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.
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For VAS score, WOMAC overall and individual component scores, KOOS and individual component scores, Lysholm score, and MOCART score
Give your inputs with references
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At leat 50% improvement in pain or function
MCID for the WOMAC was 4.2 points for the pain subscale, 1.9 points for the stiffness subscale, 10.1 points for the function subscale, and 16.1 points for the total
adjusted MCIDs for improvement ranged from 2.89 to 16.24 score points
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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.
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Thank you Francesca. The therapy I did on this patient is the same as an ultrasound video for a different patient with 34 years of chronic low back pain. It uses cine-loop to show changes in the connective tissue (thoracolumbar fascia) before and after treatment.
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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.
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See iCOAP questionnaire, user guide and article via the link (https://oarsi.org/research/outcome-measures). I'm not sure they've got a specific online tool yet but I'm sure this could be transferred into qualtrics or another survey tool for easy use on an iPad.
All the best!
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Hello,
I`d appreciate your input as to where we can buy this strain of mice (osteoarthritis model).
Thanks for your help
Cheers
JP
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Thanks so much Subhash, I have quite a few papers that Ive referred to as well, most suggest Harlan labs but not sure if they're still breeding them because I dont seem to be able find on any lab catalogues. I'll go thorough these and see.... thanks again
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Surgery or physical therapy?
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Following any means to treat OA. Strengthening of the quadriceps muscles goes a long way.
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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.
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Our 10 -year experience on early weight bearing did not show any problems with early weight bearing (Day 1)
However for those patients whose proximal femur were wired following fractures we delayed weight bearing for 6 weeks.Our choice of implants were mainly Depuy and Biomet
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i m working on osteoarthritis, i want to isolate the active compound which is responsible for preventing arthritis
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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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Thank you for raising this cool Q. This is a very interesting point with one of the suggested hypotheses explaining why gout occurs most commonly in the big toe as uric acid (UA) is sensitive to temperature changes. At cooler temperatures, UA turns into crystals. Since the toe is the farthest from the heart, it is also the coolest part of the body and, thus, the most likely target of gout.
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Do statins have useful roles in rheumatology especially in rheumatoid arthritis?
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Osteoarthritis is the second most common rheumatologic problem and it is the most frequent joint disease with a prevalence of 22% to 39% in India. OA is more common in women than men, but the prevalence increases dramatically with age.
As we all Know that Medicine get better, Technology get better, Diagnosis tool get better, Physiotherapy Prevention and management get better still the prevalence increases year by year..........
Thats mean all this get fail for reducing the prevalence of Knee OA among world.
What are the reasons for this?
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According to your risk factors for knee OA proven by existing peer reviewed research in your paper, I should be explaining to my patients that they should:
· Stop aging
· Stop being female
· Stop being obese
· Stop performing work that involves kneeling, squatting or lifting
· Stop performing high intensity exercises such as running over long periods
· Avoid mineralizing their bones too much
How much money, time and debate did it take to arrive at these conclusions?
I suggest that Sackett’s methodology when used to research knee OA is at the top of the error of your ways.
Your suggestion that “Generally speaking, researchers focus their studies on a very specific risk factor” is the pearl inside the shell of your paper. In future studies, it might be worthwhile for them to examine the impact of the interaction of two or more risk factors. A Stochastic Model of research that utilizes a multimodal treatment plan whose components are symbiotic and safe may produce better, more valid and more applicable clinical outcomes.
Theoretically, any methodology that improves overall foot and postural stability, support, strength, symmetry and balance should reduce the existence, progression and life-altering of knee OA (think foot typing).
The knee joint is akin to the transmission of a car in that it has little functional importance of stabilizing or moving the machine as a whole. It simply translates the motions and moments generated from the hips downward and the foot upwards in order to have a more efficient, more productive, less injured biomachine. While it is important for every car to have a well oiled and functional transmission, it is the ability of a car to resist degeneration, deformity and performance issues by dampening and buffering forces generated by the engine and the ability of the tires and chassis to absorb the impact shock of the road and degenerative forces of gravity, friction, etc.
You conclude that “In the future, it could also be useful to do systematic reviews of the effectiveness of care approaches that combine various treatment modalities”. Biomechanically, I have been doing that successfully for decades in real time. Perhaps with your insightful addition to the literature, more of us will consider your suggestions.
I remain available to assist any or all open minded researchers and clinicians in meeting this challenge.
Good fortune to all our knees.
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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?
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Many of the products used for arthritis like glucosamine etc are more of neutraceuticals than valid pharmaceutical agents. In early arthritis many may improve symptoms but we'll established cartilage degeneration is not repaired by any of drugs at present.
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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!
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I saw several supratrochlear foramen in the humerus where any pathology was present. No arthrosy no diseases that can produce it. The bone was perfect but with the foramen. I think mechanical effort produce that and it is more frequent in women and the left arm, you can see in bibliography about this.
