scholarly journals Etiology, pathophysiology and conservative management of degenerative joint disease

2002 ◽  
Vol 55 (1-2) ◽  
pp. 35-39
Author(s):  
Slavica Jandric

Etiology of degenerative joint diseases Etiology of degenerative joint diseases is still not clearly understood and there is no specific management for this group of diseases. Various pathological conditions cause damage of the articular cartilage and lead to clinically and radiographically recognized impairment. Biomechanical, metabolic, genetic factors inflammation and other risk factors contribute to development of osteoarthrosis. Pathophysiology of degenerative joint diseases Osteoarthrosis is characterized by progressive erosion of articular cartilage and bone overgrowth at the joint margins. Cartilage integrity requires balance between synthesis and degradation of matrix components. Chondrocytes react to various mechanical and chemical stresses in order to stabilize and restore the tissue. Failures in stabilizing and restoring the tissue lead to cartilage degeneration that may be irreversibile. For better understanding of conservative management of degenerative joint diseases it is important to know the impact of pathophysiology mechanisms on development of degenerative joint diseases. There is great variability in the rate of progression of erosive processes in articular cartilage in clinical radiographic signs and course of the disease. This is in relation with many factors, as well as with management and response to therapy. Treatment of degenerative joint diseases Treatment should vary depending on the severity of disease and patient's expectations and level of activity. Besides analgesic and anti-inflammatory drugs, conventional and not conventional treatment and techniques can be used for management of osteoarthrosis. Physical therapy and exercises are very important for maintaining muscle strength, joint stability and mobility, but should be closely monitored for optimal efficacy.

BMJ Open ◽  
2018 ◽  
Vol 8 (2) ◽  
pp. e017442 ◽  
Author(s):  
Yuan-Yang Cheng ◽  
Chung-Lan Kao ◽  
Shih-Yi Lin ◽  
Shin-Tsu Chang ◽  
Tz-Shiang Wei ◽  
...  

ObjectivesIt has been proven that statin can protect synovial joints from developing osteoarthritis through its anti-inflammatory effects. However, studies on the effect of statins on spinal degenerative joint diseases are few and limited to in vitro studies. Therefore, we investigated the relationship between the statin dosage and the development of spinal degenerative joint diseases.DesignA retrospective cohort study.SettingPatients registered in Taiwan National Health Insurance Research Database.ParticipantsPatients aged 40–65 years old from 2001 to 2010 were included. Those who received statin treatment before 2001, were diagnosed with spinal degenerative joint diseases or received any spinal surgery before 2004 or had any spinal trauma before 2011 were excluded. A total of 7238 statin users and 164 454 non-users were identified and followed up for the next 7 years to trace the development of spinal degenerative joint disease.Outcome measuresThe incident rate of spinal degenerative joint diseases and HRs among the groups treated with different statin dosages.ResultsA higher dosage of statins was associated with a significantly lower risk of developing spinal degenerative joint disease in patients with hypercholesterolaemia. Compared with the group receiving less than 5400 mg of a statin, the HR of the 11 900–28 000 mg group was 0.83 (95% CI 0.70 to 0.99), and that of the group receiving more than 28 000 mg was 0.81 (95% CI 0.68 to 0.97). Results of subgroup analysis showed a significantly lower risk in men, those aged 50–59 years and those with a monthly income less than US$600.ConclusionsOur study’s findings clearly indicated that a higher dosage of statins can reduce the incidence of spinal degenerative joint disease in patients with hypercholesterolaemia, and it can be beneficial for people with a higher risk of spine degeneration.


2017 ◽  
Vol 60 (1) ◽  
pp. 225-232
Author(s):  
Szymon Czech ◽  
Jacek Hermanson ◽  
Piotr Rodak ◽  
Tomasz Stołtny ◽  
Łukasz Rodak ◽  
...  

