jan koval

:)dziala pw na wyobraznie

mit

KOMERCJALNA BZDURA   Piskoor - mlody  bedzie wyzszy I ciezszy wkrotce  dla CIEBIE min 190, chociaz  dla typowej zabawy mantra albo gotama ok 184 w zupelnosci OK

A mi sie heli kojarzy wylacznie z praca (w ramach mojego treningu mielismy tez to) oraz przyejmnoscia - mam nadzieje uniknac darmowego przejazdu Moge strzelac - prawdopodobnie AVN glowy k udowej po zwichnieciu...... na szczescie , obecne total hip sa przyjazne narciarzom!!!!!!! Tez zycze wielu zjazdow!!!!

jakmoze zauwazyles nie mam ambicji instruktorsko/nauczycielskich przylec tutaj, razem pojezdzimy bez zbednych slow (pieprzenia) - zapewniam  nocleg na moj koszt - Ty placisz za bilet swoj i dojazd pojezdzimy smig, rzeczywiscie stromy teren i off-piste wglebokim sniegu  - po co strzepic jezyk....   do DK - ile Twoa zona ma lat? wyglada "bojowo" natomiast powinna sobie przypomniec, ze jest fragment ekwipunku , ktory nazywa sie...kije   Hammer - dla mnie brytyjski akcent na sniegu jest podejrzany, chociaz osobiscie poznajem jednego faceta z WlkB, ktory dobrze jezdzil - mial tez troche szczescia, bo wyciagnalem go z Back Country w JH - zupelnie zgubil orientacje

powsciagnalem moje ADHD i ogladnalem ten film - przelknalem brit accent tez   1/ facet  jezdzi w miare dobrze ale ....pieprzy za duzo 2/ czemu "jazda na stromym" jest pokazana na  takim sobie spadku a nie na  stromym? 3/ facet nawet kije ma za krotkie 4/ nie wiem, czym ta jazda pokazana na filmie ma byc jakas specjalna odmiana "nur fur steeps"?   nastepny odcinek to off piste - najwieksza jego zaleta to to, ze jest ...krotki...........   PS ogolnie - jedna z wielu produkcji  dostepna w net

stosujesz zle kryteria "wiary" - dla mnie info z osrodka sa tendencyjne z definicji……nie mowie, ze Wiki to alfa i omega…ale chyba przyznasz, ze Wiki ma prawo byc bardziej bezstronna strona ale to juz inna bajka. Po prostu z natury jestem podejrzliwy, a w dodatku mialem solidne przeszkolenie  nt small print i innych chwytow.. sam pare razy pojechalem te H - i mnie nie zachwycila, chociaz byl prawie doskonaly lod…owszem, trzeba  wiecej sie "zazebic' ……. i na pewno nie przekracza 40 stopni w najbardziej stromym miejscu  wszyscy lubia Naj…….stad postawa M-B : nie chca stracic nazwy "najbardziej stromej trasy".. ot co

1/ 45 stopni przez 10m to nie jest zadne wyzwanie 2/ info z M-B Team niezupelnie moze byc prawdziwe - w koncu sa oni zainteresowani, zeby harakiri straszyla - jakbys mial jakies oficjalne, BEZSTRONNE  zrodlo to bylo by lepiej   Prawie, a 40  to jest duuuuuuuuuuuuuuza roznica   PS wlasnie sprawdzilem (z Wiki) - widac, ze mialem racje o tym M-B Team......Ponizej jasno stoi ze najwieksze nachylenie to 78% With incline of up to 78%, vertical drop of 375 metres and a length of about 1500 metres, it is the steepest groomed slope in Austria

typowo PISARSKI temat

EEEEE juz przejezdzony i plytki…... chociaz lepsze to niz kazde boisko  

    http://www.mountainy...sMountains.html   Przepraszam dopiero teraz wyedytowalem z odp link'iem   Popatrz uwaznie na zdjecie przy Big Sky - tam jest 50 stopni, nie 40 Popatrz na pozostale links i "coloured contours" - jako geologicznie wyksztalcoenmu, powie Ci to wiele o miejscach takich jak Big Sky, Jackson etc. Kazdy, kto chce dyskutowac o jezdzie w stromym terenie, powinien przejrzec podana strone razem z links tam sa PRAWDZIWE TRASY  po  40-50 stopni . Porownaj sobie te miejsca z Twoim filmem (nie chce sie sprzeczac, ale dokladnie wiem, jak wyglada 40+ , bo calymi dniami wlasnie w takich miejscach lubie jezdzic. OSOBISCIE zjechalem wszystkie  z tej listy za wyj Silvertone (w planie) i Telluride (nie wiem, czy tam sie wybiore, bo Colorado jakos niespecjalnie lubie) I stale podtrzymuje twierdzenie, ze 99% tutaj piszacych nawet sie do 40 nie zblizylo - chyba , ze z podrecznym nocnikiem…...   PS Tomal - to nie moj film - a co do GoPro mam identyczne odczucia - sprzedalem po sezonie….

