Science topic
Osteoarthritis - Science topic
Osteoarthritis is a progressive, degenerative joint disease, the most common form of arthritis, especially in older persons. The disease is thought to result not from the aging process but from biochemical changes and biomechanical stresses affecting articular cartilage. In the foreign literature it is often called osteoarthrosis deformans.
Questions related to Osteoarthritis
In Osteoarthritis collagen type I is increased and assume that is one of the illness factor, then why most of products and studies use of hydrolyzed collagen type one for treatment?
Is there any conclusive evidence to suggest an association of Type 2 Diabetes and Osteoarthritis?
Why does the incidence increase progressively with age?
Why are some joints rarely affected?
How do mechanical forces cause joint degeneration?
What biologic and mechanical factors slow or accelerate the rate of joint degeneration?
For VAS score, WOMAC overall and individual component scores, KOOS and individual component scores, Lysholm score, and MOCART score
Give your inputs with references
I have been treating this patient for 20 years. She is 80 years old now. In the past 10 years her degenerative scoliosis (DS) has progressively worsened. We did xrays before starting the combination of lumbosacral Flexion/Distraction (Cox Technic) and Fascial Plane Therapy. Her scoliotis improved almost 13.5 degrees. Her pain improved (NPS) 6-8/10 to 1-2/10. I cannot find anything in the literature, non-surgically, to compare this to.
Does anyone know of an on-line tool or program to collect the OARSI measurement tool called the ICOAP (Measure of Intermittent and Constant Osteoarthritis Pain (ICOAP))? Looking for an easy, cheap way to collect this data from patients using an I-pad.
Hello,
I`d appreciate your input as to where we can buy this strain of mice (osteoarthritis model).
Thanks for your help
Cheers
JP
Surgery or physical therapy?
Incorporation of bone into the components of the non-cemented arthroplasty takes time, and it is difficult to know when the incorporation is sufficient enough to withstand full load.
Psoriatic Arthritis (PsA)
Risk Signs for Psoriatic Arthritis
1. Skin Psoriasis (Ps)
2. Nail Psoriasis
3. Over-weight
4. Young age @ Onset of Ps
5. Family member with PsA
6. Strep Throat Infection
7. Joint Injury
8. HIV
Clinical Review on Psoriatic Arthritis
Psoriatic arthritis (PsA) is a systemic musculoskeletal disease with a wide range of clinical presentations, including peripheral or axial arthritis, inflammation at sites where ligaments and tendons attach to bone, diffuse swelling of a finger or toe, or plaque psoriasis. Its severity ranges from mild to disabling. PsA is distinguished from other inflammatory arthritis by abnormal bone turnover, leading to osteoporosis and extensive resorption accompanied by new bone formation.
Five clinical subtypes of PsA have been identified, with some overlap: (1) spondyloarthritis, (2) arthritis mutilans, (3) predominant distal interphalangeal disease, (4) symmetric polyarthritis, and (5) asymmetric oligoarthritis.
Recommended first-line treatment of moderate-to-severe PsA consists of methotrexate (MTX) or biologic therapy, or a combination of both. A 2012 study failed to demonstrate any significant difference between MTX and placebo in PsA. However, MTX is still in widespread use, in part because of its low cost. Anti-tumor necrosis factor (TNF) agents such as etanercept, adalimumab, infliximab, golimumab, and certolizumab have been shown to safely reduce symptoms and inhibit the radiographic progression of joint space narrowing and bone erosion in PsA, and thus have become the Gold standard for treatment. However, up to 50% of patients with PsA are either intolerant of anti-TNF therapy or fail to achieve an adequate response, and the majority of patients who fail therapy with anti-TNF biologics do not respond to a switch in TNF agents.
Despite the need to manage symptoms and comorbidities and to improve quality of life (QoL), many patients with PsA are currently under-treated, untreated, or dissatisfied with the treatments they are provided.
