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Medicina (Kaunas, Lithuania) Nov 2020Osteoarthritis (OA) is the most well-known degenerative disease among the geriatric and is a main cause of significant disability in daily living. It has a... (Review)
Review
Osteoarthritis (OA) is the most well-known degenerative disease among the geriatric and is a main cause of significant disability in daily living. It has a multifactorial etiology and is characterized by pathological changes in the knee joint structure including cartilage erosion, synovial inflammation, and subchondral sclerosis with osteophyte formation. To date, no efficient treatment is capable of altering the pathological progression of OA, and current therapy is broadly divided into pharmacological and nonpharmacological measures prior to surgical intervention. In this review, the significant risk factors and mediators, such as cytokines, proteolytic enzymes, and nitric oxide, that trigger the loss of the normal homeostasis and structural changes in the articular cartilage during the progression of OA are described. As the understanding of the mechanisms underlying OA improves, treatments are being developed that target specific mediators thought to promote the cartilage destruction that results from imbalanced catabolic and anabolic activity in the joint.
Topics: Aged; Cartilage, Articular; Cytokines; Humans; Inflammation; Knee Joint; Osteoarthritis
PubMed: 33207632
DOI: 10.3390/medicina56110614 -
Cureus Jun 2023Osteoarthritis (OA) is a common chronic degenerative disease. The prevalence tends to increase with age and is influenced by underlying risk factors such as gender,... (Review)
Review
Osteoarthritis (OA) is a common chronic degenerative disease. The prevalence tends to increase with age and is influenced by underlying risk factors such as gender, obesity, joint injuries (work/sports activities), and geographic region. OA has a distinctive picture, namely, damage to the joint cartilage and the formation of new bone at the edges of the bones, also called osteophytes, due to biochemical, metabolic, physiological, and pathological changes in the joint cartilage and subchondral bone. Symptoms that can be caused include joint pain, inhibition of joint movement, crepitus, deformity, asymmetrical swelling of the joints, signs of inflammation, and changes in gait. Currently, there are various methods of managing OA in terms of reducing pain, including regeneration and non-regeneration therapy. Non-regeneration treatments include physiotherapy (exercise, biomechanical intervention, electrotherapy, diathermy), pharmacology, intra-articular injections (corticosteroids, hyaluronic acid, geniculate nerve blocks), extra-articular injections, and radiofrequency. In comparison, regeneration management includes laser and intra-articular injection (prolotherapy and PRP).
PubMed: 37503484
DOI: 10.7759/cureus.40966 -
Current Reviews in Musculoskeletal... Apr 2020The goal of this review is to introduce surgical decision-making pearls for reverse shoulder arthroplasty and describe optimization of surgical exposure for reverse... (Review)
Review
PURPOSE OF REVIEW
The goal of this review is to introduce surgical decision-making pearls for reverse shoulder arthroplasty and describe optimization of surgical exposure for reverse shoulder arthroplasty.
RECENT FINDINGS
While the technology of reverse shoulder replacement and the associated prosthetic options have expanded, the principles involved in successfully exposing the humerus and glenoid in arthroplasty remain the same. Reverse shoulder replacement should be considered in arthroplasty situations with rotator cuff disease, deformity, bone loss, and instability as part of the diagnosis. Optimal exposure in reverse shoulder arthroplasty can be obtained by (1) releasing deltoid adhesions, (2) removal of humeral osteophytes, (3) generous humeral head cuts, (4) thorough humeral and glenoid capsular release and (5) optimal glenoid retractor placement. Neuromuscular paralysis can also aid glenoid exposure.
PubMed: 32147779
DOI: 10.1007/s12178-020-09613-3 -
Aging Dec 2020Osteoarthritis is a chronic degenerative disease that can lead to restricted activity or even disability. Bone marrow mesenchymal stem cells can repair cartilage damage...