Abstract An adequate level of physical activity has a substantial effect on both mental and physical human health. Physical activity is largely dependent on the function of the musculoskeletal and articular system. One of the most frequent diseases of this system is degenerative joint disease. Due to the changing and more demanding lifestyles and patients’ willingness to be involved in sports activity, the expectations of hip joint arthroplasty are becoming increasingly high. Alleviating pain ceases to be the only reason for which patients choose surgical interventions, while the expectations often include involvement in various sports. Only few studies contain recommendations concerning the frequency, type and intensity of sports activity which are acceptable after hip joint arthroplasty. The aim of the study was to evaluate function and physical activity of people following cementless short-stem hip joint arthroplasty in the observation of at least five years. The study group comprised 106 patients who underwent total hip arthroplasty due to degenerative joint diseases, chosen according to inclusion criteria. Patients underwent routine physical examinations following the Harris Hip Score protocol, responded to the UCLA scale and questionnaires concerning pre-surgical and current physical activity. Our results demonstrated that hip joint arthroplasty in people suffering from degenerative joint diseases has a beneficial effect on their level of functioning and physical activity. Although physical activity and the level of functioning obviously reduced as a person aged, the level of physical activity continued to be very high in both groups, with function of the hip joint evaluated as very good.


2021 ◽  
Author(s):  
Ding-Chao Zhu ◽  
Yi-Han Wang ◽  
Jia-Hao Lin ◽  
Zhi-Min Miao ◽  
Jia-Jing Xu ◽  
...  

Osteoarthritis (OA) is a common degenerative joint disease characterized by articular cartilage degeneration and inflammation. Currently, there is hardly any effective treatment for OA due to its complicated pathology and...


2021 ◽  
Vol 7 (1) ◽  
pp. 9-13
Author(s):  
A. Vol'nyagina ◽  
Elena Belyaeva

Osteoarthritis (OA) is the most common joint disease with high comorbidity. Among comorbid diseases in patients with OA, diseases of the cardiovascular system are in the first place. It is known that comorbid diseases mutually aggravate the course of each of the existing nosologies.It is important to study the impact of concomitant diseases in patients with OA on the quality and duration of life, to analyze the factors that contribute to an increased risk of cardiovascular disasters in patients with degenerative and destructive joint diseases.


2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Guiqiang Miao ◽  
Xuehui Zang ◽  
Huige Hou ◽  
Hui Sun ◽  
Lihui Wang ◽  
...  

Osteoarthritis (OA) is a chronic degenerative joint disease, where chondrocyte apoptosis is responsible for cartilage degeneration. Bax is a well-known proapoptotic protein of the Bcl-2 family, involved in a large number of physiological and pathological processes. However, the regulation mechanisms of Bax underlying chondrocyte apoptosis in OA remain unknown. In the present study, we determined the role of Bax in human OA and chondrocyte apoptosis. The results showed that Bax was upregulated in chondrocytes from the articular cartilage of OA patients and in cultured chondrocyte-like ATDC5 cells treated by IL-1β. Bax was identified to be the direct target of miR-29a by luciferase reporter assay and by western blotting. Inhibition of miR-29a by the mimics protested and overexpression by miR-29a inhibitors aggravated ATDC5 apoptosis induced by IL-1β. These data reveal that miR-29a/Bax axis plays an important role in regulating chondrocyte apoptosis and suggest that targeting the proapoptotic protein Bax and increasing expression levels of miR-29a emerge as potential approach for protection against the development of OA.


Cells ◽  
2020 ◽  
Vol 9 (4) ◽  
pp. 927 ◽  
Author(s):  
Szu-Yu Chien ◽  
Chun-Hao Tsai ◽  
Shan-Chi Liu ◽  
Chien-Chung Huang ◽  
Tzu-Hung Lin ◽  
...  

Osteoarthritis (OA) is a chronic inflammatory and progressive joint disease that results in cartilage degradation and subchondral bone remodeling. The proinflammatory cytokine interleukin 1 beta (IL-1β) is abundantly expressed in OA and plays a crucial role in cartilage remodeling, although its role in the activity of chondrocytes in cartilage and subchondral remodeling remains unclear. In this study, stimulating chondrogenic ATDC5 cells with IL-1β increased the levels of bone morphogenetic protein 2 (BMP-2), promoted articular cartilage degradation, and enhanced structural remodeling. Immunohistochemistry staining and microcomputed tomography imaging of the subchondral trabecular bone region in the experimental OA rat model revealed that the OA disease promotes levels of IL-1β, BMP-2, and matrix metalloproteinase 13 (MMP-13) expression in the articular cartilage and enhances subchondral bone remodeling. The intra-articular injection of Noggin protein (a BMP-2 inhibitor) attenuated subchondral bone remodeling and disease progression in OA rats. We also found that IL-1β increased BMP-2 expression by activating the mitogen-activated protein kinase (MEK), extracellular signal-regulated kinase (ERK), and specificity protein 1 (Sp1) signaling pathways. We conclude that IL-1β promotes BMP-2 expression in chondrocytes via the MEK/ERK/Sp1 signaling pathways. The administration of Noggin protein reduces the expression of IL-1β and BMP-2, which prevents cartilage degeneration and OA development.