In a recent survey, 31.3% of patients with psoriasis and 40.7% of patients with PsA indicated that primary goals of therapy were not met by their current treatment. Dissatisfaction with the long-term safety of biologic therapy was reported by 31.8% of patients with psoriasis and 25.2% of patients with PsA. Most survey participants (87.8% of patients, 98.0% of dermatologists, and 98.0% of rheumatologists) believed there was a strong or moderate need for better therapies. Among patients, 51.5% indicated that current therapies can be worse than the condition itself, compared with 30.7% of dermatologists and 12.0% of rheumatologists. In addition, 48.5% of dermatologists and 31.0% of rheumatologists reported that an important issue is patients leaving their practice because of frustration or dissatisfaction with currently available therapies.
Multiple IL-17–related genes have been shown by genome-wide association studies to be associated with PsA. IL-17A, IL-17C, and IL-17F levels are elevated in psoriatic skin lesions and can act directly on keratinocytes, inducing expression of other proinflammatory molecules. The IL-17 inhibitor secukinumab received FDA approval for the treatment of patients with active PsA in January 2016, after having received approval in 2015 for the treatment of patients with moderate-to-severe plaque psoriasis. Approval for the treatment of PsA was based on the FUTURE-1 and FUTURE-2 studies, both of which had a primary endpoint of a minimum 20% improvement in the American College of Rheumatology response criteria (ACR20) at 24 weeks. In both trials, ACR20 response rates were significantly higher in patients receiving secukinumab than in those receiving placebo.Analysis of all primary and secondary endpoints from the FUTURE-1 study, on an intent-to-treat basis, continued to Week 104. Secukinumab showed sustained efficacy across multiple domains of PsA through Week 104, including signs and symptoms, disease activity, QoL, physical function, skin symptoms, dactylitis, and enthesitis. At Week 104, 84.3% of patients in the secukinumab 150 mg group and 83.8% in the secukinumab 75 mg group showed no radiographic disease progression. Ixekizumab, an IL-17 monoclonal antibody, received FDA approval for moderate-to-severe plaque psoriasis in March 2016 and is in late-stage trials for PsA.
In the recently reported double-blind, phase III SPIRIT-P1 trial, biologic-naïve patients with active PsA who were randomized to ixekizumab treatment saw improvements in disease activity and physical function, as well as in the inhibition of structural damage progression. At Week 25, ACR20 response rates, which was the primary endpoint, were 57.9% for patients who received ixekizumab 80 mg every 4 weeks and 62.1% for patients who received ixekizumab 80 mg once every 2 weeks. Results from the extension phase of the trial showed that over 52 weeks, ixekizumab demonstrated clinically significant improvement in the signs and symptoms of PsA, including arthritis, dactylitis, enthesitis, and skin manifestations, across treatment groups. In a placebo-controlled, phase 2 study, brodalumab, an IL-17 receptor monoclonal antibody (140 or 280 mg every 2 weeks) was evaluated in patients with active PsA. The ACR20 responses were achieved by 37% and 39% of patients in the respective brodalumab groups at Week 12 compared with 18% for placebo.
Abatacept, a selective T-cell costimulation modulator, and tofacitinib, an oral Janus kinase inhibitor, were approved by the FDA in 2017 to treat PsA. In a phase 3 trial involving 424 patients with PsA (approximately 60% with prior exposure to a TNF inhibitor and 60% on concomitant methotrexate), 39.4% of patients given abatacept experienced at least 20% improvement in the ACR20, compared with 22.3% among placebo-treated controls.
Ustekinumab, a fully human anti-IL-12/23p40 monoclonal antibody, also has FDA-approval alone or in combination with methotrexate for the treatment of adult patients (18 years or older) with active psoriatic arthritis.21
Apremilast, a phosphodiesterase 4 (PDE4) inhibitor, was approved by the FDA on March 21, 2014 for the treatment of adult patients with active psoriatic arthritis.
Tofacitinib is FDA-approved for the treatment of adults with PsA who have had an inadequate response or intolerance to methotrexate or other disease-modifying antirheumatic drugs, based on the results of the OPAL Broaden and OPAL Beyond studies, which demonstrated significant improvement in ACR20 response compared to placebo.22
Summary
Psoriatic arthritis is a systemic musculoskeletal disease with a broad constellation of clinical presentations, ranging from mild to disabling, including peripheral or axial arthritis, inflammation, diffuse swelling, joint destruction, and plaque psoriasis. Psoriatic arthritis is distinguished from other inflammatory arthritis by abnormal bone turnover, leading to osteoporosis and extensive resorption accompanied by new bone formation.2 Recent drug approvals have provided physicians with enhanced therapeutic options to manage this disease.