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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
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The human knee is an excellent biological model for tracking the early natural history of osteoarthritis (OA). The medial compartment is the most common anatomic region to develop OA, esp. following damage to the medial meniscus. We have found that the pathophysiology of the knee includes Loss of Osseous Homeostasis (detectable scitigraphically by Tc 99m-MDP Bone Scan) at a time long before any structural changes (e.g. Kellgren-Lawrence Scale1-3) occur radiographically. We have shown that following treatment for a torn meniscus, if joint homeostasis can be achieved and maintained (manifested by resolution to a normal bone scan post-operatively - then the process of early OA can be completely aborted/PREVENTED!
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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.
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I agree with Dr.Diachkova. Knee varus deformity predisposes to degenerative changes medially and progression.
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I do not mean steroids, all we know steroids, I mean some really new drugs. 
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You may find few in the following article: Generally the natural products derived from Food  are safe and long lasting.
 I have worked on  Apigenin flavonoid which is a good alternate found in dried parsley leaves.
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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?
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there is a mechanical association....
however it becomes relevant when there is a predisposing  factor like altered bio mechanics / .....
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1. Share some published articles, which contain scales for Osteoarthritis
2. Some site which contain more information for Osteoarthritis
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Maharishi here is a list of articles that cover the topic fully:
 Kettler, Annette; Wilke, Hans-Joachim (2005). "Review of existing grading systems for cervical or lumbar disc and facet joint degeneration". European Spine Journal. 15 (6): 705–718. ISSN 0940-6719. doi:10.1007/s00586-005-0954-y.
Ofiram, Elisha; Garvey, Timothy A.; Schwender, James D.; Denis, Francis; Perra, Joseph H.; Transfeldt, Ensor E.; Winter, Robert B.; Wroblewski, Jill M. (2009). "Cervical degenerative index: a new quantitative radiographic scoring system for cervical spondylosis with interobserver and intraobserver reliability testing". Journal of Orthopaedics and Traumatology. 10 (1): 21–26. ISSN 1590-9921. doi:10.1007/s10195-008-0041-3.
Brox, Jens; Lereim, Paul; Merckoll, Else; Finnanger, Anne Marie (2009). "Radiographic classification of glenohumeral arthrosis". Acta Orthopaedica Scandinavica. 74 (2): 186–189. ISSN 0001-6470. doi:10.1080/00016470310013932.
 Page 117 in Barbara N. W. Weissman (2009). Imaging of Arthritis and Metabolic Bone Disease. Elsevier Health Sciences. ISBN 9780323041775.
 "Glenohumeral joint space". radref.org., in turn citing: Petersson, Claes J.; Redlund-Johnell, Inga (2009). "Joint Space in Normal Gleno-Humeral Radiographs". Acta Orthopaedica Scandinavica. 54 (2): 274–276. ISSN 0001-6470. doi:10.3109/17453678308996569.
Zdravko Jotanovic, Radovan Mihelic, Gordan Gulan, Branko Sestan, Zlatko Dembic (2015). "Osteoarthritis of the hip: An overview". Periodicum biologorum. 117 (1).
Lequesne, M (2004). "The normal hip joint space: variations in width, shape, and architecture on 223 pelvic radiographs". Annals of the Rheumatic Diseases. 63 (9): 1145–1151. ISSN 0003-4967. doi:10.1136/ard.2003.018424.
 Terjesen, Terje; Gunderson, Ragnhild B (2012). "Radiographic evaluation of osteoarthritis of the hip". Acta Orthopaedica. 83 (2): 185–189. ISSN 1745-3674. doi:10.3109/17453674.2012.665331.
"Tönnis Classification of Osteoarthritis by Radiographic Changes". Society of Preventive Hip Surgery. Retrieved 2016-12-13.
"Osteoarthritis Classification Scales: Interobserver Reliability and Arthroscopic Correlation". The Journal of Bone and Joint Surgery-American Volume. 96 (14): 1145–1151. 2014. ISSN 0021-9355. doi:10.2106/JBJS.M.00929.
Hernández-Vaquero, Daniel; Fernández-Carreira, José Manuel (2012). "Relationship between radiological grading and clinical status in knee osteoarthritis. a multicentric study". BMC Musculoskeletal Disorders. 13 (1). ISSN 1471-2474. doi:10.1186/1471-2474-13-194.
Kim, Young-Mo; Joo, Yong-Bum (2012). "Patellofemoral Osteoarthritis". Knee Surgery & Related Research. 24 (4): 193–200. ISSN 2234-0726. doi:10.5792/ksrr.2012.24.4.193.
Page 722 in Gary S. Firestein, Ralph Budd, Sherine E Gabriel, Iain B. McInnes, James R O'Dell (2012). Kelley's Textbook of Rheumatology E-Book. Elsevier Health Sciences. ISBN 9781455737673.
 Massilla Mani, F.; Sivasubramanian, S. Satha (2016). "A study of temporomandibular joint osteoarthritis using computed tomographic imaging". Biomedical Journal. 39 (3): 201–206. ISSN 2319-4170. doi:10.1016/j.bj.2016.06.003.