  dokladnie popatrz na  te scenyy - te zleby maja po 40-45 stopni - tak to wyglada w tzw Alta Chutes JH - widze duza rozbieznosc z Twoim filmem - nie wiem , kto to mierzyl u Ciebie…. wejscie w teren 40+ to jak ta scena na pocz wideo - glowa w dol , wybieramy linie i w dol…….nie ma odwrotu….   Nie lubie takich glupawych GoPro nagran, w dodatku facet  stchorzyl i pojechal w prawo od glownego zlebu, na dodaatek jest slabym narciarzem. postaram sie cos wiecej dolaczyc

Ladna demonstracja smigu - ok 1'33 troche Cie obwiozlo. No i, oczywiscie, na pewno nie jest to 40st Jak Tadeusz napisal - (zmieniam troche) - miedzy 40% a 40 stopni jest przepasc.. Tak ok pow 35 KAZDY nastepny stopien pochylenia to przepasc.......... Moja ulubiona trasa w moich gorach ma SREDNIA  28 stopni - latem, w czasie  wypraw z plecakami, w zasadzie  mozna isc po czworakach i nie ma wiekszej roznicy  czy sie idzie po czworakach czy "prosto".... Od 35 to juz powazna zabawa, pow 40 krotki skret obowiazkowy albo  skret podskokiem - zaloze sie, ze moze 1% ludzi z tego forum  zjechalo kiedykolwiek dluzszy odcinek pow 40 stopni......   A ta dyskusja  dowodzi, ze internet wszystko wbaczy ( to nie do Ciebie, Mitku)........Ty przynajmniej publikujesz SWOJE  filmy. Pisarze tego unikaja i dobrze, chociaz moze bylo by smieszniej na forum.....

  tE WSZYSTKIE FILMY JAPONSKo-Koreanskich instruktorow to jak podrobka dobrego auta.......... czy m,i sie podoba  obecna jazzda na muldach na zawodach?  nie wiem, ale patrze z fascynacja (zwlaszcza na kolana!!!) - widze i rozumiem  klase, bo osobiscie  przejechalem trase olimpijska w  Whistler - polecam!!!   No to chyba czas najwyzszy ?          z moich zakamarkow nmiemieckiego  wyglada, ze tepich to chodnik...?

to sie mylisz. nowoczesna technika jazdy po muldach w wydaniu zawodniczym to tzw pancake - nioe ma nic wpsolnego ze smigiem, za wyjatkie rytmu  Nie chce namieszac i nie chce sie klocic, bo nie o to chodzi - ale zobacz na tym filmie:......   https://www.youtube....h?v=e6clufY6USY

  mOZNA TAK ROBIC, ALE RESEARCH  project  musi byc zatwierdzony przez RBI - w protokule musi byc zapisane to, ze bedzie double blinded - zwykle o tym sie informuje, ale ,zeby wzmocnic znaczenie statystyczne,  mozna  wnioskowac o wyjatek - jezeli jest to zaakceptowane, wtedy pacjenta nie trzeba informowac, ze moze dostac placebo... Ale, jak napisales, regula jest  disclosure....

mozesz robic, co tylko chcesz, a te buty po prostu maja za duzy volume czyli objetosc prawdopodobnie potrzebujesz  last 95-98 z low  volume. zalezy, jaka "gruba " lydka, jak nisko schodzi brzusiec miesnia itp polsrodkami mozesz te buty uratowac, ale po prostu byly one zle dobrane w sensie wymiarow

Nikt CIEBIE  nie ocenia , tylko podejscie  do Ciebie. cross section - przekroj poprzeczny dolu podkolanowego (anatomia)

  Hej zadne pretensje, skad, cos Ty - moze tylko troche, bo akurat Colorada nie jest moim  najlepszym miejscem - nastepnym razem przy flancowaniu, umiesc mnie prosze w Wyoming albo chociaz Utah     Mysle, ze slowo "hochsztapler" bylo w tym kontekscie , przyznaje, nieco   naciagniete. Ale chyba rozumiesz watpliwa etyke Twego leczenia?. Poza tym -  wybitny lekarz tez  moze miec potrzeby finansowe, czyz nie? Co do dolu podkolanowego juz napisalem cross section anatomy - voila Stale zycze zdrowia!     Tutaj takie rzeczy nie sa zwykle omawiane, z wielu powodow . - jak ktos ma powiklania, to boi sie wyjawnic szczegolow , gdyz moze to zmniejszyc szanse na skuteczny law suit - tutaj nie mozna sobie pozwolic na leczenie nei poparte szczegolowymi dowodami na  skutecznosc - nawet nie dostaniesz approval z insurance company - a jezeli jest cos off protocol to jest to robione jako eksperyment, ktory wymaga ton papierow, poprzednich wynikow itp itd. No i placi sie zwykle za to z Grant'u  (czyili programu naukowego)   Swiete slowa....................