Ace the Case:
A 44-year old man with a 20-year history of psoriasis presents with a 2-month history of a painful, swollen left finger and a swollen right second toe. The patient has a 20-year history of psoriasis and is not receiving any medications. O/E the left third interphalangeal joint is swollen and tender to palpation and movement. The right second toe has fusiform swelling and is tender to palpation, with impaired range of motion. The nails show yellowish-pink discoloration with pitting and onycholysis. Radiographs of the affected joints demonstrate enthesitis and marginal bone erosions, with pencil-in-cup deformities of the distal interphalangeal joints of the left middle and index fingers, as well as dactylitis of the second toe. Labs show a sedimentation rate of 38 mm/1st hr; negative rheumatoid factor and anti-CCP antibody.
What is the likely diagnosis?
(A) Lyme Disease
(B) Psoriatic Arthritis
(C) Osteoarthritis
(D) Acute Gout
Answer: B
Rationale: Psoriatic arthritis (PsA) can affect approximately 30% of patients with psoriasis and is characterized by enthesitis, dactylitis, tenosynovitis, asymmetric oligoarthritis, spondylitis, and arthritis of the distal interphalangeal joints. The nails may show characteristic pitting or onycholysis. Approximately 15% of patients who present with PsA have undiagnosed psoriasis.1 Joint pattern of involvement in patients with PsA not only can involve the distal interphalangeal joints, but also can include symmetric polyarthritis, asymmetric oligoarthritis, arthritis mutilans, and spondylitis. Erosive changes of PsA can be associated with the pencil-in-cup deformities of the distal interphalangeal joints of the thumb and middle fingers. 1
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QUESTION 1
Which of the following medications is an IL-17 inhibitor?
(A) Tofacitnib
(B) Abatacept
(C) Secukinumab
(D) Certolizumab
Q1 Answer: C.
Rationale: The IL-17 inhibitor secukinumab received FDA approval for the treatment of patients with active PsA in January 2016, after having received approval in 2015 for the treatment of patients with moderate-to-severe plaque psoriasis.23 Approval for the treatment of PsA was based on the FUTURE-1 and FUTURE-2 studies, both of which had a primary endpoint of a ARC20 at 24 weeks.14,15
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QUESTION 2
Which of the following best describes the principle mechanism of action for tofacitinib?
(A) VEGF inhibitor
(B) IL-17 monoclonal antibody
(C) Janus kinase inhibitor
(D) Anti-CD40 antibody
Q2 answer: C
Rationale: Tofacitinib, a Janus kinase inhibitor, is FDA-approved for the treatment of adults with PsA who have had an inadequate response or intolerance to methotrexate or other disease-modifying antirheumatic drugs, based on the results of the OPAL Broaden and OPAL Beyond studies, which demonstrated significant improvement in ACR20 response compared to placebo.22
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Is It Psoriatic Arthritis, Gout, or Something Else?https://www.everydayhealth.com/psoriatic-arthritis/living-with/psoriatic-arthritis-gout-something-else/
Do statins have useful roles in rheumatology especially in rheumatoid arthritis?
Osteoarthritis is characterised as the deterioration of the articular cartilage which then causes bone-to-bone contact. Glucosamine is a primary constituent of cartilage proteoglycans, which is why there are claims that glucosamine could possibly be an anti-arthritic. Despite this, there has been no current and impressive evidence supporting this claim. Has there been any current advances on this claim and if so, what are they?
Article of that kind would be pretty helpful for past (archaeological) or modern populations. As for the DJD, I meant on DISH, anklyosing spondylitis and similar.
Thank you!
Dear Friends
The classification criteria for Osteoarthritis were created by ACR 30 years back. There has been a greater understanding of Osteoarthritis since then, and many advances in imaging of Osteoarthritis have occurred. We feel that progress in treatment of Osteoarthritis is suffering due to our inability to diagnose OA very early in the course of disease.
We are attaching a link for the questionnaire to elicit your opinion to know what could constitute an early diagnosis of OA. Even if you have done it redo it on the link given below.
With kind regards.
