Intermediate Outcomes Following Percutaneous Fixation of Proximal Humeral Fractures
Alicia K. HarrisonKonrad I. GrusonBenjamin ZmistowskiJay D. KeenerLeesa M. GalatzGerald R. WilliamsBradford O. ParsonsEvan L. Flatow
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Mini-open reduction and percutaneous fixation of proximal humeral fractures historically results in good outcomes and a low prevalence of osteonecrosis reported with short-term follow-up. The purpose of this study was to determine the midterm results of our multicenter case series of proximal humeral fractures treated with percutaneous fixation.Between 1999 and 2006, thirty-nine patients were treated with percutaneous reduction and fixation for proximal humeral fractures at three tertiary shoulder referral centers. Twenty-seven of these patients were available for intermediate follow-up at a minimum of three years (mean, eighty-four months; range, thirty-seven to 128 months) after surgery; the follow-up examination included use of subjective outcome measures and radiographic analysis to identify osteonecrosis and posttraumatic osteoarthritis on radiographs.Osteonecrosis was detected in seven (26%) of the total group of twenty-seven patients at a mean of fifty months (range, eleven to 101 months) after the date of percutaneous fixation. Osteonecrosis was observed in five (50%) of the ten patients who had four-part fractures, two (17%) of the twelve patients who had three-part fractures, and none (0%) of the five patients who had two-part fractures. Posttraumatic osteoarthritis, including osteonecrosis, was present on radiographs in ten (37%) of the total group of twenty-seven patients. Posttraumatic osteoarthritis was observed in six (60%) of the ten patients who had four-part fractures, four (33%) of the twelve patients who had three-part fractures, and none (0%) of the five patients who had two-part fractures.Intermediate follow-up of patients with percutaneously treated proximal humeral fractures demonstrates an increased prevalence of osteonecrosis and posttraumatic osteoarthritis over time, with some patients with these complications presenting as late as eight years postoperatively. Development of osteonecrosis did not have a universally negative impact on subjective outcome scores.Keywords:
Shoulder Fracture
We aimed to determine whether hand OA is characterized by systemic cartilage loss by assessing if radiographically normal joints had greater joint space width (JSW) loss over 4 years in hands with incident or prevalent OA elsewhere in the hand compared with hands without OA. We used semi-automated software to measure JSW in the distal and proximal IP joints of 3368 participants in the Osteoarthritis Initiative who had baseline and 48-month hand radiographs. A reader scored 16 hand joints (including the thumb base) for Kellgren-Lawrence (KL) grade. A joint had OA if scored as KL ≥2. We identified three groups based on longitudinal hand OA status: no hand OA (KL <2 in all 16 joints) at the baseline and 48-month visits, incident hand OA (KL <2 in all 16 joints at baseline and then one or more joints with KL ≥2 at 48 months) and prevalent hand OA (one or more joints with KL ≥2 at baseline and 48 months). We then assessed if JSW in radiographically normal joints (KL 0) differed across these three groups. We calculated unpooled effect sizes to help interpret the differences between groups. We observed small differences in JSW loss that are unlikely to be clinically important in radiographically normal joints between those without hand OA (n = 1054) and those with incident (n = 102) or prevalent hand OA (n = 2212) (effect size range -0.01-0.24). These findings were robust when examining JSW loss dichotomized based on meaningful change and in other secondary analyses. Hand OA is not a systemic disease of cartilage.
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Arthropathy
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Osteoarthritis is a common joint disease in the elderly. By far the most important risk factor for osteoarthritis is aging. Age-related changes in the articular cartilage may be responsible for age-related increase in the number of people with osteoarthritis. One of the most striking changes in cartilage is the accumulation of non-enzymatic glycation (NEG) products in cartilage. NEG is the spontaneous reaction of proteins with sugars. Earlier in vitro experiments showed that NEG negatively affects the cartilage. The cartilage is stiffer and more fragile being more susceptible to damage. In addition, there is less capacity to repair the cartilage because NEGs interfere with chondrocyte activity. This combination can lead to initiation and progression of damage of the cartilage as can be seen in osteoarthritis. In this thesis the role of NEG on specificallythe occurrence of osteoarthritis is examined. In animal experiments we have shown that artificial increased NEG in the cartilage of the knee joints of dogs plays a role at the progression of osteoarthritis. We were not able to demonstrate the effect of NEG on the development of osteoarthritis. In a cohort of individuals with early signs of osteoarthritis the NEG content (measure in skin as surrogate for cartilage NEG) was higher in participants with some osteoarthritis on their X-ray than with participants without any signs of radiographic osteoarthritis. The NEG content measured at baseline was not able to predict the limited radiographic progression of osteoarthritis over 5 years follow-up. At end stage osteoarthritis, the amount of NEG in the cartilage tissue appeared inversely related to the degree of osteoarthritis in the cartilage. This was considered due to the formation of new cartilage, not yet being glycated, in an attempt to repair. Conclusion: The influence of NEG on the occurrence of osteoarthritis is not undisputedly demonstrated. We still expect that AGEs do play a role in OA, however, regarding development of OA it is hard to proof, and the causality is definitely not a strong one.