2008 ◽  
Vol 60 (1) ◽  
pp. 93-102 ◽  
Author(s):  
G. Gonçalves ◽  
E.G. Melo ◽  
M.G. Gomes ◽  
V.A. Nunes ◽  
C.M.F. Rezende

Samples of articular cartilage of femur, tibia and patella of 15 dogs with experimentally induced degenerative joint disease (DJD) were microscopically analyzed. Animals were distributed into three groups (n=5): the control group received no medication; the second group was treated with chondroitin sulfate and the third received sodium hyaluronate. Samples were processed and stained with HE and toluidine blue for morphological evaluation. The metabolic and proliferative activity of the chondrocytes was evaluated by the measurement of nucleolar organizer regions (NORs) after impregnation by silver nitrate. Significant differences were not observed (P>0.05) in the morphology among the groups, however, the group treated with sodium hyaluronate had a higher score suggesting a trend to a greater severity of the lesions. Significant differences were not observed (P>0.05) in the measurement of NORs, cells and NORs/cells among the groups. Although differences were not significant, sodium hyaluronate group showed higher NOR and cell counts which suggested an increase of the proliferation rate of chondrocytes. In addition, a higher NOR/cell ratio in the group treated with chondroitin sulfate suggested that this drug may have stimulated the metabolic activity of the chondrocytes, minimizing the lesions resulting from DJD.


Biomolecules ◽  
2020 ◽  
Vol 10 (4) ◽  
pp. 637 ◽  
Author(s):  
Paula Carpintero-Fernandez ◽  
Marta Varela-Eirin ◽  
Alessandra Lacetera ◽  
Raquel Gago-Fuentes ◽  
Eduardo Fonseca ◽  
...  

Osteoarthritis (OA) is the most common degenerative joint disease characterized by articular cartilage degradation and joint degeneration. The articular cartilage is mainly formed by chondrocytes and a collagen-proteoglycan extracellular matrix that contains high levels of glycosylated proteins. It was reported that the shift from glycoproteins containing α-2,6-linked sialic acids to those that contain α-2,3 was associated with the onset of common types of arthritis. However, the pathophysiology of α-2,3-sialylation in cartilage has not been yet elucidated. We show that cartilage from osteoarthritic patients expresses high levels of the α-2,3-sialylated transmembrane mucin receptor, known as podoplanin (PDPN). Additionally, the Maackia amurensis seed lectin (MASL), that can be utilized to target PDPN, attenuates the inflammatory response mediated by NF-kB activation in primary chondrocytes and protects human cartilage breakdown ex vivo and in an animal model of arthritis. These findings reveal that specific lectins targeting α-2,3-sialylated receptors on chondrocytes might effectively inhibit cartilage breakdown. We also present a computational 3D molecular model for this interaction. These findings provide mechanistic information on how a specific lectin could be used as a novel therapy to treat degenerative joint diseases such as osteoarthritis.


Author(s):  
T. Vaughan-Scott ◽  
J.H. Taylor

Osteoarthritis or degenerative joint disease is a condition characterised by degeneration of articular cartilage often associated with the formation of new bone at joint surfaces or margins. Commonly encountered in dogs, osteoarthritis may have a gradual onset, but may also occur acutely. Osteoarthritis can be a primary disease of joint cartilage, but is more often secondary to abnormal stresses on joints. This article describes the pathogenesis and progression of cartilage degeneration as well as the dietary, lifestyle and pharmacological management of osteoarthritis. Recent pharmacological developments allow the clinician not only to control clinical signs of the disease, but also to slow the progression of cartilage degeneration.


Sign in / Sign up

Export Citation Format

Share Document