Meniscal ramp lesions should be considered in anterior cruciate ligament-injured knees, especially with larger instability or longer delay before surgery.

PURPOSE: To determine the incidence of meniscal ramp lesions in an anterior cruciate ligament (ACL) injured knees and to clarify whether ramp lesions are related to chronic ACL deficiency and increased knee instability. METHODS: Consecutive ACL injured patients were evaluated arthroscopically for a ramp lesion via a trans-notch view and evidence of menisco-capsular injury was recorded. Other concomitant injuries to the knee were also noted. Incidence of meniscal ramp lesions, delay before surgery, and anterior-posterior stability was analyzed. All patients underwent bilateral KT-2000 evaluation. RESULTS: One hundred and three consecutive ACL injured patients with a mean age of 24 years were included in this study. In total, a ramp lesion was found in 10 knees (9.7%) via a trans-notch view. None of these lesions could be identified by the standard view from the anterolateral portal. Other medial meniscal lesions were found in 26 knees (25.2%) by standard arthroscopic viewing. The ramp lesion group had significantly longer delay before surgery with a median of 191 days (p < 0.01) as well as a larger side-to-side difference of KT-2000 measurement (7.3 ± 1.8 mm; p < 0.01), compared with the intact medial meniscus group (53 days and 5.5 ± 1.5 mm, respectively). CONCLUSION: Ramp lesions that were identified using a trans-notch view were not visualized with standard arthroscopic views. Increased anterior tibial translation and longer delay before surgery were seen in knees with ramp lesions. Careful inspection of the posteromedial menisco-capsular region is required as hidden menisco-capsular lesions may occur which may result in residual knee instability. LEVEL OF EVIDENCE: Level II.

Influence of Age on Healing Capacity of Acute Tears of the Anterior Cruciate Ligament Based on Magnetic Resonance Imaging Assessment.

OBJECTIVE: The purpose of this study was to evaluate the influence of patient age on the effects of conservative treatment of the anterior cruciate ligament (ACL). METHODS: A total of 102 consecutive patients with acute ACL injury were allowed to heal without surgery. Final magnetic resonance imaging images of the ACL were classified from grade I, indicating good morphological recovery, to grade IV, indicating poor recovery. Chi-square analysis was used to determine significant differences in the incidence of grades I and II among those less than 20 versus those 20 years or more of age. RESULTS: The mean follow-up to final magnetic resonance imaging was 9 months. A significant difference in the frequency of grades I and II was observed between age groups (<20 years, 13.0%; ≥20 years, 69.6%; P < 0.0001). CONCLUSION: ACL injury was more severe, and morphological recovery with conservative treatment was poorer among younger patients than among adults.

Enhanced lateral inhibition in the barrel cortex by deletion of phospholipase C-related catalytically inactive protein-1/2 in mice.

We previously demonstrated that the deletion of phospholipase C-related catalytically inactive protein-1/2 (PRIP-1/2) enhances the desensitization of GABAA receptors (GABAARs), while it facilitates their resensitization at the offset of GABA puff, causing a hump-like tail current (tail-I) in layer 3 (L3) pyramidal cells (PCs) of the barrel cortex. In the present study, we investigated whether inhibitory synaptic transmission in L3 PCs in the barrel cortex is altered in the PRIP-1/2 double-knockout (PRIP-DKO) mice, and if so, how the interaction between excitation and inhibition is subsequently modified. PRIP-1/2 deletion resulted in the prolongation of the decay phase of inhibitory postsynaptic currents/potentials (IPSCs/IPSPs) in L3 PCs evoked by stimulation of L3, leaving the overall features of miniature IPSCs unchanged. An optical imaging revealed that the spatiotemporal profile of a horizontal excitation spread across columns in L2/3 caused by L4 stimulation in the barrel cortex was more restricted in PRIP-DKO mice compared to the wild type, while those obtained in the presence of bicuculline were almost identical between the two genotypes. These findings suggest that PRIP-1/2 deletion enhances the lateral inhibition by prolonging inhibitory synaptic actions to limit the intercolumnar integration in the barrel cortex. Considering the present findings together with our previous study including a mathematical simulation, the prolongation of inhibitory synaptic actions is likely to result from an enhancement of desensitization followed by an enhanced resensitization in GABAARs.