Nicolas Holzer, Davide Salvo, Anne Karien Marijnissen, Aminudin Che Ahmad, Emanuele Sera, Pierre Hoffmeyer, Anne Lübbeke Wolff, Mathieu Assal (2017-09-14). "How to assess ankle osteoarthritis: comparison of the Kellgren and Lawrence scale with functional outcome and digital image analysis". Orthopaedic Proceedings. 94–B.
Imai, Kan; Ikoma, Kazuya; Kido, Masamitsu; Maki, Masahiro; Fujiwara, Hiroyoshi; Arai, Yuji; Oda, Ryo; Tokunaga, Daisaku; Inoue, Nozomu; Kubo, Toshikazu (2015). "Joint space width of the tibiotalar joint in the healthy foot". Journal of Foot and Ankle Research. 8 (1). ISSN 1757-1146. doi:10.1186/s13047-015-0086-5.
Quintana, José M.; Escobar, Antonio; Arostegui, Inmaculada; Bilbao, Amaia; Azkarate, Jesús; Goenaga, J. Ignacio; Arenaza, Juan C. (2006). "Health-Related Quality of Life and Appropriateness of Knee or Hip Joint Replacement". Archives of Internal Medicine. 166 (2): 220. ISSN 0003-9926. doi:10.1001/archinte.166.2.220.
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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!
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Please let me know if this citation (and reference below) is useful to you.
“Why joints pop
Like nearly all the joints in your body, the knee joint is covered by a protective membrane containing synovial fluid. This fluid lubricates the joint, allowing it to move smoothly and easily.
Occasionally, tiny gas bubbles build up in this fluid. When the joint moves, the bubbles are released, causing the nearby ligaments to emit a snap or pop sound. The technical term for this phenomenon is crepitus, which also describes all grinding or crackling sounds and sensations in the body.
When to be concerned about joints popping
Most of the time, this popping and creaking of joints is harmless. However, crepitus is also a symptom of the joint degeneration that leads to osteoarthritis.
 You should worry about joint popping if:
•It's occurring frequently in one location
•It's accompanied by pain
•It's accompanied by joint swelling, tenderness, or stiffness
•You're also having pain as a result of prolonged joint movement, such as when walking
If you're experiencing pain when a joint pops or you have any other of the symptoms listed above, talk with your doctor. If your symptoms and test results indicate it, your doctor may diagnose osteoarthritis and start treatment. Treatments for osteoarthritis can ease pain, improve mobility, and slow disease progression—especially if it's caught early.”
Reference:
Dennis
Dennis Mazur
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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?
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I recommend reading Vandesompele, J., De Preter, K., Pattyn, F., Poppe, B., Van Roy, N., De Paepe, A. and Speleman, F., 2002. Accurate normalization of real-time quantitative RT-PCR data by geometric averaging of multiple internal control genes. Genome biology, 3(7), pp.research0034-1. This landmark paper discusses the issue of housekeeping gene expression variability and provides a solution (geometric mean of multiple housekeeping genes).
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He is known case of Ca prostate and recently sustained right sided hemiplegia.
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All comments have merit. I am always high on THA or cemented Bipolar if the patients potential life expectations is moderate to high with the note that a hip surgeon performs the surgery. This case is beyond the skill set of a general orthopaedic surgeon (in my opinion) Panayot is correct in comment of high risk of failure.
Todays skill set for an experienced hip surgeon can replace this hip within 45 to 60 minutes and provide a stable hip for the remained of this patients life. I would also recommend a cemented stem.
Non surgical approach would be restricted to the ability of skilled hip surgeon availability and or potential life expectation of this patient.
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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, 
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Boy or girl ? If girl- what about menarchy ? In any case the oblique pelvis is a problem making the centering of the femoral head problematic (degenerative changes later in the years). As far as I understood the decision was already made for "wait and see" tactics. So monitoring, measuring the dynamics of the LLD. If the condition (LLD) does not imrove (after 6-12 months) then corrective valgus osteotomy should be discussed earlier or later.
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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.
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According to Sally Frautschy one 900 mg capsule a day can be safely taken with some fatty food. Taking in empty stomach is not advisable
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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?
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Though higher in concentration they are structurally different 
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Bilateral hip replacement in patient, women 55yrs old, with congenital bilaterl hip dislocation
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Stretching of Hamstrings and Flexors and Extensors of Hip-. If Adductor Tendon is Tight release of or tenotomy is done routinely
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Aceclofenac causes the gastric discomfort on administration, so there is need of additional PPI (Rabeprazole) SR.
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I think maintaining a mucousal  protection of stomach following ingestion of NSAID is more important than reducing the acidity in the stomach itself. Sucralfet do this function and I routinely use it 
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Osteoarthritis, T cells.