No i powoli dyskusja, ktora byla na niebezpiecznym zakrecie, przynosi owoce - jak sie powstrzyma emocje, to od razu mozna cos skorzystac     NIe dziwie sie i nie potepiam Twej decyzji - watpliwosci mam jedynie co do  etycznej strony - dla mnie bylo by  dopuszczalne, gdybys byla poinformowana,ze beirzesz udzial w leczeniu eksperymentalnym, nieudokumentowanym itp (przepraszam za Ty - jezeli to razi to zaznacz prosze) - ale wtedy leczacy nie powinien brac pieniedzy Na szczescie  nie zgodzilas sie na sterydy     z ukrwieniem to nie do konca prawda....   Tutaj nie ma roznicy - zawsze trzeba wytlumaczyc wszystko - i udokumentowac   Mitek to normalna reakcja   Dziekuje  za info - wlasnie - zgoda na eksperymentalne leczenie to skomplikowana sprawa - dobrze , ze w Polsce jest to tez przestrzegane

mam nadziej, ze stale rozumiem j polski Dla mnie jest kolosalna roznica miedzy: ".....Udowodniono również, że odpowiednie komórki macierzyste (w tym dorosłego dawcy) mogą różnicować się w komórki podścieliska krwiotwórczego, kość, chrząstkę,..."  a np : udowodniono, ze PRP/SC "naprawiaja" chrzastke , lakotki itp.... Jak mowilem, na pewno cos z tych wskazan  w sumie sie zdeklaruje, ale nie znaczy, ze jest to uznana metoda w kolanie.   Biovico - nastepny etap?

nie wiem, jak to teraz w POlsce wyglada tzw informed consent -  czyli zdobycie zgody na  dane leczenie....czy lekarze maja na to czas? odpowiadaja na pytania  pacjentow? czy zbywaja brakiem czasu? Bo jezeli maja czas, to w przypadku PRP czy podobnych, powinni wytlumaczyc np tak:".... obecnie nie ma dowodow na to, ze PRP dziala w Pani(a) przypadku. Proponowana terapia jest terapia doswiadczalna. Mamy nadzieje, ze, opierajac sie na logice i wiedzy podstawowej, ta metoda moze pomoc, ale przekonywujacych danych na ten temat nie ma..." w moim przypadku "wymusilem " PRP , gdyz  jest malo inwazyjne (nie zgodzil bym sie na podanie przez dol podkolanowy i wstrzykniecie do lakotki), wykonany byl niejako "przy okazji" z zerowym ryzykiem i nikt za to mnie nie wydoil..... PS gdybys sie odniosl do IC bylbym wdzieczny

nie oceniam pracy tylko POSTAWE , ktora jest nieetyczna - niestety, czesto spotykana w Polsce.... Typowy przyklad to ladowanie  malaczasteczkowej heparyny po kazdej rekonstrukcji ACL , nawet u b mlodych ludzi bez czynnikow ryzyka DVT - jezeli nie wiadomo, dlaczego, to chodzi o ...pieniadze - polaczenia z firmami farmaceutycznymi, wycieczki itp. W USA, leczenie metoda, ktora nie jest uznana, oznacza koniec kariery - no , ale co ja wiem nt medycyny w USA......   PS . to co pisze, nie jest  krytyka medycyny w Polsce, tylko jej fragmentow. znam osobiscie wspanialych lekarzy polskich...............