Enhanced desensitization followed by unusual resensitization in GABAA receptors in phospholipase C-related catalytically inactive protein-1/2 double-knockout mice.

Phospholipase C-related catalytically inactive proteins (PRIP-1/2) are previously reported to be involved in the membrane trafficking of GABAA receptor (GABAAR) and the regulation of intracellular Ca(2+) stores. GABAAR-mediated currents can be regulated by the intracellular Ca(2+). However, in PRIP-1/2 double-knockout (PRIP-DKO) mice, it remains unclear whether the kinetic properties of GABAARs are modulated by the altered regulation of intracellular Ca(2+) stores. Here, we investigated whether GABAAR currents (IGABA) evoked by GABA puff in layer 3 (L3) pyramidal cells (PCs) of the barrel cortex are altered in PRIP-DKO mice. The deletion of PRIP-1/2 enhanced the desensitization of IGABA but induced a hump-like tail current (tail-I) at the GABA puff offset. IGABA and the hump-like tail-I were suppressed by GABAAR antagonists. The enhanced desensitization of IGABA and the hump-like tail-I in PRIP-DKO PCs were mediated by increases in the intracellular Ca(2+) concentration and were largely abolished by a calcineurin inhibitor and ruthenium red. Calcium imaging revealed that Ca(2+)-induced Ca(2+) release (CICR) and subsequent store-operated Ca(2+) entry (SOCE) are more potent in PRIP-DKO PCs than in wild-type PCs. A mathematical model revealed that a slowdown of GABA-unbinding rate and an acceleration of fast desensitization rate by enhancing its GABA concentration dependency are involved in the generation of hump-like tail-Is. These results suggest that in L3 PCs of the barrel cortex in PRIP-DKO mice, the increased calcineurin activity due to the potentiated CICR and SOCE enhances the desensitization of GABAARs and slows the GABA-unbinding rate, resulting in their unusual resensitization following removal of GABA.

Generation of resonance-dependent oscillation by mGluR-I activation switches single spiking to bursting in mesencephalic trigeminal sensory neurons.

The primary sensory neurons supplying muscle spindles of jaw-closing muscles are unique in that they have their somata in the mesencephalic trigeminal nucleus (MTN) in the brainstem, thereby receiving various synaptic inputs. MTN neurons display bursting upon activation of glutamatergic synaptic inputs while they faithfully relay respective impulses arising from peripheral sensory organs. The persistent sodium current (IN aP ) is reported to be responsible for both the generation of bursts and the relay of impulses. We addressed how IN aP is controlled either to trigger bursts or to relay respective impulses as single spikes in MTN neurons. Protein kinase C (PKC) activation enhanced IN aP only at low voltages. Spike generation was facilitated by PKC activation at membrane potentials more depolarized than the resting potential. By injection of a ramp current pulse, a burst of spikes was triggered from a depolarized membrane potential whereas its instantaneous spike frequency remained almost constant despite the ramp increases in the current intensity beyond the threshold. A puff application of glutamate preceding the ramp pulse lowered the threshold for evoking bursts by ramp pulses while chelerythrine abolished such effects of glutamate. Dihydroxyphenylglycine, an agonist of mGluR1/5, also caused similar effects, and increased both the frequency and impedance of membrane resonance. Immunohistochemistry revealed that glutamatergic synapses are made onto the stem axons, and that mGluR1/5 and Nav1.6 are co-localized in the stem axon. Taken together, glutamatergic synaptic inputs onto the stem axon may be able to switch the relaying to the bursting mode.

Teeth clenching reduces arm abduction force.