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Pro inflammatory T cell are said to the the key inflammatory mediator for cartilage destruction triggering release of interleukin 1 and tumor necrosis factors 
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Treatment of osteoarthitis
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Gene therapy: an attractive concept and maybe more. Gene therapy (Table 2) in articular joint tissues can be used as a drug delivery system to modify or reestablish the balance between catabolic/anabolic factors or to modulate proinflammatory cytokines. Ideally, this must be done to the cell or must be tissue specific. The potential for the use of biologic molecules as therapeutic agents is limited. Lately, much attention has been focused on the use of gene transfer techniques. Their potential for the treatment of OA is of very significant interest, since a consistently high local concentration of the therapeutic protein in the joint can be provided and sustained delivery maintained over time. Several strategies to replace defective or deficient protein products are now under study (Table 2). Treatment approaches consist of various ex vivo or in vivo techniques using viral or nonviral vectors (102). One strategy consists of insertion into the cells of a gene enabling the production of a protein not normally expressed or expressed in low and insufficient amounts by the OA cells. The viral system is favored because it generally allows for a very effective transfer to a large percentage of cells while maintaining a sustained high level of protein expression that can be extended over significant periods of time. Ex vivo transfer of marker genes to OA cells has been demonstrated in experimental models with the use of a retroviral vector (89).
Table 2. Gene therapy for osteoarthritis*
*
In both cartilage and synovium, catabolic factors (for example, metalloproteases [MMPs], nitric oxide [NO]) and cytokines (for example, interleukin-1β [IL-1β], tumor necrosis factor α [TNFα]) should be either reduced or eliminated. In contrast, some growth factors and the cytokine receptor antagonist (interleukin-1Ra [IL-1Ra]) or soluble receptors (soluble IL-1 receptor type II [sIL-1RII], soluble tumor necrosis factor receptor [sTNFR]) should be stimulated.
Potential targets
 Cartilage
  Catabolic factors (for example, MMPs, NO)
  Anabolic factors (growth factors)
  Apoptotic factors (for example, caspases, ceramides)
 Synovium
  Cytokines (for example, IL-1β, TNFα)
  Antiinflammatory cytokines (IL-4, IL-10, IL-13)
  Cytokine receptor antagonist (IL-1Ra)
  Soluble receptors (sIL-1RII, sTNFR)
Strategies
 Gene replacement
 Gene addition
 Gene control
The selection or combination of the gene(s) that would offer the best protection against OA remains to be determined. The transfer of genes such as IL-1Ra, IL-10, and IL-13 has been studied using OA or inflammatory animal models (103). However, more specifically with regard to OA, the use of IL-1Ra gene therapy has elicited much attention. The rationale is based mainly on the fact that this antagonist has the ability in vitro to arrest cartilage degradation and in vivo to reduce the progression of experimental OA (30, 89, 90)
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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. 
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Try "Tergazyme" from Alconox.  Their cocktail is not public information, but its properties may be appropriate for your project.
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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? 
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I am not sure  but I think lumber segment L1 or L2 because some hip case presents with knee pain.
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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?
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Type II supracondylar fractures usually do well with Closed Manipulative Reduction and immobilization. The question is how to determine if the reduction with be lost during late post reduction
1) Assess if the first reduction is stable after manipulation. If suspicious, better add two percutaneous wires
2) Immobilise with elbow in a flexion of 90 deg and below An obluse angle will hardly maintain the reduction.Obtuse position is advised if one suspect a vascular compromise.
3) A fracture line which is oblique in coronal or sagittal plane has high risk of displacement
4) Varus anglulation if any  after reductionnot acceptable
5) posterior tilt if any will limit a later flexion movements
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Loss of somatosensory function with regards to neuropathic pain indicates abnormal function mediated by small and large nerve fiber.
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In thinking about your interesting question, as a rheumatologist, I am not certain exactly what your question is referring to. Ciro refers to autoimmune processes that would imply the arthropathy is not OA, but certainly connects arthritis with SNHL or Corneal involvement (so does syphilis). If you are referring to neuropathic pain and conceptualization of loss of function in Somatosensory pathways to cortex as negative symptoms and gain of function as positive symptoms, then this Medscape article that uses a BMJ figure explains both aspects and likely pathways quite clearly. See link to figure one below. 
 How to imagine the MOA of OA to trigger peripheral and/or central NP , neuropathic pain with both loss and gain of function OR negative and positive symptoms would invoke theories of afferent input modulation and neuroplasticity evolving in a chronic fashion. Emil suggests swelling that may be one means by pressure on mechanoreceptors that sprout into dorsolateral columns lamina and overlap with type c nociceptive pathways and cross over each other and up the contralateral spinothalamic tract. However, swelling may be associated not only with pressure on surrounding nerve fibers of various sorts, but also with various cytokines and soluble inflammatory factors that modulate various type of nerve stimulation and conduction. I hope this helps you.
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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.
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If the results are mixed, then the indications should be made clear. I never use viscosupplemenation injectoins in advanced OA (i.e.grade 4 ) because in the majority of these patients it fails, and the patients are disappointed.
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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? 
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Severity of Knee osteoarthritis should actually be measured without radiographs by measuring the loss of function due to same. After all, it is loss of knee function affecting his quality of life which brings the patient to the clinician!
There are multiple knee function scoring systems available which would enable this measurement, e.g. KOOS, SF-36, WOMAC, Oxford knee score........!