Ponizej fragment nwszego artykulu przegladowego nt GFs i PRP i SCT  w aspekcie  choroby zwyrodnieniowej stawow . Prosze zwrocic uwage na slownictwo uzyte w tym aspekcie : pelno trybu przypuszczajcego," w trakcie badan", "w przyszlosci moze tak byc" etc. moze komus sie to przyda. Sam  jestem przekonany, ze np total joint replacement (endoprotezy stawow) za kilkanascie lat beda zastapione hodowla tkanki chrestnej i jej wbudowanie w stawy. Na razie jednak pow metody sa w fazie badan PS sorry za angielski, ale nie mam czasu przetlumaczyc     Growth factors & stem cell therapy   During development biosynthesis is stimulated by a variety of anabolic cytokines and growth factors, such as TGF-β, bone morphogenetic proteins and FGF. In OA, many factors, such as inflammatory cytokines TNF-α and IL-1, are produced by the synovium and the chondrocytes. In normal adult cartilage, chondrocytes synthesize matrix components very slowly and there is strict regulation of matrix turnover: a delicate balance between synthesis and degradation. In OA, however, this balance is disturbed, with both degradation and synthesis usually enhanced until changes in both bone cells and chondrocytes favor catabolic activity: proinflammatory cytokines, including IL-1, TNF-α and IL-6, act to increase the synthesis of MMPs, decrease MMP enzyme inhibitors and decrease extracellular matrix synthesis. The initiation of such degradative alterations in the joint leads to the depletion of cell reservoirs, loss of the condrogenic potential of cartilage bringing about the preponderance of a fibrogenic phenotype and the structural and functional failure of the joint [144]. Current treatments for cartilage defects in early OA include surgical interventions (microfracture and osteochondral auto/allo-grafts), which have shown promise in clinical trials [145]. Such catabolic changes may have the potential to be reversed by the use of a pool of growth factors [146]. The FGF family of growth factors regulates branching morphogenesis and limb development [147]. FGF-18 is thought to have an anabolic effect on cartilage, leading to increased deposition of FGF-18 in the ribs, trachea, spine and joints. Preclinical data of the anabolic effects of FGF-18 is now being followed-up by Merck Serono in Phase I clinical trials [147]. Investigators are currently looking into the therapeutic potential of endogenous plasma rich in growth factors that may have the potential to modulate gene expression of chondrocytes, synoviocytes, macrophages and MSCs. Therapies involving the utilization of growth factors could have the possibility to stimulate an anabolic microenvironment within an affected joint. A possible approach to maintaining the homeostasis of damaged OA joint tissue could be the use of growth factors, which in turn could improve cartilage/bone dysregulation and lead to reduced pain and improved function [146,148]. Platelet-derived elements, such as platelet-rich plasma, human platelet lysate and platelet supernatants, are carriers of endogenous morphogens, which can be stimulated by endogenous or exogenous activators to modulate cell fate, encouraging cell proliferation and matrix synthesis, alongside anti-inflammatory effects owing to the downregulation of catabolic pathways [148,149]. Platelet-derived elements are convenient and easy to extract, with a high-speed recovery potential offering multiple growth factors at an affordable cost [149]. Platelet-rich plasma injections have had beneficial effects in the treatment of mild-to-moderate OA in approximately 6 months compared with hyaluronic acid and neutral saline injections [148]. Experimental, preclinical and clinical studies are being reported suggesting short-term (1–2 years) improvement, but long-term results on cartilage injuries and joint pain are unknown [149]. MSCs are multipotent precursors of connective tissue cells that can be isolated from a wide variety of adult human tissues, including synovial joints. Endogenous MSCs could possibly act as reservoirs for cell repair or immunomodulatory sentinels reducing inflammation [144]. Current methods rely on the paracrine properties of MSCs that release several growth factors, such as HGF, IGF and TGF, along with anti-inflammatory factors, including cytokines, IL-1ra, indoleamine 2, 3-dioxygenase and HLA antigen-G5 [150]. Chondrocyte and osteoblast phenotypes are established via the activation of pathways induced by paracrine factors, such as the SMAD cascade by BMP-2, TGF-3 or Wnt signaling [151]. Thus, the paracrine factors delivered by the MSCs may be more important for MSC therapeutic potency than stimulating repair responses for the differentiation of cells [144]. Early exploratory research studies used MSC-derived chondrocytes to regenerate cartilage in OA. A hydrated collagen matrix covered with