Osteoarthritis is a chronic degenerative disease that can lead to restricted activity or even disability. Bone marrow mesenchymal stem cells can repair cartilage damage and treat osteoarthritis via cell therapies or in-tissue engineering. Research has shown that the paracrine mechanism is the main mode of action of mesenchymal stem cells. Exosomes are the smallest known membrane-bound nanovesicles. Exosomes are also important carriers of paracrine delivery agents and promote communication between cells. We demonstrated that bone marrow mesenchymal stem cell-derived exosomes can delay the progression of osteoarthritis. Exosomes alleviate cartilage damage, reduce osteophyte formation and synovial macrophage infiltration, inhibit M1 macrophage production and promote M2 macrophage generation. In synovial fluid, the expression levels of the proinflammatory cytokines, IL-1β, IL-6, and TNF-α were decreased and the release of the anti-inflammatory cytokine, IL-10 was increased. , macrophages treated with exosomes maintain chondrocytes' chondrogenic characteristics and inhibit hypertrophy. Our results demonstrated that bone marrow mesenchymal stem cell-derived exosomes may relieve osteoarthritis by promoting the phenotypic transformation of synovial macrophages from M1 to M2.
Topics: Animals; Anterior Cruciate Ligament; Cartilage, Articular; Chondrocytes; Disease Models, Animal; Exosomes; Hypertrophy; Injections, Intra-Articular; Interleukin-10; Interleukin-1beta; Interleukin-6; Macrophages; Menisci, Tibial; Mesenchymal Stem Cells; Mice; Osteoarthritis; Osteophyte; Phenotype; RAW 264.7 Cells; Rats; Synovial Fluid; Synovial Membrane; Tumor Necrosis Factor-alpha
PubMed: 33350983
DOI: 10.18632/aging.104110 -
Annals of the Rheumatic Diseases Nov 2023Prior studies noted that chondrocyte SIRT6 activity is repressed in older chondrocytes rendering cells susceptible to catabolic signalling events implicated in...
OBJECTIVES
Prior studies noted that chondrocyte SIRT6 activity is repressed in older chondrocytes rendering cells susceptible to catabolic signalling events implicated in osteoarthritis (OA). This study aimed to define the effect of deficiency on the development of post-traumatic and age-associated OA in mice.
METHODS
Male cartilage-specific -deficient mice and intact controls underwent destabilisation of the medial meniscus (DMM) or sham surgery at 16 weeks of age and OA severity was analysed at 6 and 10 weeks postsurgery. Age-associated OA was assessed in mice aged 12 and 18 months of age. OA severity was analysed by micro-CT, histomorphometry and scoring of articular cartilage structure, toluidine blue staining and osteophyte formation. SIRT6-regulated pathways were analysed in human chondrocytes by RNA-sequencing, qRT-PCR and immunoblotting.
RESULTS
deficient mice displayed enhanced DMM-induced OA severity and accelerated age-associated OA when compared with controls, characterised by increased cartilage damage, osteophyte formation and subchondral bone sclerosis. In chondrocytes, RNA-sequencing revealed that depletion significantly repressed cartilage extracellular matrix (eg, ) and anabolic growth factor (eg, insulin-like growth factor-1 ()) gene expression. Gain-of-function and loss-of-function studies in chondrocytes demonstrated that SIRT6 depletion attenuated, whereas adenoviral overexpression or MDL-800-induced activation promoted IGF-1 signalling by increasing Akt phosphorylation.
CONCLUSIONS
SIRT6 deficiency increases post-traumatic and age-associated OA severity in vivo. SIRT6 profoundly regulated the pro-anabolic and pro-survival IGF-1/Akt signalling pathway and suggests that preserving the SIRT6/IGF-1/Akt axis may be necessary to protect cartilage from injury-associated or age-associated OA. Targeted therapies aimed at increasing SIRT6 function could represent a novel strategy to slow or stop OA.