It has been reported that the 90° arm abduction force counteracting external adduction loads appeared to be smaller under teeth clenching condition than under non-clenching condition. To elucidate the physiological mechanism underlying the possible inhibitory effect of teeth clenching on the arm abduction, we have attempted to quantify the difference in the force induced against the fast and slow ramp load between the arm abductions under teeth non-clenching and clenching conditions. When the load of adduction moment was linearly increased, the abductor force increased to a maximal isometric contraction force (MICF) and further increased to a maximal eccentric contraction force (MECF) with forced adduction. The MICF measured under teeth clenching was significantly lower than that under non-clenching, despite no significant difference in the MECF between the two conditions. The reduction in MICF caused by teeth clenching was enhanced by increasing the velocity of the load. These results suggest that clenching inhibits abduction force only during isometric contraction phase. The invariability of MECF would indicate the lack of involvement of fatigue in such inhibitory effects of clenching. To discover the source of the inhibition, we have examined the effects of teeth clenching on the stretch reflex in the deltoid muscle. The stretch reflex of deltoid muscles was inhibited during clenching, contrary to what was expected from the Jendrassik maneuver. Taken together, our results suggest that the teeth clenching reduced the MICF by depressing the recruitment of deltoid motoneurones presumably via the presynaptic inhibition of spindle afferent inputs onto those motoneurones.

Life Course Epidemiology of Hip Osteoarthritis in Japan: A Multicenter, Cross-Sectional Study.

BACKGROUND: The incidence of developmental dysplasia of the hip (DDH) in Japanese newborns has reduced drastically following a primary prevention campaign initiated around 1972 to 1973; this perinatal education campaign promoted maintaining the hips of newborns in the naturally flexed-leg position. The purpose of the present study was to describe the life course epidemiology of hip osteoarthritis (OA) in adolescent and adult patients and to assess its association with exposure to the primary prevention campaign for DDH. METHODS: We included new patients with hip OA diagnosed from January 1, 2022, to December 31, 2022, at 12 core hospitals (8 special-function hospitals and 4 regional medical care support hospitals). The trend in the percentage of hips with a history of DDH treatment in childhood was estimated with use of a centered moving average using the birth year of the patient. We compared the prevalence of severe subluxation (Crowe type II, III, or IV) between patients with secondary hip OA due to hip dysplasia who were born in or before 1972 and those who were born in or after 1973. RESULTS: Overall, 1,095 patients (1,381 hips) were included. The mean age at the time of the survey was 63.5 years (range, 15 to 95 years). A total of 795 patients (1,019 hips; 73.8% of hips) were diagnosed with secondary OA due to hip dysplasia. Approximately 13% to 15% of hips among patients born from 1963 to 1972 had a history of DDH treatment in childhood; however, the percentage decreased among patients born in or after 1973. The prevalence of severe subluxation (Crowe type II, III, or IV) among patients born in or after 1973 was 2.4%, which was significantly less than that among patients born in or before 1972 (11.1%; odds ratio, 0.20; p < 0.001). CONCLUSIONS: As of 2022, secondary hip OA due to hip dysplasia is still responsible for most new cases of adolescent and adult hip OA seen in core hospitals in Japan. However, the perinatal education campaign initiated 50 years ago, which utilized a population approach and advocated for maintaining the hips of newborns in the naturally flexed-leg position, may have improved the environmental factors of DDH, as indicated by the apparently reduced need for treatment of DDH in childhood and the associated severe subluxation. This may result in a reduced need for challenging hip surgery later in life. LEVEL OF EVIDENCE: Prognostic Level III . See Instructions for Authors for a complete description of levels of evidence.

Protocol for the RETHINK study: a randomised, double-blind, parallel-group, non-inferiority clinical trial comparing acetaminophen and NSAIDs for treatment of chronic pain in elderly patients with osteoarthritis of the hip and knee.