Prof. S. K. Das
Dr. Urmila Dhakad
Dr. Pooja Dhaon
Osteoarthritis (OA) is a common occupational dangerous case for service members. I wanted to know how body borne load impacts knee biomechanics for participants who do and do not present varus thrust during running.
I do not mean steroids, all we know steroids, I mean some really new drugs.
Many physicians and physiotherapists advise their patients who have knee osteoarthritis whether in earlier stage or late and chronic stage to stop stair climbing and use lifts if available.
Is this logic suitable for all types of patients with knee osteoarthritis?
Is there any evidence or published article that discuss this issue?
1. Share some published articles, which contain scales for Osteoarthritis
2. Some site which contain more information for Osteoarthritis
What are the reasons of knee cracking in young people who do not suffer from any symptoms? In particular, cracking that comes with normal activities.
Is this normal for such type of knee cracking? Should we treat this issue?
Any suggested article that explain this issue would be appreciated!
I performed real-time PCR to find out the expression of different genes in osteoarthritis and normal rat model and for that, I used GAPDH as a standard. The issue I am facing is that the GAPDH expression in Osteoarthritis is low while its high in the normal model. I am confused as its a housekeeping gene so why its expression is not the same?
He is known case of Ca prostate and recently sustained right sided hemiplegia.
I thank colleagues for their suggestions. In annex x-ray images, clinical did not seem to be a problem of rotation. Our decision not to operate because of the fear of possible postoperative .. .prolonged the same legs works of accelerated growth, and at the same time we are not sure that our decision is correct
best regards,
Curcumin (diferuloylmethane) is the principal biochemical component of the spice turmeric and has been shown to possess potent anti-catabolic, anti-inflammatory and antioxidant, properties.
Could anyone explain the reasons to supplement A2M to OA knee mainly because there is a lower concentration of A2M in SF than serum (plasma)? Why did the higher A2M in OA's SF (results shown in Fig. 1) not inhibit MMP-13 or other proteases? Perhaps the nature or properties of OA's A2M is/are different than those of normal A2M, and itself may be the problem?
Bilateral hip replacement in patient, women 55yrs old, with congenital bilaterl hip dislocation
Aceclofenac causes the gastric discomfort on administration, so there is need of additional PPI (Rabeprazole) SR.
I would like to digest the entire porcine glenoid cartilage to create some Osteoarthritis like damage using MMP-1 and mechanical test the glenoid with the joint simulator to see the effect of the damage. how can I determine how much MMP-1 I need for the whole glenoid? I have attached the joint that I would like to digest. Could you please recommend me groups that might do similar work or recipes that I could use.
Many thanks for your help in advance.
I have to write a research proposal as an assignment. It is about the effect of spinal cord stimulation in a rat model of osteoarthritis (OA). I am inducing OA with a monoiodoacetate injection in the knee.
However, I can not find anywhere within the spinal cord segment as the best to stimulate in a rat.
Can anybody please help me with this?
Most orthopaedic surgeons recommend operative stabilization of type II supracondylar humerus fractures because of concerns for further displacement and resultant malunion/deformity.
Are there any radiographic, patient-related, or injury/mechanistic risk factors for further displacement of type II supracondylar humerus fractures treated non-operatively?
Can a subset of these injuries be treated non-operatively without substantial risk of displacement?
Loss of somatosensory function with regards to neuropathic pain indicates abnormal function mediated by small and large nerve fiber.
Recently AAOS recommended against any benefit provided by viscosupplementation. The insurance companies stopped supporting this treatment. After this, there was an editorial in the journal "Arthroscopy" against the recommendations of AAOS. To this editorial, the AAOS authors gave a rebuttal.
I have personally used this treatment in many patients. The results are mixed. But still there are quite a good number of patients who feel significant improvment in their symptoms.
The kellgren and lawrence system and the Ahlbäck grading system for knee osteoarthritis disease severity classification are based on knee radiograph. Can knee osteoarthritis disease severity be classified without a radiograph?
I am preparing a stock solution of sodium monoiodoacetate solution and planning on storing it in -20 to use in future experiments to minimize my exposure to its toxic powder. So I am wondering if anyone who has worked with Iodoacetate has any thoughts on how to properly store a stock solution of it. Thanks!
it is said that the most Knee OA is age related: wear and tear due to daily joint use causes some damage to the knee joint which is not followed by the repair process. Sp
what is the physiological pathway which is protecting the knee joint in normal people? and what is the pathophysiological pathway which leads to damage of cartilage in the knee Joint in knee OA?