KOOS remains one of the most validated scoring system out of these.
Attaching a couple of articles comparing/reviewing these knee function rating scales/instruments. Hope you find these useful!
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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! 
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I did, and they had no information regarding that issue. Thanks
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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? 
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Cause Osteoarthritis is complex and multifactorial. It is a result of problems that deriving from the morphology of the cartilage and the mechanical properties of it, as well as changes in the biochemistry of the area.
Few factors that are described as causes of OA are
Anatomical abnormalities
Trauma (either major fractures or microfractures as result of repeated low degree trauma)
Loss of joint stability
Abnormal loading due to alteration of the weight bearing axis
Meniscal surgery (medial meniscectomy almost doubles the incidence of OA)
Altered kinetics of the knee
Gait modification.
Repetitive increase load in a particular area of the knee
Inflammatory factors (increase of them)
Increase of activities of the immune system in the joint environment
Metabolic disorders
Obesity.
In females if they have 6 or more pregnancies.
Vitamin D deficiency (about 2.5 times more OA)
and so on.
All mechanical problems influence the Proteoglycans and all inflammatory problems increase the Proteolytic Enzymes.
Obesity is found to increase the Leptin within the joint which is influencing the chondrocytes.
These are part of the Causes leading to Osteoarthritis and mentioned here in brief.
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As the patients do exercises,Can they use drugs less than other patients that they do not exercise???
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Physical exercises are necessary for the Rheumatoid patients as the joints remain flexible and soft tissues mobile. Despite this it will be better to do them when the inflammation is better (so better not during acute inflammatory phases where the patient will be benefitted by rest). Medication has to be monitored and controlled by having regular follow up reviews and the regime has to be changed accordingly.
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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?
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Very good points. This is the way to avoid the upper cross syndrome.
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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? 
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Here are some possible publications related to a 3 week, outpatient based multidisciplinary pain program that could be helpful for you to review--W. Michael Hooten had been the main physician champion in the past.
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Almost all the physiotherapy articles on OA  shows clinically significant in management osteoarthritis(Hip & Knee). Whether this significant changes are also capable of changing pathology of OA , so can we believe on each and every articles showing clinically significant ..............?
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This is a philosophical question which can be explained in an easy or complicated way. If we are talking about established tri-compartmental arthritis the answer is a straight "no". The only thing that may happen is for physiotherapy to delay the total knee replacement, as you already mentioned. In a case of post-traumatic uni-compartmental arthritis (either anterior or medial compartments) in a very young patient, the possibility and sometimes necessity is to delay surgery, but again changes are not reversible. The treatment is there only to help the soft tissues, but not the articular cartilage. So again the word is "delay". All this is already rightfully mentioned above. But now, this is the philosophical part of it. Physiotherapy, in the broad spectrum, is possible an educational tool to change the way of life and it can help, as it is changing our attitudes, to prevent OA (although this is not the only way; causes of OA are multifactorial and cannot be answered in such simplistic way). But do we know to whom we will apply this "treatment"? The answer is to all. This is not possible though and so we continue to live and walk towards a total knee replacement.
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What would be effect of inhibition of osteoblast proliferation when Rheumatoid arthritis patient is administered with DMARD capable of inhibiting osteoblast proliferation?
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In Rheumatoid arthritis, the inflammatory cytokines (TNF alpha, IL1, IL17 etc)  inhibit osteoblast proliferation and promote osteoclast differentiation. This causes bone erosions & periarticular osteopenia locally and generalised osteoporosis at distant sites.
The effect of inflammation in negatively affecting bone loss is very high. Almost all DMARDs have a salutatory effect on bone health by reducing this inflammation. Though invitro studies show that there is some deleterious effect on osteoblast proliferation, this effect is very small compared to the deleterious effects of inflammation itself. Thus, in clinical terms, the net effect is positive by stopping the bone loss or at least reducing the rate significantly.
The newer Biologic DMARDs like the TNF inhibitors (Infliximab, etanercept etc) have even shown reversal of bone erosions in a few studies (by MRI imaging) and possibly have a more positive effect on bone health than the non Biologic DMARDs like methotrexate. 
Hope this helps
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I want to know the relation of severity with the specific clinical findings of crepitus sound.
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An interesting question. Years back I started my career with this question.  We tried to record the sound from the joint using a microphone attached to the knee - an experiment not entirely successful. 
Crepitus apparently has no direct relationship to knee OA. It frequently decreases when a knee becomes inflamed or has fluid in the joint, a common occupancy as knee OA becomes more severe. 
Best best in can be an early sign of OA if it is present. 
Siddharth Das 
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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?
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I think there are several problems with using heparin with little or no advantage
  1. Heparin binds to receptors on the platelets thus potentially changing platelet physiology, whereas Citrate is well established as a safe anticoagulant working by  chelating the free calcium, and is easily reversible by the addition of more calcium.
  2. heparin increases the sensitivity of platelets to activation and causes platelet aggregation. Whether this is significant or not in the clinical situation where the PRP is being reinjected within minutes has yet to be ascertained.