INTRODUCTION: In patients with chronic pain, oral analgesics are essential treatment options to manage pain appropriately, improve activities of daily living abilities and achieve a higher quality of life (QOL). It is desirable to select analgesics for elderly patients based on comparative data on analgesic effect and risk of adverse events; however, there are few comparative studies so far. The purpose of this study is to determine whether the efficacy and safety of acetaminophen are non-inferior to non-steroidal anti-inflammatory drugs (NSAIDs) in the treatment of chronic pain associated with osteoarthritis of the hip and knee in elderly patients. METHODS AND ANALYSIS: This study is a multicentre, randomised controlled, double-blind, parallel-group study to compare the analgesic effect and adverse events between acetaminophen or NSAIDs (loxoprofen or celecoxib). A total of 400 elderly patients with osteoarthritis of the hip and knee will be recruited from five institutions in Japan. Patients of 65 years or older with osteoarthritis-related pain will be registered and randomly assigned to acetaminophen, loxoprofen or celecoxib with 2:1:1 allocation. The primary endpoint is change in the Brief Pain Inventory (BPI) item 3 (worst pain) score from baseline to week 8. The secondary endpoints are BPI item 3 score change from baseline to week 4, health-related QOL measured by Short Form-8 Health Survey, and occurrence of adverse events including gastrointestinal disorders and abnormal liver function. Data will be analysed in accordance with a predefined statistical analysis plan. ETHICS AND DISSEMINATION: This study protocol was approved by the Kyushu University Hospital Certified Institutional Review Board for Clinical Trials on 28 January 2021 (KD2020004) and the chief executive of each participating hospital. The results of the study will be submitted to international peer-reviewed journals, and the main findings will be presented at international scientific conferences. TRIAL REGISTRATION NUMBER: jRCTs071200112.

Cellular mechanisms underlying the rapid depolarization caused by oxygen and glucose deprivation in layer III pyramidal cells of the somatosensory cortex.

Cortical pyramidal neurons show rapid and irreversible membrane depolarization in response to oxygen-glucose depolarization (OGD). In this study, we investigated cellular mechanisms responsible for rapid depolarization caused by OGD in layer III pyramidal neurons of the mouse somatosensory cortex. When OGD solution was perfused in the presence of Ca2+ chelator and inhibitors of ryanodine receptors (RyRs) and inositol 1,4,5-trisphosphate receptors (IP3Rs) in the pipette solution or in the presence of inhibitors of NMDA receptors (NMDARs), voltage-gated Ca2+ channels (VGCCs), and canonical transient receptor potential (TRPC) channels in the perfusion solution, the latency of the rapid depolarization was significantly prolonged compared to the control. In addition, when OGD solution was perfused in the presence of scavengers of nitric oxide and reactive oxygen species in the perfusion solution or in the presence of calcineurin inhibitors in the pipette solution, the latency of the rapid depolarization was significantly prolonged compared to the control. These data indicate that OGD-induced intracellular Ca2+ increases mediated by Ca2+ influx through NMDARs, VGCCs and TRPC channels as well as by Ca2+ release from RyRs and IP3Rs lead to mitochondrial impairment, which may facilitate the generation of the rapid depolarization via dysfunction of Na+-K+-ATPase due to decreased ATP production.

Varus-valgus laxity correlates with pain in osteoarthritis of the knee.

Pain during osteoarthritis (OA) of the knee does not necessarily correlate with the severity of the radiographic grade, and the mechanism of pain has not been completely clarified. The purpose of this study was to evaluate risk factors for pain in the knee OA using epidemiologic analyses. We evaluated 518 out of 4183 people over the age of 40 (156 males and 362 females) from Shinyoshitomi village, Japan. Mean ages were 63.8 years for men and 60.7 years for women. Screening included a physical examination of the knee and a standing AP roentgenogram of the bilateral knee. Radiographic OA was defined as a Kellgren-Lawrence grade 2 or higher. All data were coded and pain risk factors were evaluated using a multiple logistic regression model. Radiographic OA was observed in 18.4% of men and 26% of women. Of these subjects with OA, 10.9% of men and 32.5% of women complained of knee pain. Seven factors-age, gender, BMI, radiographic grade, varus-valgus laxity, torque of quadriceps muscles, and varus-valgus alignment-were evaluated as potential risk factors for pain. A significant increase in the odds ratio was observed with varus-valgus laxity (p=0.005; odds ratio, 3.04). Our results suggest that varus-valgus laxity is a risk factor for pain during knee OA.

The anabolic response to parathyroid hormone is augmented in Rac2 knockout mice.