Topics: Male; Animals; Mice; Humans; Aged; Insulin-Like Growth Factor I; Osteophyte; Proto-Oncogene Proteins c-akt; Osteoarthritis; Chondrocytes; Cartilage, Articular; RNA; Sirtuins; Disease Models, Animal
PubMed: 37550003
DOI: 10.1136/ard-2023-224385 -
Frontiers in Cell and Developmental... 2023Osteoarthritis (OA) is one of the leading causes of pain and disability in the elderly. Synovitis, cartilage destruction and osteophyte formation histologically manifest... (Review)
Review
Osteoarthritis (OA) is one of the leading causes of pain and disability in the elderly. Synovitis, cartilage destruction and osteophyte formation histologically manifest OA. Unfortunately, there is currently no effective therapy to delay its progression and the underlying mechanisms of OA require further exploration. Macrophage is a main cellular component of joint synovium. It is highly plastic and can be stimulated to polarize to different phenotypes, namely, the pro-inflammatory phenotype (M1) and the anti-inflammatory/tissue-repairing phenotype (M2). Ample evidence has demonstrated the vital roles of macrophages in the progression of OA. Imbalanced M1/M2 ratio is significantly related to OA severity indicating macrophage polarization might be a promising therapeutic target for OA. In this review, we summarized the involvements of polarized macrophages in synovitis, cartilage degradation, osteophyte formation and OA-related chronic pain. Promising therapies targeting macrophage polarization including the intra-articular cell/derivates-based therapy and the alternative non-invasive intervention such as photobiomodulation therapy were reviewed as well.
PubMed: 37954210
DOI: 10.3389/fcell.2023.1269724 -
Osteoarthritis and Cartilage Jul 2020To evaluate progression of individual radiographic features 5 years following exercise therapy or arthroscopic partial meniscectomy as treatment for degenerative... (Randomized Controlled Trial)
Randomized Controlled Trial
OBJECTIVE
To evaluate progression of individual radiographic features 5 years following exercise therapy or arthroscopic partial meniscectomy as treatment for degenerative meniscal tear.
DESIGN
Randomized controlled trial including 140 adults, aged 35-60 years, with a magnetic resonance image verified degenerative meniscal tear, and 96% without definite radiographic knee osteoarthritis. Participants were randomized to either 12-weeks of supervised exercise therapy or arthroscopic partial meniscectomy. The primary outcome was between-group difference in progression of tibiofemoral joint space narrowing and marginal osteophytes at 5 years, assessed semi-quantitatively by the OARSI atlas. Secondary outcomes included incidence of radiographic knee osteoarthritis and symptomatic knee osteoarthritis, medial tibiofemoral fixed joint space width (quantitatively assessed), and patient-reported outcome measures. Statistical analyses were performed using a full analysis set. Per protocol and as treated analysis were also performed.
RESULTS
The risk ratios (95% CI) for progression of semi-quantitatively assessed joint space narrowing and medial and lateral osteophytes for the surgery group were 0.89 (0.55-1.44), 1.15 (0.79-1.68) and 0.77 (0.42-1.42), respectively, compared to the exercise therapy group. In secondary outcomes (full-set analysis) no statistically significant between-group differences were found.
CONCLUSION
The study was inconclusive with respect to potential differences in progression of individual radiographic features after surgical and non-surgical treatment for degenerative meniscal tear. Further, we found no strong evidence in support of differences in development of incident radiographic knee osteoarthritis or patient-reported outcomes between exercise therapy and arthroscopic partial meniscectomy.
TRIAL REGISTRATION
www.clinicaltrials.gov (NCT01002794).
Topics: Adult; Disease Progression; Exercise Therapy; Female; Follow-Up Studies; Humans; Magnetic Resonance Imaging; Male; Meniscectomy; Middle Aged; Osteoarthritis, Knee; Osteophyte; Patient Reported Outcome Measures; Physical Therapy Modalities; Tibial Meniscus Injuries
PubMed: 32184135
DOI: 10.1016/j.joca.2020.01.020