  3. There have been cases of contaminated heparin and so if one were to use heparin tubes it would be important to ascertain the origins of the heparin used.
Because citrate uprates glycloysis in the platelets there is over several hours an increased rate of spontaneous activation which is reduced if ACD-A anticoagulant is used. I have a separate question here on whether there is any significant difference in the spontaneous activation rates between pure citrate and ACD-A for periods less than 60mins. Nobody has yet offered any concrete evidence either way but there is the suggestion that on a theoretical basis ACD-A could be preferred. 
Another question (also asked here) is how much citrate is necessary to achieve anticoagulation. The present protocols are based on historical blood bank requirements where the blood should remain anticogulated for 3-4 weeks. In reality the amount of citrate can be significantly reduced to 0.5ml 3.8% citrate in 8.5ml blood without any coagulation at several days, thus potentially decreasing the increased activation related to uprated glycolysis.
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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.
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There are some good studies than can give you ideas about where to look, I would start looking the combinations with Diclofenac the possible synergistic effects of Vitamin B complex an are not clear but the possible answer could be in some of these mechanism: increase in the availability of substances that Blockade nociceptive transmitters, also it have been reported a opioid mechanism and nitric oxide liberation and this have been probed to some degree with the inhibition of the analgesic effect of vitamin B complex trough the administration of naloxone an L-NAME.
Here are some works that will give you a good idea about where to look including one in osteoarthritis patients.
1. Magaña-Villa M, Rocha-González H, Fernández del Valle-Laisequilla C, Granados-Soto V, Rodríguez-Silverio J, Flores-Murrieta F, et al. B-vitamin Mixture Improves the Analgesic Effect of Diclofenac in Patients with Osteoarthritis: A Double Blind Study. Drug Research. 2013 Mar 22;63(06):289–92.
2. Dehghan M. Comparative Effectiveness of B and E Vitamins with Diclofenac in Reducing Pain Due to Osteoarthritis of the Knee. Medical Archives. 2015;69(2):103.
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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.?
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I fully agree with Drs TANCHEV and SATISH on that subject... On my opinion, and except for uncemented implants that follow specific biologic rules and scheduled radiologic controls, the time during which walking aids are necessary is usually related to the results of the post-operative rehabilitation. These results are themselves related to the initial physiological capabilities - in direct relationship with the age - and to the pain relief... So I don't have specific rules for it and on my experience, younger and healthy patients heal really very fast and therefore older ones need further treatments and help. I usually let them manage their own personal and socio-professional reinsertion following their inner feelings and their ability to properly lock their knee and move it up to a satisfying ROM. The average time is about 3-6 weeks... Despite all this ans as previously said, preoperative contractures and per-operative instability or insufficient ROM should lead to closer surveys and advices..
Best regards to you all!
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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 ?
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Panayot is right here: if the femur is valgus and the tibia varus the ligaments and cartilage in the medial compartment of the knee are overloaded under weight and that destined for alteration.
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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.
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Thanks Eric. Thank you very much.
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From clinic to community.
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The water should have at least 28, better 31 degrees C. The same kind of exercises, as performed on land can be done much better in the breast deep water, due to the updrive through water (like walking, bending, sitting position from sitting to standig, etc.) 
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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.
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Dear Professor Tanchev,
In Turkey, hyaluronic acid  preparations are not paid by insurance, patients pay the bill. My experience is that the short and long term efficacy of intraarticular corticosteroids injections is superior to intra articular hyaluronic acid.
We reported that even a 10 day spa therapy course in a spa resort may have beneficial short and medium term effects in terms of pain and function in severe knee osteoarthritis (Clin Rheumatol. 2007 Dec;26(12):2063-71.) 
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I am trying to find out level of cartilage destroying enzymes which is associated with crepitus sound with pain.
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Crepitation suggests sever chondromalacia (gr II and III). I have no experience with the measuring the level of destroying enzymes.
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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?
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Dear Kanwal,
In theory you can modify any questionnaire, but if it is not validated, obtained results are not "valid" by regulators.  Publications could be more difficult, but if you explain and justify in detail the modifications, and those are accepted by the publisher, then you could publish.
As suggested above, I would go for a validated questionnaire for the pathology and for your country. Otherwise, I would try to validate a modificated questionnaire previously to be used in a larger clinical trial.
Hope it helps.
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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-
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Gustavo,  Important changes, regarding daily time spent performing an activity, may be measured in increments of time such as 10 or 15 min vs. an increased level of workload or a combination of both as well as considering the level of pain that may be limiting the activity.
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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!)
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There is an infrequent condition known as intermittent hydrarthrosis (IH). Its onset is usually seen in childhood or adolescence. It usyally affects the knees, causing considerable effusion of the joints. The synovial fluid may be mildly (no more than 5000 white cells/mL) or non-inflammatory.
Since I see the Institution where you are working, may be you could ask to your clinician colleagues to collect synovial fluid from their IH patients.
I don't know if such substance could be considered "normal" for your purposes, but IH synovial fluids are the closest and most abundant sources of it, to the best of my knowledge.