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Knee pain
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Purpose of review We discuss recent published epidemiologic data regarding risk factors for incident and progressive knee osteoarthritis and related knee pain to identify targets for primary and secondary prevention. We also discuss recently identified methodologic challenges to the study of knee osteoarthritis, particularly osteoarthritis progression. Recent findings Recent epidemiologic studies and systematic reviews of knee osteoarthritis have confirmed that being overweight and obese, and knee injuries increase the risk for incident knee osteoarthritis. Biomechanical risk factors such as leg-length inequalities and malalignment require further study. Obesity also appears to play a role in accelerating osteoarthritis worsening. However, with the exception of malalignment, no risk factors for knee osteoarthritis progression have been identified. Novel approaches to the study of knee pain have demonstrated a strong association between structural abnormalities and knee pain, contrary to the 'so-called' structure-symptom discordance, as well as between fluctuations of knee pain with changes in specific structural lesions. A number of methodologic issues, including conditioning on an intermediate stage of disease and depletion of susceptibles may explain, in part, the difficulty in identifying risk factors for knee osteoarthritis. Summary There is strong epidemiologic evidence that being overweight or obese and knee injury are associated with increased risk of developing knee osteoarthritis. Further study is required to confirm associations of leg-length inequality and malalignment with incident knee osteoarthritis. Few new risk factors for progression of knee osteoarthritis have been identified in the past few years. Without such knowledge, secondary prevention of osteoarthritis remains challenging.
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Abstract Osteoarthritis, has existed as far back as the prehistoric eras-it has been found in dinosaur skeletons, and affects all mammals. Studies of skeleton X-rays from all ages show that if one lives long enough, osteoarthritis will develop in some joints. However, even though more than 80% of X-rays in people older than 75 years have osteoarthritis of the knee, less than 30% of people will ever develop knee pain from their osteoarthritis. Other estimates are that 10-15% of all Americans suffer from osteoarthritis knee pain. Clearly there is a large discrepancy between those that have X-ray evidence of osteoarthritis and those who eventually develop joint pain; however, the reasons for this are not yet clear. The older we get, the higher the chance of getting osteoarthritis, with a nearly 90% chance of X-ray findings in some joint by age 75. However, after the seventh decade the incidence appears to plateau, and this may mean that those who reach this age without symptoms are not likely to get them or that it has not yet been carefully studied in older individuals. While osteoarthritis appears to be an inescapable cause of aging, there is still no clear link between the normal aging process and the articular cartilage loss seen with osteoarthritis. Here we will review the risk factors for developing osteoarthritis (summarized in Table 3, at the end of the section).
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We investigated the clinical and radiographic disease course of hand osteoarthritis as well as determinants of poor clinical outcome and radiographic progression over a period of six years in 289 patients with hand osteoarthritis. Because these patients had osteoarthritis at multiple joints this enabled us to not only assess the association between progression of osteoarhtiritis in different hand joints groups but also between progression of hand osteoarthritis and osteoarthritis change at the knee. In addition, genetic factors in hand osteoarthritis progression were investigated as well as the influence of illness perceptions. The hand osteoarthritis subsets erosive osteoarthritis and thumb base osteoarthritis are further characterised. In the last part of the thesis the clinimetric properties of a pain score for osteoarthritis and radiographic outcome measures for hand osteoarthritis are evaluated.