MSCs was implanted into the joint; cartilage regeneration was complete after 6 months, although 20–100% of the new tissue had not integrated into the original cartilage [151,152]. Intervention with local delivery of ex vivo cultures of MSCs, as the chondrogenic potential of adult chondrocytes are lost and regression into a fibrotic phenotype initiates, in preclinical models of joint disease has led to promising outcomes and is now being tested in clinical trials recently started in 2013 [144]. Several early-stage clinical trials testing the delivery of MSCs via intra-articular injection into the knee are underway; however, the optimal dose and vehicle are still being optimized [144]. Bader and Macchiarini recently demonstrated the uses of stem cell techniques in several pioneering transplant surgeries, seeding an inert tracheal scaffold with either patient or donor bone marrow MSCs [153]. Further work is needed to characterize factors that could avert MSC derived chondrocyte to undergo premature hypertophy and understand what facilitates terminal development pathways for stable hyaline cartilage regeneration [154]. In the case of both anabolic agents, such as FGF-18, and stem cell therapy trials currently underway, it will be interesting to observe if therapies targeted at regeneration of damaged cartilage in people with OA will translate into improved outcomes for pain and function in the medium to long term. Go to: Pain sensitization in OA In chronic arthritis, a complex set of activation signals lead to the persistence of nociceptive pain. These include known molecular mediators of pain, such as substance P, prostaglandin E2, NGF, TNFR-α, bradykinin, GDNF and TRPV1 (Figure 3). Recent work has focused on tools to measure pain peripherally and centrally in people with OA (Figure 4). Several groups, including work in our unit, have reported the use of quantitative sensory testing in people with OA [155–158]. Pain threshold testing using algometers has become more widely accepted for measuring pain perception objectively since it is reproducible over time and has been validated in large studies with knee OA [159] or intra-oral pain [160]. We have found quantitative sensory testing to be a useful objective measure of hand OA pain [158] where people with hand OA showed evidence of peripheral sensitisation. A recent meta-analysis of pain pressure threshold testing in OA showed that pain pressure thresholds demonstrated good ability to differentiate between people with OA and healthy controls [156]. Lower pain pressure thresholds in people with OA in affected sites may suggest peripheral, and in remote sites central, sensitization. Recent studies have also shown that certain patients with OA may remain sensitized to pain even after joint replacement surgery [161]. Figure 4 Sensitisation in osteoarthritis Brain neuroimaging tools have also been used to investigate sensitization in OA. Gwilym et al. reported increased activation of brain pain processing centers with functional MRI in chronic hip OA, including the thalamus, anterior cingulate and insular cortex, upon quantitative sensory testing [162]. Kulkarni et al. reported similar activation using fludeoxyglucose PET in knee OA, suggesting activation of distinct brain regions in patients with chronic arthritic pain [163]. Several authors have described the phenomenon of chronic pain center activation during arthritis as central sensitization, a process thought to derive from hypersensitivity to stimuli by long-term activation of peripheral receptors in arthritic joints. A study by our group in people with hand OA showed significant activation in the thalamus, cingulate and insular cortex but not controls [164]. Of interest, the cingulate cortex is involved in developing emotion formation, learning and memory, suggesting that people with OA are adapting their responses to sensory cues in their hand and developing unique pain activation systems compared with controls. Others have suggested that the cingulate cortex is important in mediating affective processing of pain [165]. With increasing information regarding sensitization in OA, recent trials have reported the use of centrally acting agents, such as the selective serotonin and noradrenaline reuptake inhibitor duloxetine in the treatment of OA [166]. In a recent review, Brown and Boulay discuss the evidence for the efficacy of duloxetine use in four chronic pain conditions including OA [167]. They report that the studies published so far demonstrate a superior analgesic effect of duloxetine compared with placebo that is sustained with continued use and is also safe and effective when used concomitantly with NSAIDs. Further information on the cost utility of duloxetine has shown that it would be cost effective when evaluated in a US population and could