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In patients with a meniscal tear and moderate osteoarthritis, does partial menis- cectomy improve functional outcomes than physical therapy does?
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It depends to patient complaints, patient expectation and lifestile and severity of lesion.
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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. 
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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.
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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?
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Arthroscopic management is generally useful and effective in the well-selected patients over 50 years. The main problems in these patients are degenerative meniscal tear or chondral damage (chondromalacia.). We can treat degenerative meniscal tear and grade II-III chondromalacia effectively.
However,only arthroscopic treatment is inadequate for chronic meniscal root tear with degeneration and III-IV chondromalacia. Especially, meniscal root tear is at high risk of retear due to low healing potential after arthroscopic fixation regardless of the method.  Accordingly, we perform HTO after arthroscopic debridment  in active patients with chronic meniscal root tear accompanied by grade III-IV chondromalacia, and think that this method is very effective. 
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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.
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Subhash,
we tested PHB/HAp scaffold for bone and UHMWPE implant for cartilage defects replacement. But the last one was not porous.
In case of PHB/HAp there were sites of neo-osteogenesis after 3 weeks of orthotopic transplantation in rats bone. Over time there was resorption of the material and replacing it with bone. 
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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,
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What sort of X-Gal staining are you doing?  Is it for aging, a reporter or to validate recombination?  It can be a bit tricky andI have found better results are obtained by staining with a Life Technologies antibody for the later two cases.
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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.
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OA is not really a disease. It is a structural state that can be the end result of just about any disruption of joint integrity, including PsA, RA, too much football, congenital dysplasia and old age. Inflammation is probably mostly just a result of mechanical irritation secondary to the structural changes. I suspect it is too heterogeneous a category to be worth comparing. If you are looking at patterns of inflammation gout or RA might be of more interest.
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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
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Dear Dr. Subash,
TGF-beta-3 is the key factor promoting the differentiation of MSCs to cartilage either by mono-layer,micro-mass or pellet culture systems.With the little experience i have,i would believe that the number of days defines articular cartilage and hypertrophy.Extended differentiation would up-regulate the hypertrophic marker ColX. Essentially 12-16 days of differentiation would result in healthy articular cartilage.Extending it for another 10-15 days will result in hypertrophy.
Hope this helps!
Regards,
Charan
Stempeutics Research
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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.
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Oh, this is also the question I am asking. I take DAS's view. we need a RCT.
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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?
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Dear Dhara,
The ultimate goal of exercise in OA is to prevent or delay disability. An exercise program should incorporate elements to lessen pain during activity and to
increase or at least maintain joint range of motion, periarticular muscle strength, joint stability, and aerobic capacity or level of conditioning.
Exercise in OA should be adapted according to the presence and severity of pain.
In painful episodes:
- Isometric exercise or exercise in a non weight-bearing
(e.g., biking, rowing with adapted tools) or
- In a partial weight-bearing position (e.g., aquatic ex) should be recommended.
In painless (or at least less painful) periods:
- Exercise program may include progressive muscle performance exercises.
The above exercise programs may delay disability but does not help regenerationof the cartilage. Hence, it can't recover the actual joint pathology, so the final choise of treatment will remain joint reconstruction or replacement surgery untill we get a new line of treatment.
Regards
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I am giving a lecture to a audience of sports physicians, physiotherapists and physical trainers on the topic.
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Dear Christan,
Good question. Exercises on OA knee has been performing form many decades and it has built strong positive evidence. As you are going to talk in front of experts I would suggest to prepare the material/ slides using recent guidelines/ position statements/ review etc. Below is some of the recent guidelines on Exercise and OA Knee. Hope this will serve the purpose...
Many more recent publication are also there but couldn't attached all of them...
Regards
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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.
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In principle for the primary case you don't have such problems. The previous answer is correct to look at https://www.researchgate.net/go.Deref.html?url=http%3A%2F%2Fwww.orthobullets.com%2Frecon%2F5016%2Fsagittal-plane-gap-balancing.
But for this special situation a revision prosthesis is necessary .
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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?
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Dear Subhash
These articles may be useful for you
1) Am J Vet Res. 1997 Oct;58(10):1132-40.
Effects of intravenous administration of sodium hyaluronate on carpal joints in exercising horses after arthroscopic surgery and osteochondral fragmentation.
Kawcak CE1, Frisbie DD, Trotter GW, McIlwraith CW, Gillette SM, Powers BE, Walton RM.
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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)?
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Dr. Swan, I am sorry but I have to disagree with you as far as inflammatory changes in chronic posttraumatic OA are concerned. There are many such cases in which chronic non-specific inflammatory synovitis is observed. So I do not see any reason for rejecting the use of NSAID in similar cases. Actually, in late stages the etiology of OA is no longer so important (except for RA, Bechterew) and the pathoanatomic changes are similar - cartilage degeneration, joint deformity, ligament laxity accompanied by chronic non-specific inflammatory synovitis (not always !).
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Dear Ezequiel
These articles may be useful for you
1) J Bone Joint Surg Am. 2012 Dec 5;94(23):e1721-7.