As the patients do exercises,Can they use drugs less than other patients that they do not exercise???
Some of the Yoga experts suggest neck rotation in the problem of cervical spondylitis, whereas some suggests not to perform this practice. Can we get the right answer?
Chronic, non-specific and widespread pain is very common among older adults. Traditional interventions which usually use physical means to deal with individual joints only cannot address the problem. Is there any effective interventions that incorporate physical, psychological and social needs of this population?
What would be effect of inhibition of osteoblast proliferation when Rheumatoid arthritis patient is administered with DMARD capable of inhibiting osteoblast proliferation?
I want to know the relation of severity with the specific clinical findings of crepitus sound.
3.8% citrate chelates Calcium less than EDTA. One can use 0.5ml citrate in 8ml to get adequate anticoagulation rather than the usual 1.0ml resulting in less dilution and less calcium that needs to be added to reverse the citrate chelation effect
It is possibly reasonable to assume that PRP injected into skin will not need activation with calcium because of the diluting effect of extracellular fluid but what is the effect in the joint cavity? The cavity is enclosed so the PRP cannot escape. If the platelets are not activated immediately this is not necessarily bad? but my gut feeling is that the PRP will soon be activated with both the dilution of the citrate and the mechanical trauma.
Any thoughts?
I have osteoarthritis patient DNA. Now I want to study the interaction of the DNA with Vitamin B complex. What is the procedure to do so? What types of materials and methods are used to study this interaction? Is there any specific Protocol for study this interaction? Is there any paper on this topic?
Please tall me.
Thank you.
How soon should a patient with a successful total knee arthroplasty do away with any form of walking aid, even when there is no pain any longer.?
In some patients we observe an oblique joint line (i.e. in cases of a femoral valgus which is compensated by a tibial varus deformity) even though the overall alignment of the affected leg is straight. Does anybody know papers on the biomechanical influence of an oblique joint line in such patients ?
I am looking at the possibility to exploit the molecules that enhance calcium deposits as means to combat osteoarthritis and other diseases that contribute to loss of calcium from the body.
i m working on osteoarthritis, i want to isolate the active compound which is responsible for preventing arthritis
The results in the literature are very controversial. One can find some sort of disagreement when comparing clinical results with advertising papers (TV, media, etc.).
There is also another dilemma: peroral or intrarticular? Here the ratio expectations/price may be sometimes a troublesome matter to discuss with patients.
I am trying to find out level of cartilage destroying enzymes which is associated with crepitus sound with pain.
Anybody please suggest can i use any established questionnaire like WOMAC with modification of time frame, addition or deletion of questions according to my population without any problem in publication and with authorities of that questionnaire? Actually it is changed but i am using few of question from there along with their scoring pattern. Will there any problem or anybody who has worked with knee osteoarthritis and developed his own questionnaire guide me?
1) What would you consider an important change in daily time spent in lifestyle physical activities (e.g., mopping, gardening, walking to do errands)?
2) How about moderate activities (e.g., lawn mowing, doubles tennis, brisk walk)? What would you consider an important change in daily time spent in those activities?
I'd really appreciate your thoughts.
Thank you very much-
I am developing a biomarker assay for the detection of aggrecan fragments in patient synovial fluid samples and need to source synovial fluid or at the very least a 'SF like substance' for my standard curve. I am currently only able to compare SF assay results to that of a standard curve in buffer (which needless to say acts considerably differently to SF!)
In patients with a meniscal tear and moderate osteoarthritis, does partial menis- cectomy improve functional outcomes than physical therapy does?
Many of us have maintained that filling depleted bones with dead (osteoclast) bone cells is not really increasing bone mass except in a superficial way. But that is exactly how the current model of treatment works in allopathic medicine today. I hope by opening up this discussion we will explore deeply the experiences and knowledge of how to best address the huge masses in many countries that are experiencing the dread chronic diseases of osteoarthritis, osteopenia, and osteoporosis. Only a frank and unbiased approach will be of value, that which is best for our patients rather than what is best for the bottom line of a system that is fraught with introducing additional health challenges to the population.
