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Modern trends in joint biotribology are presented. The extent of the achievements in this field at the turn of the 21st century is discussed. This period is distinguished by the discovery of liquid-crystalline and quasi-electret states in synovial liquids; ascertainment by AFM of new boundary lubrication mechanisms in joints, which are realized at the nanolevel; and development of methods for in vitro study of friction in joints using electromagnetic fields able to simulate the natural articular biofield. A relationship is shown between biotribology and the chief directions in contemporary orthopedics including: intraarticular chondroprotection exercised via local therapeutic methods based on tribological monitoring of pharmaceutic substances; injection of drugs based on blood serum; and development of a new generation of articular endoprostheses able to simulate the biophysical properties of synovial joints. It is shown that progress in modern biotribology has provided scientific substantiation of orthopedic treatment procedures.

Resumen El manejo de la artrosis (OA) constituye un importante reto. La mayoria de las recomendaciones publicadas van dirigidas a controlar los sintomas de la OA, es decir, reducir el dolor y mejorar la funcion articular. Sin embargo, el principal objetivo a alcanzar en el tratamiento de la OA seria retrasar o detener la progresion de la enfermedad. En funcion de este objetivo, las diferentes terapias deben ayudar a preservar la integridad de la articulacion a traves del control de la degradacion del cartilago, la inflamacion sinovial y la esclerosis del hueso subcondral, los 3 tejidos involucrados en la fisiopatologia de la OA. Esto debe tenerse en cuenta tanto para el desarrollo de futuros tratamientos como para los farmacos disponibles actualmente. El condroitin sulfato (CS) forma parte de los denominados SYSADOA (del ingles symptomatic slow acting drugs for osteoarthritis) que define a un grupo de farmacos de accion lenta para el tratamiento sintomatico de la OA. Existe, sin embargo, un cuerpo de evidencia creciente que demuestra su efecto DMOAD (del ingles disease modifying osteoarthritis drugs), es decir, farmacos de accion lenta para la OA capaces de modificar la estructura. Esta revision tiene por objeto recopilar y sintetizar la informacion acerca del efecto protector que el CS ejerce sobre el cartilago, asi como su capacidad de preservar las cualidades del hueso subcondral.

Summary Objective To perform a molecular mechanism-based investigation of the chondroprotective potential of hylan G-F 20. Method The effects of hylan G-F 20 on IL-1β-induced glycosaminoglycan (GAG) depletion and matrix metalloproteinase (MMP) expression in bovine and human cartilage explants were evaluated. Three weekly intra-articular hylan G-F 20 or control injections were administered 4 weeks post-operatively to rabbits with surgically induced osteoarthritis (OA). Cartilage histopathologic scores and osteophyte size were evaluated at 1, 4, and 8 weeks post-injections. Histomorphometry and immunostaining were used to quantify cartilage area and type II collagen (Col II) intensity, and real-time polymerase chain reaction (PCR) was used to examine the mRNA levels of Col2A1 , MMP-13 , - 16 and IL-1β at 1 week. Results Hylan G-F 20 retained GAG in IL-1β-exposed bovine and human cartilage explants and abrogated IL-1β-mediated increases in MMP-1, -3, and -13 in human explant culture. Hylan G-F 20‒treated OA joints had significantly better cartilage integrity at 1 and 4 weeks post-treatment and significantly smaller osteophytes at 4 weeks compared with control. Col2A1 mRNA increased with hylan G-F 20 treatment, which correlated with a trend toward increased Col II immunostaining. MMP - 13 and - 16 mRNAs increased in OA cartilage, but were not significantly altered by hylan G-F 20. IL-1β mRNA was undetectable in cartilage and unaltered in the synovium. Conclusions Hylan G-F 20 improved cartilage integrity and decreased osteophyte formation in the rabbit model of OA. Our results suggest that hylan G-F 20 may stimulate cartilage repair by increasing Col II, and inhibit IL-1β-mediated matrix degradation by decreasing MMPs.

Objetivo Evaluar la eficacia y seguridad de una unica inyeccion intraarticular de acido hialuronico (AH)+manitol en artrosis de rodilla (AR). Material y metodo Estudio prospectivo, abierto, no-comparativo con 80 pacientes diagnosticados de AR, de los cuales 79 finalizaron el estudio. Recibieron una inyeccion intraarticular de 2ml de AH al 2%+manitol al 0,5% (dia 0) y fueron monitorizados durante 6 meses. Los dias 0, 15, 30, 60, 90, 120, 150 y 180 se evaluaron dolor y funcionalidad articular mediante una escala analogica visual (EAV) y el indice WOMAC, eficacia y seguridad segun medico y paciente, y medicacion de rescate como medida indirecta del dolor. Resultados Disminucion significativa del dolor articular, rigidez e incapacidad funcional en comparacion con el valor inicial en todas las visitas (p