PTH is the only currently available anabolic therapy for osteoporosis. In clinical practice, the skeletal response to PTH varies and because therapy is limited to 2 yr, approaches to maximize the therapeutic response are desirable. Rac2 is a small GTPase that is expressed only in hematopoietic tissue. Rac2(-/-) mice have a slight increase in bone mass and osteoclasts isolated from these animals have reduced basal resorptive activity and reduced chemotaxis. To evaluate the anabolic response to PTH in Rac2(-/-) mice, we treated 18 Rac2(-/-) and 17 control, age-matched wild-type animals once daily for 28 d with 80 ng/g body weight of h(1-34)PTH. Treatment resulted in significantly greater increments in spinal, femur, and total bone density in the Rac2(-/-) as compared with wild-type animals. Microcomputed tomography analysis demonstrated greater increases in trabecular thickness and cortical thickness in the knockout mice. Interestingly, histomorphometric analysis showed an equivalent increase in osteoblast and osteoclast number in response to PTH treatment in both groups of animals. However, as judged by changes in serum markers, the resorptive response to PTH was impaired. Thus, telopeptide of type 1 collagen was 15.9+/-6.9 ng/ml after PTH treatment in the knockout animals and 26.8+/-11.1 ng/ml in the PTH-treated wild-type group. In contrast, serum aminoterminal propeptide of type 1 collagen and osteocalcin were equivalent in both groups. We conclude that, in the genetic absence of Rac2, the anabolic response to PTH is increased. This appears to be due to attenuated resorptive activity of osteoclasts.

Colony-stimulating factor-1 increases osteoclast intracellular pH and promotes survival via the electroneutral Na/HCO3 cotransporter NBCn1.

Colony-stimulating factor-1 (CSF-1) promotes the survival of osteoclasts, short-lived cells that resorb bone. Although a rise in intracellular pH (pH(i)) has been linked to inhibition of apoptosis, the effect of CSF-1 on pH(i) in osteoclasts has not been reported. The present study shows that, in the absence of CO(2)/HCO(3)(-), CSF-1 causes little change in osteoclast pH(i). In contrast, exposing these cells to CSF-1 in the presence of CO(2)/HCO(3)(-) causes a rapid and sustained cellular alkalinization. The CSF-1-induced rise in pH(i) is not blocked by 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid, an inhibitor of HCO(3)(-) transporters but is abolished by removing extracellular sodium. This inhibition profile is similar to that of the electroneutral Na/HCO(3) cotransporter NBCn1. By RT-PCR, NBCn1 transcripts are present in both osteoclasts and osteoclast-like cells (OCLs), and by immunoblotting, the protein is present in OCLs. Moreover, CSF-1 promotes osteoclast survival in the presence of CO(2)/HCO(3)(-) buffer but not in its absence. Preventing the activation of NBCn1 markedly attenuates the ability of CSF-1 to 1) block activation of caspase-8 and 2) prolong osteoclast survival. Inhibiting caspase-3 or caspase-8 in OCLs prolongs osteoclast survival to the same extent as does CSF-1. This study provides the first evidence that osteoclasts express a CSF-1-regulated Na/HCO(3) cotransporter, which may play a role in cell survival.

Nicotinic activity depresses synaptic potentiation in layer V pyramidal neurons of mouse insular cortex.

The insular cortex is a critical brain region involved in nicotine addiction. However, its specific cellular and synaptic mechanisms underlying nicotine addiction remains largely unknown. In the present study, we examined how nicotine modulates synaptic transmission and plasticity in layer V pyramidal neurons of the mouse insular cortex. We also examined which type of neurons express functional nicotinic acetylcholine receptors (nAChRs) in layer V of the insular cortex. We found that nicotine suppresses synaptic potentiation induced by combination of presynaptic stimulation with postsynaptic depolarization (paired training). An application of nicotine significantly enhanced both spontaneous excitatory postsynaptic currents (EPSCs) and inhibitory postsynaptic currents (IPSCs): the former effect was mediated by activation of ß2-containing nAChRs while the latter one was mediated largely by activation of ß2-containing nAChRs and to a minor extent by activation of α7-containing nAChRs. The application of nicotine significantly enhanced evoked IPSCs but had no effect on evoked EPSCs. We also found that in layer V of the mouse insular cortex, majority of non-fast-spiking (non-FS) interneurons have ß2-containing nAChRs while about half of pyramidal neurons and FS interneurons have functional nAChRs. Blockade of GABAA receptors or ß2-containing nAChRs prevented the effects of nicotine on synaptic potentiation. Taken together, these results suggest that in layer V pyramidal neurons of the insular cortex, activation of ß2-containing nAChRs expressed in non-FS interneurons suppresses synaptic potentiation through enhancing GABAergic synaptic transmission. These findings provide important insights into the cellular and synaptic mechanisms of insular cortical changes in nicotine addiction.

