarsal in a bunion deformity are multiplanar. It is not universally understood whether the pathologic changes in the hallux or first metatarsal drive the deformity. We have observed that frontal plane rotation of the hallux can result in concurrent positional changes proximally in the first metatarsal in hallux abducto valgus. In the present study, we observed the changes in common radiographic measurements used to evaluate a bunion deformity in 5 fresh frozen cadaveric limbs. We measured the tibial sesamoid position, 1-2 intermetatarsal angle, and first metatarsal cuneiform angle on anteroposterior radiographs after frontal and transverse plane manipulation of the hallux. When the hallux was moved into an abducted and valgus position, a statistically significant increase was found in the tibial sesamoid position (p = .016). However, we did not observe a significant increase in the intermetatarsal angle (p = .070) or medial cuneiform angle (p = .309). When the hallux was manipulated into an adducted and varus position, a statistically significant decrease in the intermetatarsal angle (p = .02) and a decrease in the tibial sesamoid position (p = .016) was seen, with no significant change in the medial cuneiform angle (p = .360). We also observed a consistent rounding of the lateral aspect of the first metatarsal head and an increase in the concavity of the lateral metatarsal shaft, with valgus rotation of the hallux. From these observations, it is possible that the hallux could drive the proximal changes in the first ray that lead to metatarsus primus adducto valgus deformity.

Principles of management of growth plate fractures in the foot and ankle.

Providers treating pediatric injuries must understand the properties of the pediatric skeleton and be sensitive to the psychological and social expectations of patients and their families. Immediate needs must be addressed, and the long-term prognosis must be explained. Detailed understanding of fracture mechanism and fracture patterns is essential for diagnosis and treatment. The provider must remain vigilant for changes in the osseous and soft tissue structures during treatment. Failure to recognize signs of growth interruption and changes in position may lead to functional abnormalities. This article presents an overview of pediatric growth plate injury management.

Anatomical variance in acetabular anteversion does not predict hip fracture patterns in the elderly: a retrospective study in 135 patients.

It has been suggested that variances in the anatomy of the acetabulum determine the type of hip fracture in elderly patients. Based on this concept, an overly anteverted acetabulum would lead to impingement of the femoral neck against the posterior rim of the acetabulum, causing a femoral neck fracture, whereas with a retroverted acetabulum, external rotation of the hip would be limited by the capsular tissues attached to the trochanteric region, causing a trochanteric fracture. To test the hypothesis that acetabular version predicts hip fracture type in elderly patients, we measured acetabular version using computed tomography scans for 135 patients with hip fracture. Logistic regression analysis was used to check for an association between version angle and fracture type. No significant relationship between acetabular version and fracture type was found. Therefore, we conclude that acetabular version angle does not predict hip fracture type in the elderly, and our data do not support the impingement concept as the mechanism of hip fractures.

Bone density and cortical thickness in normal, osteopenic, and osteoporotic sacra.

It is unclear if a decrease in cancellous bone density or cortical bone thickness is related to sacral insufficiency fractures. We hypothesized that reduction in overall bone density leads to local reductions in bone density and cortical thickness in cadaveric sacra that match clinically observed fracture patterns in patients with sacral insufficiency fractures. We used quantitative computed tomography to measure cancellous density and cortical thickness in multiple areas of normal, osteopenic, and osteoporotic sacra. Cancellous bone density was significantly lower in osteoporotic specimens in the central and anterior regions of the sacral ala compared with other regions of these specimens. Cortical thickness decreased uniformly in all regions of osteopenic and osteoporotic specimens. These results support our hypothesis that areas of the sacrum where sacral insufficiency fractures often occur have significantly larger decreases in cancellous bone density; however, they do not support the hypothesis that these areas have local reduction of cortical bone thickness.