Platelet-rich plasma increases matrix metalloproteinases in cultures of human synovial fibroblasts.
Browning SR1, Weiser AM, Woolf N, Golish SR, SanGiovanni TP, Scuderi GJ, Carballo C, Hanna LS.
2) Foot Ankle Clin. 2013 Sep;18(3):437-48.
Conservative treatment of asymmetric ankle osteoarthritis.
Schmid T1, Krause FG.
3) Clin Med Insights Arthritis Musculoskelet Disord. 2013 Sep 4;6:65-72.
Regenerative injection therapy with whole bone marrow aspirate for degenerative joint disease: a case series.
Hauser RA1, Orlofsky A.
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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?
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Thank you to all of you. I will take a look to all these publications. In fact we would need TMG data stratified by sex, age and probably by physical activity for "normal" subjects in order to be able to compare results of TMG in OA patients. And it is clear that the procedure should be performed similarly to also be able to compare results.
Thank you again.
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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?
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I routinely do a papain digest on connective tissues such as cartilage (60 degrees C overnight) which will dissolve the majority of the cartilage and result in a solution that is suitable for both sGAG assay (by the DMMB assay) and DNA assay (I usually use the Hoechst assay as its cheap and easy). It really depends whether you want to know the proportion of your proteoglycan in the tissue or how it relates to the cell number in the tissue. In agreement with previous answers, its usual with cartilage to relate to total protein (although the DNA content is valid data in its own right) and its always more accurate to start with a freeze-dried tissue but not absolutely necessary.
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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.
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Dear Subhash
These articles may be useful for you
1) Allogenous bone with collagen for repair of deep osteochondral defects.
Schleicher I, Lips KS, Sommer U, Schappat I, Martin AP, Szalay G, Schnettler R.
J Surg Res. 2013 Dec;185(2):667-75.
2) Role of autologous chondrocyte transplantation in articular cartilage defects: An experimental study
Amit Rastogi, Pradeep Srivastava,1 Zafer Iqbal, Vinay Kumaraswamy, and Ravindra Pratap Singh
Indian J Orthop. 2013 Mar-Apr; 47(2): 129–134.
3) Rabbit articular cartilage defects treated with autologous cultured chondrocytes
Brittberg M, Nilsson A, Lindahl A, Ohlsson C, Peterson L. .
Clin Orthop Relat Res. 1996;326:270–83
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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?
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Dear Subash,
TGF-beta-1 is mostly related to fibrosis and wound healing and TGF-beta-3 is mostly used for chondrogenic induction and yes TGF-beta-1 has also been used for chondrogenic induction by a few groups.
TGF-beta family functions are widespread in their areas of development and function.
I am attaching a brilliant article published in Cell Stem Cell.Take a look.
Hope this helps
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What is the best method for induction of surgical osteoarthritis in rabbit knee joint?
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Dear Gamal,
There are several surgical methods that have been developed such as unilateral anterior ligament transection and menisectomy to mimic the OA in different animals but unfortunately no method is ideal because each has advantages and disadvantages. It all depends on what you expect to show. I invite you to read the attached article which has revised your question. Good luck.
SM
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I am starting a new project in the osteoarthritis field and need to introduce a new chondrocyte culture into the lab.
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Hi,
primary/immortalized chondrocytes of any origin constitute a difficult system since they easily lose the chondrocytic phenotype, additionally if considering cell isolation, it is difficult to gain efficient cell population for culturing. You can try chondrocytic cell line SW-1353 (ATCC,HTB-94, human chondrosarcoma) - these cells produce molecules/proteins typical to cartilage and respond in a way similar to primary chondrocytes. I used this cell to study the effect of some col II mutants on ER stress, UPR and ECM pathobiology etc: doi: 10.1016/j.bbrc.2010.04.056; doi: 10.1002/humu.21506. Alternatively, you can buy D1 cell line (ATCC CRL-12424) that derives from mouse bone marrow stromal precursor. First, cultivate the cells w/o stimuling factors, freeze stocks, and then use it in the presence of stimulating factor and differentiate to chondrocytes. After that it will be important to standardize the cells with respect to population doublings/expression of chondrocyte markers for your experiments. ie SOX-9, MIA, col II,matrillins. Good luck!
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Varisation osteotomy is an established treatment for younger patient with arthritis of knee due to valgus malalignment. Since the majority of those deformities is located on the femur, supracondylar varisation osteotomy is indicated in the majority of the cases. Nevertheless, in some case in tibial deformities osteotomy of the proximal tibia can be performed. Is there an indication for double osteotomies in patients with a mixed type (femoral and tibial) deformity?
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Dear Gustavo, by doing it in the way of your recommendation, you will probably be right in the majority in the cases, but you will certainly not perform your correction at the site of the deformity in those with a femoral varus or a tibial valgus deformity ... my questions actually yielded on those patients with a severe mixed type (combined femoral and tibial) deformity ... in order to avoid an oblique joint line double osteotomy certainly seems an interesting option