The oblique posterior femoral condylar radiographic view following total knee arthroplasty.

BACKGROUND: It is often difficult to evaluate the posterior aspects of the femoral condyles after total knee arthroplasty. We have developed an imaging technique involving the use of the oblique posterior condylar view for the evaluation of the posterior aspects of the femoral condyles. The purpose of the present study was to compare the efficacy of this view with that of the true-lateral view. METHODS: Three orthopaedic surgeons analyzed fifty-five sets of radiographs (consisting of oblique posterior condylar and true-lateral views) for patients who had undergone total knee arthroplasty. The accuracy and reproducibility of the oblique posterior condylar view for the detection of radiolucencies were compared with those of the true-lateral view. RESULTS: The oblique posterior condylar view was significantly better than the true-lateral view for the detection of radiolucencies of the posterior aspects of the femoral condyles (p < 0.0005). CONCLUSIONS: Radiographic analysis with use of the oblique posterior condylar view is technically easy and is accurate for the evaluation of radiolucencies of the posterior aspects of the femoral condyles after total knee arthroplasty.

Alignment in total knee arthroplasty following failed high tibial osteotomy.

In total knee arthroplasty (TKA) following failed high tibial osteotomy, the mechanical axis does not intersect the center of the tibial component if the tibia has been resected perpendicular to the anatomical axis. Therefore, tibial resection referencing the predicted postoperative mechanical axis instead of the tibial shaft axis is advocated. To obtain the optimal tibial resection, characteristics of the tibial proximal deformity were measured radiographically and predicted postoperative lower limb alignment was calculated using full-length, weight-bearing, lower limb anteroposterior radiographs. Two finite element analysis models also were examined. The proximal tibia was resected perpendicular to the tibial shaft axis in model 1, and perpendicular to the predicted postoperative tibial mechanical axis in model 2. When the proximal tibia was resected perpendicular to the tibial shaft axis, the predicted lower limb mechanical axis was significantly shifted medially to the center of the tibial joint surface. The results of the finite element analysis reflected the medial shift of the lower limb mechanical axis in model 1, where stresses were increased in the medial tibial compartment. Tibial resection referencing the predicted postoperative tibial mechanical axis, instead of the tibial shaft axis, should be performed, especially in cases with a deformed tibia.

[Bone quantity and quality to its mechanical integrity].

Bone strength is made up of quantity (mass, mineralization), geometry (anatomy, micro architecture, collagen structure), and turnover/damage accumulation. While most of the mechanical behavior can be explained by measures of porosity, several additional descriptors of the geometry have been proposed for better predictions of fracture risk. This review introduces various aspects of these relationships between bone quantity and quality to its mechanical integrity.

LIM kinase 1 deficient mice have reduced bone mass.

The cytoskeleton determines cell shape and is involved in cell motility. It also plays a role in differentiation and in modulating specialized cellular functions. LIM kinase 1 (LIMK1) participates in cytoskeletal remodeling by phosphorylating and inactivating the actin-severing protein, cofilin. Severing F-actin to release G-actin monomers is required for actin cytoskeletal remodeling. Although less well established, LIMK1 may also influence the cell cycle and modulate metalloproteinase activity. Since the role of LIMK1 in bone cell biology has not been reported, the skeletal phenotype of LIMK1(-/-) mice was examined. LIMK1(-/-) mice had significantly reduced trabecular bone mass when analyzed by microCT (p<0.01). Histomorphometric analyses demonstrated a 31% reduction in the number of osteoblasts (p=0.0003) and a 23% reduction in osteoid surface (p=0.0005). The number of osteoclasts was no different in control and knock out animals. Consistent with the in vivo findings in osteoblasts, the number of osteoblast colony forming units in LIMK1(-/-) bone marrow was reduced by nearly 50%. Further, osteoblasts isolated from LIMK1(-/-) mice showed significantly reduced rates of mineralization in vitro. Osteoclasts from LIMK1(-/-) mice evidenced more rapid cytoskeletal remodeling in response to treatment with CSF1. In keeping with this latter finding, basal levels of phospho-cofilin were reduced in LIMK1(-/-) osteoclasts. LIMK1(-/-) osteoclasts also resorbed dentine slices to a greater extent in vitro and were more active in a pit assay. These data support the hypothesis that LIMK1 is required for normal osteoblast differentiation. In addition, its absence leads to increased cytoskeletal remodeling and bone resorption in osteoclasts.