be particularly useful in the over 65-year age group when NSAIDs have been prohibitive owing to side effects [168]. Other work by Micca et al. has shown that duloxetine is safe in younger and older people with knee OA [169]. Analgesics, such as duloxetine, may have an important role to play as pain-relieving options in patients who are unable to tolerate other classes of drugs or have demonstrated lack to efficacy in response to, for example, NSAIDs and/or opiate drugs. Findings from several large international studies suggest that the correlation between pain and structural change may not be a linear, particularly in a chronic disease, such as OA, when flares may occur (Figure 5). Emerging studies suggest that newer techniques such as quantitative sensory testing and brain neuroimaging may help to further phenotype pain subgroups in OA, which could help to develop pathways for the treatment of OA pain in the future. If it is accepted that pain sensitization is influenced by both physical factors occurring in the joint and psychological influences on pain, then it could be argued that an early combined approach of both pharmacotherapy plus other interventions, such as pain management programs, to inhibit the development of sensitization, for example, before chronic pain develops, could have an effect on clinical pain. Such interventions, early in the disease process, may be effective in modulating the development of chronic pain in OA, but will need to be tested in the context of clinical trials. Figure 5 Complex nature of pain in osteoarthritis Go to: Conclusion OA is a heterogeneous and debilitating disorder for which there are no universally accepted disease-modifying treatments. It affects large weight-bearing joints including the hip and knee but also smaller joints often in a nodal distribution in the hands. Recognized risk factors include obesity, genetic risk and previous mechanical injury. Since OA is a chronic disease that often progresses after the third or fourth decades, any intervention for pain that is used needs to be safe, with minimal side effects and of long-term benefit. It is interesting to note that many of the agents discussed in this review that could have a therapeutic effect, are also associated with potential harmful effects. For example, NSAIDs, such as indomethacin, can lead to destruction of cartilage, as can treatment with anti-NGF and corticosteroid therapy, suggesting that a positive effect on joint pain may also be associated with accelerated joint destruction, which is an extremely important factor in a chronic, long-term condition such as OA. Recent work highlighted in this review also suggests that the relation between pain and structural damage does not always follow a linear pattern in OA (Figure 5). Recent focus has been on optimizing efficacy of analgesics including NSAIDs and opiates. Emerging data from meta-analyses suggests a limited role for nutraceuticals including glucosamine and chondroitin. The physician looking after OA patients may need to consider the use of centrally acting analgesics, such as duloxetine, if there is lack of efficacy with NSAID/opiates over time and possibly clinical evidence of sensitization. It is only when risk factor reduction, lifestyle advice and pharmacological intervention have been unsuccessful that joint replacement surgery can be considered primarily for OA of the hip and knee. Go to: Future perspective Compared with other inflammatory rheumatic diseases, for example, rheumatoid arthritis, there are no disease-modifying treatments for OA. Promising new avenues for understanding the pathophysiology of pain include recognition of NGF as a potential therapeutic target in certain groups with OA, in addition to structure modifying agents including growth factors, such as FGF-18, or stem cell therapies, which are currently in early clinical trials. ​ Pathological changes in the osteoarthritic joint Risk factor modification for OA Osteophytes & their effect on OA pain Influence of bone marrow lesions on OA pain Targeting synovitis to treat OA pain NSAIDs & nutraceuticals for treating OA pain NGF monoclonal antibodies Growth factors & stem cell therapy Pain sensitization in OA Go to: Acknowledgments Financial & competing interests disclosure A Kuttapitiya was funded by a Wellcome Trust Value in People Award, grant number 087846/Z/08/Z. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. No writing assistance was utilized in the production of this manuscript. Go to: References Papers of special note have been highlighted as: • of interest; •• of considerable interest Woolf AD, Erwin J, March L. The need to address the burden of musculoskeletal conditions. Best Pract. Res. Clin. Rheumatol. 2012;26(2):183–224. [PubMed] Hunter DJ, Guermazi A, Roemer F, Zhang Y, Neogi T. Structural correlates of pain in joints with osteoarthritis. Osteoarthritis Cartilage. 