The best way for healthcare professionals and researchers to combat the huge and recent rise in osteoporosis is to give right advice. Asian women who have a small frame often have a high rate of osteoporosis. We need to exercise more and move more. 'The average person today has way too little movement in their life early on, which already impacts bone density and gets even worse as they age, for most have never developed a habit of it in their lifestyle. Bone builds and re-builds based on its needs. So if you don’t use them, you literally lose them. Part of this exercise can include daily brisk walking, yoga and various cardio exercises, but the key really is having some resistance or weight training exercise.'
Next, I stay away from an acidic diet (coffee, soda, alcohol and fast, processed foods high in bad fats, excess sugar and salt).
Third, I make sure I get enough sunlight and vitamin D so that the calcium really gets absorbed into the bone matrix to strengthen and harden the bones.
Lots of authors see that in old age the main cause of pain is osteoarthritis not degenerated meniscus, so what would you do with that meniscus?
Biomaterial or scaffold for stem cells to transplant in osteo-chondral defects in rat or rabbit. There are large number of biomaterial experts are out there on RG site. My stem cells placed in osteo-chondral defects and later covered with fibrin glue is not helping much for the survival of stem cells checked after few weeks. Many thanks.
Wondering if someone has done X-gal staining on decalcified bone section in rat or mouse. My fear is that if decalcification process would interfere with X-gal staining,
Thanks,
Other links in pathogenesis are also welcome. I am looking at serum levels of miRNAs in PsA and have found some links between the disease. Now I am wondering what potential links exist between the two disease types.
Anyone wants to share their experience of MSCs differentiation into articular cartilage and growth plate cartilage, and exact growth factors used for either type, i.e, Tgb and Bmp
We receive such patients who refuse replacement surgery and expect a 100% recovery by PT Rx in terms of pain, function, gait and even joint space and deformity. We try counseling but they keep on complaining.
Do you face such problems? What's your opinion?
I am giving a lecture to a audience of sports physicians, physiotherapists and physical trainers on the topic.
In one of my recent surgeries on an obese female, the extension and flexion gaps (after the releases) were just sufficient enough for the largest insert (17.5) I had available. I was wondering what the options to tackle this situation would be if the gap was bigger.
Synovial Fibrosis
Does anyone have experience in synovial fibrosis in surgically-induced OA rat knee or mouse or other animal model? Has anyone tried to reduce synovial fibrosis while trying to treat OA by any means (like stem cells etc)? Any comments on fibrosis vs OA in induced OA reference?
How should a medical doctor attempt to reduce arthrofibrosis? What are any of the latest treatments besides mild exercises to reduce stiffness?
Do you integrate some of the following principles/drugs in your clinical regimen as NSAID, chondroprotection (e.g. antioxidants, inhibition of apoptosis, protection of cell membrane integrity), inhibition of pro-inflammatory mediators (e.g. anti-TNFα, anti-IL-1/IL-1RA, NO-inhibitors), anabolic cytokines (e.g. BMP-7, bFGF, IGF-1, PRP), matrix protection/remodeling (e.g. MMP-inhibitors)?
We're planning to conduct a clinical trials in patients with OA in which we will assess muscular status using tensiomyography. But we need publications on reference values.
Can someone advise on this?
I have homogenized cartilage from guinea pig and I would like to estimate the sGAGs for this. My question is, is it possible to estimate the GAG and normalize to total protein instead of the DNA?
I suppose extracting DNA from this homogenate is tough.
Is there an alternative?
I need to test chondrocytes for their in vivo ability to repair articular cartilage defects in rat femoral patellar groove. Need to know the depth of defect I should create.
It's believed to be an inflammatory disease with presence of both uric acid and calcium in synovial fluid of the OA knees that triggers production of interleukin-1 (IL-1), a key mediator of cartilage breakdown in OA.
Though Tgfb1 and Tgfb3 play different roles in fibrosis and wound healing, there is no difference in their chondrogenic ability and nature of cartilage they induce from MSCs. Can anyone elaborate on the difference between these two?
What is the best method for induction of surgical osteoarthritis in rabbit knee joint?
I am starting a new project in the osteoarthritis field and need to introduce a new chondrocyte culture into the lab.