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Abstract Aims To assess the probability of individuals with early‐diagnosed hip or knee osteoarthritis experiencing a fall and/or fracture compared to a cohort without osteoarthritis. Methods Data were analyzed from the Osteoarthritis Initiative dataset. We identified all people who were diagnosed with hip or knee osteoarthritis within a 12 month period, compared to those without osteoarthritis. We determined whether there was a difference in the occurrence of falls, with or without consequential fractures, between people newly diagnosed with hip or knee osteoarthritis compared to those who had not, using odd ratios ( OR ) and 95% confidence intervals (95% CI ). Results Five hundred and fifty‐two individuals with hip osteoarthritis were compared to 4244 individuals without hip osteoarthritis; 1350 individuals with knee osteoarthritis were compared to 3445 individuals without knee osteoarthritis. People with knee osteoarthritis had a 54% greater chance of experiencing a fall compared to those without ( OR : 1.54; 95% CI : 1.35–1.77). People with hip osteoarthritis had a 52% greater chance of experiencing a fall compared to those without hip osteoarthritis ( OR : 1.52; 95% CI : 1.26–1.84). People with knee and hip osteoarthritis demonstrated over an 80% greater chance of experiencing a fracture in the first 12 months of their diagnosis compared to those without hip or knee osteoarthritis (total knee arthroplasty: OR 1.81; total hip arthroplasty: OR 1.84). Conclusions There is an increased risk of falls and fractures in early‐diagnosed knee and hip osteoarthritis compared to those without osteoarthritis. International guidelines on the management of hip and knee osteoarthritis should consider the management of falls risk.
Hip Fracture
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Accelerated knee osteoarthritis may be a unique subset of knee osteoarthritis, which is associated with greater knee pain and disability. Identifying risk factors for accelerated knee osteoarthritis is vital to recognizing people who will develop accelerated knee osteoarthritis and initiating early interventions. The geometry of an articular surface (e.g., coronal tibial slope), which is a determinant of altered joint biomechanics, may be an important risk factor for incident accelerated knee osteoarthritis. We aimed to determine if baseline coronal tibial slope is associated with incident accelerated knee osteoarthritis or common knee osteoarthritis.We conducted a case-control study using data and images from baseline and the first 4 years of follow-up in the Osteoarthritis Initiative. We included three groups: 1) individuals with incident accelerated knee osteoarthritis, 2) individuals with common knee osteoarthritis progression, and 3) a control group with no knee osteoarthritis at any time. We did 1:1:1 matching for the 3 groups based on sex. Weight-bearing, fixed flexion posterior-anterior knee radiographs were obtained at each visit. One reader manually measured baseline coronal tibial slope on the radiographs. Baseline femorotibial angle was measured on the radiographs using a semi-automated program. To assess the relationship between slope (predictor) and incident accelerated knee osteoarthritis or common knee osteoarthritis (outcomes) compared with no knee osteoarthritis (reference outcome), we performed multinomial logistic regression analyses adjusted for sex.The mean baseline slope for incident accelerated knee osteoarthritis, common knee osteoarthritis, and no knee osteoarthritis were 3.1(2.0), 2.7(2.1), and 2.6(1.9); respectively. A greater slope was associated with an increased risk of incident accelerated knee osteoarthritis (OR = 1.15 per degree, 95 % CI = 1.01 to 1.32) but not common knee osteoarthritis (OR = 1.04, 95 % CI = 0.91 to 1.19). These findings were similar when adjusted for recent injury. Among knees with varus malalignment a greater slope increases the odds of incident accelerated knee osteoarthritis; there is no significant relationship between slope and incident accelerated knee osteoarthritis among knees with normal alignment.Coronal tibial slope, particularly among knees with malalignment, may be an important risk factor for incident accelerated knee osteoarthritis.
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GENERAL INFORMATION The Definition of Osteoarthritis Epidemiology of Osteoarthritis Pathology of Osteoarthritis Pathogenesis of Osteoarthritis DIAGNOSIS OF OSTEOARTHRITIS Clinical Features of Osteoarthritis Pitfalls in the Diagnosis of Osteoarthritis Synovial Fluid Analysis Radiography of Osteoarthritis Monitoring the Patient with Osteoarthritis THERAPY Nonmedicinal Therapy for Osteoarthritis Pain Systemic Pharmacologic Therapy Local Therapy for OA Pain A Rational Strategy for Selecting the Initial Pharmacologic Agent for the Management of Osteoarthritis Pain Disease-Modifying Drugs for Osteoarthritis (DMOADs) Tidal Irrigation of the Knee Surgical Intervention Index
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