It has been demonstrated that pulsed electromagnetic field (PEMF) stimulation has a chondroprotective effect on osteoarthritis (OA) progression in the knee joints of the 12-month-old guinea pigs. The aim of the present study was to discover whether the therapeutic efficacy of PEMFs was maintained in older animals also in more severe OA lesions. PEMFs were administered daily (6 h/day for 6 months) to 15-month-old guinea pigs. The knee joints (medial and lateral tibial plateaus, medial and lateral femoral condyles) were evaluated by means of a histological/histochemical Mankin modified by Carlsson grading score and histomorphometric measurements of cartilage thickness (CT), fibrillation index (FI), subchondral bone thickness (SBT) and epiphyseal bone microarchitecture (bone volume: BV/TV; trabecular thickness: Tb.Th; trabecular number: Tb.N; trabecular separation: Tb.SP). Periarticular knee bone was also evaluated with dual X-ray absorptiometry (DXA). PEMF stimulation significantly changed the progression of OA lesions in all examined knee areas. In the most affected area of the knee joint (medial tibial plateau), significant lower histochemical score (p

Summary Objective To compare the effects of glucosamine (GlcN), curcumin, and diacerein in immortalized human C-28/I2 chondrocytes at the cellular and the gene expression level. This study aimed to provide insights into the proposed beneficial effects of these agents and to assess the applicability of the C-28/I2 cell line as a model for the evaluation of chondroprotective action. Methods Interleukin-1beta (IL-1β)-stimulated C-28/I2 cells were cultured in the presence of GlcN, curcumin, and diacerein prior to the evaluation of parameters such as viability, morphology and proliferation. The impact of GlcN, curcumin, and diacerein on gene expression was determined using quantitative real-time RT-PCR (qPCR). Results At the transcriptional level, 5mM GlcN and 50μM diacerein increased the expression of cartilage-specific genes such as aggrecan (AGC) and collagen type II (COL2), while reducing collagen type I (COL1) mRNA levels. Moreover, the IL-1β-mediated shift in gene expression pattern was antagonized by GlcN and diacerein. These effects were associated with a significant reduction in cellular proliferation and the development of chondrocyte-specific cell morphology. In contrast, curcumin was not effective at lower concentrations but even damaged the cells at higher amounts. Conclusions Both GlcN and diacerein promoted a differentiated chondrocytic phenotype of immortalized human C-28/I2 chondrocytes by altering proliferation, morphology, and COL2/COL1 mRNA ratios. Moreover, both agents antagonized inhibitory effects of IL-1β by enhancing AGC and COL2 as well as by reducing COL1 mRNA levels.

Many compounds are being investigated for the control of symptoms of osteoarthritis in people and animals. Ideally, treatment should include analgesia, inflammation control, and chondroprotection. With further progress in this area, combination therapies tailored to the needs of the individual animal should enable us to maximize efficacy and minimize side effects. Only a few of the newer therapies and pharmaceutic agents have been investigated in the horse, however. With more rigorous investigation, they may be determined to be ineffective or unsafe. Meanwhile, as much information should be gathered from manufacturers as possible so as to ensure that appropriate recommendations are made.

Systematic review of overlapping meta-analyses shows that platelet-rich plasma improves knee pain and function in patients with knee osteoarthritis. Ultimately, biologics hold promise for chondroprotection in addition to symptomatic relief.

Osteoarthritis is the most prevalent rheumatic disease. Inasmuch as osteoarthritis is predominantly idiopathic, current treatment is aimed not at a cure but palliative management. Research, however, has made considerable forward strides with respect to feasibility of new methods for diagnostic markers of early disease and disease progression, as well as methods to conserve articular damage. This article briefly describes the authors' experience with the use of one type of surgical repair and five different medicinal agents for cartilage conservation.

Rationale The aim of the treatment of osteoarthritis (OA) is to improve symptoms and function; ideally, treatment would also prevent the structural progression of the disease. The targets of structure-modifying OA drugs (STMOADs) can be one of the various lesions of OA, including cartilage destruction, osteophytes, bone sclerosis, cysts, and bone attrition. However, prevention of cartilage destruction (chondroprotection) is currently accepted as the most promising target of STMOADs. The possibility of preventing progression of cartilage damage has been demonstrated in various animal models of OA. Chondroprotection is now being investigated in human OA. Several trials are in progress, and two positive studies have already been reported 1,2 . The goal of these initial trials was mainly to demonstrate that a reduction of the natural progression of OA joint space narrowing is possible in humans. Today, chondroprotection is no longer considered a myth, and the questions now are whether STMOADs provide a clinical benefit for the patient and how to evaluate that benefit. These new and relevant questions are difficult to answer. Can we expect a clinical benefit from STMOADs? Drugs evaluated for a structure-modifying effect may or may not also have symptomatic effects in the short term. STMOADs with a symptomatic effect can be expected to lead to clinical improvement in the OA patient in the long term. Evaluation of the clinical benefit of STMOADs could be possible with the tools presently used for the assessment of symptom-modifying drugs in OA. The clinical benefit that can be expected from a drug without known symptomatic effects but with a structuremodifying effect and how to measure that clinical benefit are as yet unknown. An effective STMOAD is not expected to induce a repair of the structural lesions of OA, but it is expected to stop or decrease their progression. Such a structural effect in the long term might result in symptom improvement or might only prevent a progression of symptoms. It also might have no clinical effect, since symptoms and lesions are poorly correlated in OA patients. The time required to demonstrate the clinical benefit of a STMOAD is unknown. It is possible that there may be a long delay (several years) between the beginning of STMOAD efficacy and the realization of any clinical benefit. The extent of clinical benefit could be related to the degree of effectiveness of the STMOAD. If this were true, the delay in clinical benefit could be very long for drugs able to only partially reduce the structural progression of the disease. Finally, the clinical benefit of a STMOAD might be missed by our usual tools and could require new methods of evaluation.