2013;21(9):1170–1178. [PubMed]• Useful paper discussing the relation of structural changes with pain in osteoarthritis (OA). Page CJ, Hinman RS, Bennell KL. Physiotherapy management of knee osteoarthritis. Int. J. Rheum. Dis. 2011;14(2):145–151. [PubMed] Hawker GA, Stewart L, French MR, et al. Understanding the pain experience in hip and knee osteoarthritis – an OARSI/OMERACT initiative. Osteoarthritis Cartilage. 2008;16(4):415–422. [PubMed]• Important reference discussing the importance of pain in OA. Haviv B, Bronak S, Thein R. The complexity of pain around the knee in patients with osteoarthritis. Isr. Med. Assoc. J. 2013;15(4):178–181. [PubMed] Wenham C, Conaghan P. Call for new treatments in OA. new horizons in osteoarthritis. Age Ageing. 2013;42(3):272–278. [PubMed] Hochberg MC, Lawrence RC, Everett DF, Cornoni-Huntley J. Epidemiologic associations of pain in osteoarthritis of the knee: data from the national health and nutrition examination survey and the national health and nutrition examination-I epidemiologic follow-up survey. Semin. Arthritis Rheum. 1989;18(4 Suppl. 2):4–9. [PubMed] Danielsson L, Hernborg J. Morbidity and mortality of osteoarthritis of the knee (gonarthrosis) in Malmo, Sweden. Clin. Orthop. Relat. Res. 1970;69:224–226. [PubMed] Feldmann M, Maini RN. Anti-TNF alpha therapy of rheumatoid arthritis: What have we learned? Annu. Rev. Immunol. 2001;19:163–196. [PubMed] Goldring SR. Alterations in periarticular bone and cross talk between subchondral bone and articular cartilage in osteoarthritis. Ther. Adv. Musculoskelet. Dis. 2012;4(4):249–258. [PMC free article] [PubMed] Mankin HJ, Lippiello L. Biochemical and metabolic abnormalities in articular cartilage from osteo-arthritic human hips. J. Bone Joint Surg. Am. 1970;52(3):424–434. [PubMed]• One of the earliest studies describing cartilage lesions in OA. Zhang Y, Nevitt M, Niu J, et al. Fluctuation of knee pain and changes in bone marrow lesions, effusions, and synovitis on magnetic resonance imaging. Arthritis Rheum. 2011;63(3):691–699. [PMC free article] [PubMed] Roemer FW, Kassim Javaid M, et al. Anatomical distribution of synovitis in knee osteoarthritis and its association with joint effusion assessed on non-enhanced and contrast-enhanced MRI. Osteoarthritis Cartilage. 2010;18(10):1269–1274. [PubMed]• Important paper highlighting synovitis in OA. Kwok WY, Plevier JW, Rosendaal FR, Huizinga TW, Kloppenburg M. Risk factors for progression in hand osteoarthritis: a systematic review. Arthritis Care Res. (Hoboken) 2013;65(4):552–562. [PubMed] Spector TD, MacGregor AJ. Risk factors for osteoarthritis: genetics. Osteoarthritis Cartilage. 2004;12(Suppl A):S39–S44. [PubMed] Doherty M. Genetics of hand osteoarthritis. Osteoarthritis Cartilage. 2000;8(Suppl. A):S8–S10. [PubMed] Stern AG, de Carvalho MR, Buck GA, et al. Association of erosive hand osteoarthritis with a single nucleotide polymorphism on the gene encoding interleukin-1 beta. Osteoarthritis Cartilage. 2003;11(6):394–402. [PubMed] Stefánsson SE, Jónsson H, Ingvarsson T, et al. Genomewide scan for hand osteoarthritis: a novel mutation in matrilin-3. Am. J. Hum Genet. 2003;72(6):1448–1459. [PMC free article] [PubMed] Merlotti D, Santacroce C, Gennari L, et al. HLA antigens and primary osteoarthritis of the hand. J. Rheumatol. 2003;30(6):1298–1304. [PubMed] Wakitani S, Imoto K, Mazuka T, Kim S, Murata N, Yoneda M. Japanese generalised osteoarthritis was associated with HLA class I–a study of HLA-A, B, cw, DQ, DR in 72 patients. Clin. Rheumatol. 2001;20(6):417–419. [PubMed] Neogi T, Soni A, Doherty SA, et al. Contribution of the COMT Val158Met variant to symptomatic knee osteoarthritis. Ann. Rheum. Dis. 2014;73(1):315–317. [PMC free article] [PubMed] Valdes AM, De Wilde G, Doherty SA, et al. The Ile585Val TRPV1 variant is involved in risk of painful knee osteoarthritis. Ann. Rheum. Dis. 2011;70(9):1556–1561. [PMC free article] [PubMed] Malfait AM, Seymour AB, Gao F, et al. A role for PACE4 in osteoarthritis pain: evidence from human genetic association and null mutant phenotype. Ann. Rheum. Dis. 2012;71(6):1042–1048. [PMC free article] [PubMed] arcOGEN Consortium, arcOGEN Collaborators. Zeggini E, et al. Identification of new susceptibility loci for osteoarthritis (arcOGEN): a genome-wide association study. Lancet. 2012;380(9844):815–823. [PMC free article] [PubMed] Guermazi A, Roemer FW, Haugen IK, Crema MD, Hayashi D. MRI-based semiquantitative scoring of joint pathology in osteoarthritis. Nat. Rev. Rheumatol. 2013;9(4):236–251. [PubMed] Sofat N, Ejindu V, Kiely P. What makes osteoarthritis painful? The evidence for local and central pain processing. Rheumatology (Oxford) 2011;50(12):2157–2165. [PubMed] Lim YZ, Wang Y, Wluka AE, et al. Are biomechanical factors, meniscal pathology, and physical activity risk factors for bone marrow lesions at the knee? A systematic review. Semin. Arthritis Rheum. 