Two subtypes of radiographic osteoarthritis in the distal interphalangeal joint of the hand.

BACKGROUND: The etiology and pathogenesis of hand osteoarthritis (OA) are not completely clarified, and several factors may cooperate in a multifactorial fashion in its development. The purpose of this study was to clarify the effects of the dominant hand that contribute to the development of distal interphalangeal (DIP) joint OA using epidemiological analyses. METHODS: A total of 518 subjects (156 men, 362 women) in a rural community were analyzed. Their mean age was 63.8 years for men and 60.7 years for women. Anteroposterior (AP) standing radiographs of bilateral knees, lateral views of the lumbar spine, and AP views of bilateral hands were obtained. Furthermore, a survey of their life patterns was conducted using self-administered questionnaires. Radiographic osteoarthritis was defined as Kellgren and Lawrence grade 2 or higher. Hand OA was limited to Heberden's nodes. Generalized OA (GOA) was defined as bilateral knee OA plus lumbar spine OA. RESULTS: GOA was observed in 13.0% of the subjects. The incidence of DIP joint OA was significantly higher in the GOA group than that in the non-GOA group. In the GOA group, the incidence of right-hand DIP joint OA in right-handed and left-handed subjects was 37.5% and 40.0%, respectively, without a significant difference. In the non-GOA group, however, the incidence of right-hand DIP joint OA in right-handed and left-handed subjects was 16.4% and 3.2%, respectively, with a significant difference. With a multiple logistic regression model, the P value of the handedness was marginal (0.060), but a clear tendency of increase in the odds ratio (7.129) was observed in the dominant hand for the non- GOA group. In contrast, there was no effect of the handedness on right-hand DIP joint OA in the GOA group. CONCLUSIONS: There are two subtypes of hand DIP joint OA in terms of the etiology. One is environmental, and the other is genetic.

Mechanical effects of the intraarticular administration of high molecular weight hyaluronic acid plus phospholipid on synovial joint lubrication and prevention of articular cartilage degeneration in experimental osteoarthritis.

OBJECTIVE: To examine in vivo the effects of a mixture of high molecular weight hyaluronic acid (HA) plus phospholipids on joint lubrication and articular cartilage degeneration. METHODS: Experimental osteoarthritis (OA) of the right knee was induced by anterior cruciate and medial collateral ligament transection in 40 rabbits. The animals were subjected to 8 consecutive weekly intraarticular administrations of high molecular weight HA (the HA200 group), conventional molecular weight HA (the HA80 group), or high molecular weight HA plus L-delta dipalmitoyl phosphatidylcholine liposomes (the PHA group) and were killed 1 week after the final injection. The remaining transected right knees (the OA group) and randomly selected nontransected contralateral left knees (the control group) were collected simultaneously. Each group (n = 10) was divided into 2 equal subgroups, one of which was evaluated histologically while the other was subjected to a lubricating ability test using a pendulum friction tester. RESULTS: The injected knees had a tendency to demonstrate less damage to the articular cartilage compared with the OA group, and the histologic findings in all groups except for the PHA group differed significantly from the control group. There was a significant difference in the mean +/- SD friction coefficient between the control group (0.0100 +/- 0.00300) and the OA (0.0206 +/- 0.00649), HA200 (0.0190 +/- 0.00427), and HA80 (0.0177 +/- 0.00712) groups (P < 0.05 for each comparison), but not between the control group and the PHA group (0.0150 +/- 0.00330) (P = 0.15). CONCLUSION: To our knowledge, this is the first in vivo study to examine whether intraarticular injections of phospholipids influence joint lubrication by acting as a boundary lubricant, thus protecting articular cartilage from degenerative changes.