2013;43(2):187–194. [PubMed] Felson DT, Zhang Y, Hannan MT, et al. Risk factors for incident radiographic knee osteoarthritis in the elderly: the Framingham study. Arthritis Rheum. 1997;40(4):728–733. [PubMed] Toivanen AT, Heliovaara M, Impivaara O, et al. Obesity, physically demanding work and traumatic knee injury are major risk factors for knee osteoarthritis – a population-based study with a follow-up of 22 years. Rheumatology (Oxford) 2010;49(2):308–314. [PubMed] Cooper C, Snow S, McAlindon TE, et al. Risk factors for the incidence and progression of radiographic knee osteoarthritis. Arthritis Rheum. 2000;43(5):995–1000. [PubMed] Oliveria SA, Felson DT, Cirillo PA, Reed JI, Walker AM. Body weight, body mass index, and incident symptomatic osteoarthritis of the hand, hip, and knee. Epidemiology. 1999;10(2):161–166. [PubMed] Spector TD, Hart DJ, Doyle DV. Incidence and progression of osteoarthritis in women with unilateral knee disease in the general population: the effect of obesity. Ann. Rheum. Dis. 1994;53(9):565–568. [PMC free article] [PubMed] Roddy E, Doherty M. Changing life-styles and osteoarthritis: What is the evidence? Best Pract. Res. Clin. Rheumatol. 2006;20(1):81–97. [PubMed] Jansen MJ, Viechtbauer W, Lenssen AF, Hendriks EJ, de Bie RA. Strength training alone, exercise therapy alone, and exercise therapy with passive manual mobilisation each reduce pain and disability in people with knee osteoarthritis: a systematic review. J. Physiother. 2011;57(1):11–20. [PubMed] Iversen MD. Rehabilitation interventions for pain and disability in osteoarthritis: a review of interventions including exercise, manual techniques, and assistive devices. Orthop. Nurs. 2012;31(2):103–108. [PubMed] Fransen M, McConnell S. Exercise for osteoarthritis of the knee. Cochrane Database Syst Rev. 2008;8(4):CD004376. [PubMed] Fransen M, McConnell S, Hernandez-Molina G, Reichenbach S. Does land-based exercise reduce pain and disability associated with hip osteoarthritis? A meta-analysis of randomized controlled trials. Osteoarthritis Cartilage. 2010;18(5):613–620. [PubMed] Bannuru R, Abariga S, Wang C. How effective is t’ai chi mind-body therapy for knee osteoarthritis? A systematic review and meta-analysis. osteoarthritis research society international world congress; 2012; Barcelona, Spain. Osteoarthritis Cartilage. 2012;20(Suppl. 1):S281–S282. Kang JW, Lee MS, Posadzki P, Ernst E. T’ai chi for the treatment of osteoarthritis: a systematic review and meta-analysis. BMJ Open. 2011;1(1):e000035. [PMC free article] [PubMed] Nguyen US, Felson DT, Niu J. The impact of knee instability with and without buckling on balance confidence, fear of falling and physical function: the Multicenter Osteoarthritis Study. Osteoarthritis Cartilage. 2014 doi: 10.1016/j.joca.2014.01.008. (Epub ahead of print) [PMC free article] [PubMed] Beckett J, Jin W, Schultz M, et al. Excessive running induces cartilage degeneration in knee joints and alters gait of rats. J. Orthop. Res. 2012;30(10):1604–1610. [PubMed] Fernandes L, Hagen KB, Bijlsma JW, et al. EULAR recommendations for the non-pharmacological core management of hip and knee osteoarthritis. Ann. Rheum. Dis. 2013;72(7):1125–1135. [PubMed]•• Current European guidelines for OA management are discussed well in this article. McAlindon TE, Bannuru RR, Sullivan MC, et al. OARSI guidelines for the non-surgical management of knee osteoarthritis. Osteoarthritis Cartilage. 2014 doi:10.1016/j.joca.2014.01.003. (Epub ahead of print) [PubMed]•• Current OARSI guidelines for OA management are discussed well in this article. Christensen R, Bartels EM, Astrup A, Bliddal H. Effect of weight reduction in obese patients diagnosed with knee osteoarthritis: a systematic review and meta-analysis. Ann. Rheum. Dis. 2007;66(4):433–439. [PMC free article] [PubMed] Brandt KD. Osteophytes in osteoarthritis. clinical aspects. Osteoarthritis Cartilage. 1999;7(3):334–335. [PubMed] van der Kraan PM, van den Berg WB. Osteophytes: Relevance and biology. Osteoarthritis Cartilage. 2007;15(3):237–244. [PubMed] Aigner T, Dietz U, Stoss H, von der Mark K. Differential expression of collagen types I, II, III, and X in human osteophytes. Lab Invest. 1995;73(2):236–243. [PubMed] Menkes CJ, Lane NE. Are osteophytes good or bad? Osteoarthritis Cartilage. 2004;12(Suppl. A):S53–S54. [PubMed] Gelse K, Soder S, Eger W, Diemtar T, Aigner T. Osteophyte development–molecular characterization of differentiation stages. Osteoarthritis Cartilage. 2003;11(2):141–148. [PubMed] 50. Felson DT, Gale DR, Elon Gale M, et al. Osteophytes and progression of knee osteoarthritis. Rheumatology (Oxford) 2005;44(1):100–104. [PubMed]• Role of osteophy