Cricket Scotland have provided some guidance on the new Home Office definitions that will affect overseas amateurs and paid players, in relation to visa requirements and allowances. The letter is pasted below, with the additional documents referred to attached to this post. We encourage all clubs to make themselves familiar with the guidance, particularly if looking to have an overseas player in 2019.
"Following recent updates from the government on the 'Home Office Immigration Rules for Cricket', (overview attached) which was released on 14th December 2018, there are areas of concern around the signing of certain cricketers from outside the UK/EEA.
Whilst Cricket Scotland, and the ECB, have concerns regarding these rules, and have attempted to progress them with the Home Office, as things stand these remain the rules that clubs will be required to adhere to.
I have attached documentation that should allow you as a club to understand the type of visa that someone from outside UK/EEA will require to hold in order to be correctly registered as an Overseas Paid Player or Overseas Amateur cricketer.
I would note that it is the responsibility of the individual involved and the club to ensure that any player registered as an Overseas Paid Player or Overseas Amateur cricketer is in the UK on the correct Visa. It should be noted that the buck stops with the Club Chair (or appropriate equivalent) and that there are SUBSTANTIAL fines should they have not carried out the correct checks or chosen to ignore the Home Office requirements.
The information provided below has been taken from various Home Office documents and needs careful consideration before registering a player with your League. Please pay particular attention to the 'Player Pathway'** definition, as any person that has played cricket from U17 upwards at state / province / territory level (paid or unpaid) may be considered a 'Professional Sportsperson'.
I would suggest that if you are planning on signing a person that may be considered on a 'Pathway' your first action is to seek written approval from the Home Office that the player disclosed all relevant information on their visa application and has been deemed an amateur by the Home Office. There is an Enquiry Bureau Helpline – 0300 123 4699.
I have also attached a summary documents that may be of use (See 'Home office Overseas Players Amateur v Professional Definition' which was last issued on 25th January 2019).
A "Professional Sportsperson", is someone, whether paid or unpaid, who : is providing services as a sportsperson, playing or coaching in any capacity, at a professional or semi-professional level of sport; or being a person who currently derives, who has in the past derived or seeks in the future to derive, a living from playing or coaching, is providing services as a sportsperson or coach at any level of sport, unless they are doing so as an "Amateur".
Deriving a living is defined as receiving payment for playing cricket and does not need to be the sole earnings. A person may also be considered as "seeking to derive a living" if they have played as part of a player pathway.
**Player "Pathway": A player may be considered to be on a "Pathway" and therefore classified as a "Professional Sportsperson", if that person has played cricket from U17 upwards at state/ province/ territory level (paid or unpaid) in any country.
Clubs wishing to use the services of a player who is in the UK, but not on a Tier 5 Creative & Sporting visa, must ensure that the visa the person has, allows them to play and/or coach.
They must make their own checks, and not solely rely on information that Agents provide them.
Inform the appropriate league management group and request that they take the appropriate action as per the league rules.
League Association only: Inform Cricket Scotland that the above has occurred.
(The same process will apply if a player, in breach of the visa rules, was denied registration in one league to be found registered in another).
As far as the Home Office is concerned, "Employment" can be paid or unpaid.
In cricket, the club Chair (or equivalent) holds the legal responsibility for all activities in the club and is therefore the "Employer".


text:
Devil May Cry 5 Final Trailer Brings the Hype
By Jeff Scott On Feb 28, 2019 04:21 PM EDT
If you've been patiently waiting for Devil May Cry 5, that wait is nearly over. And to help quench your thirst, Capcom dropped their Devil May Cry 5 final trailer. Unfortunately, the footage just makes us want the latest entry in the series now instead of next week.
The synopsis of the Devil May Cry 5 final trailer reads that "The world as we know it is falling apart after a sudden demonic invasion, and it's up to Nero, Dante and the mysterious V to team up and face the ultimate challenge." Yes, it's quite the basic description, but for good reason. For the trailer itself is riddled with some low level spoilers that many might prefer to avoid.
The game revolves around the aforementioned trio of Dante, Nero, and the new character "V". The gameplay on display looks similar to former outings, with a focus on quick and stylish action. Each character has their own weapons and abilities, if V brining a play style entirely different to the table.
As for the narrative, the story is set a few years after the events of Devil May Cry 4. Dante, still manning the Devil May Cry offices, is hired by the newcomer V to help eliminate a series of demon threats throughout the world.
Nero has since established his own demon hunting agency out of his van, yet still named Devil May Cry itself. Within the early stages of the story, Nero's Devil Bringer arm is stolen by a mysterious hooded thief. Nero's investigation into the thief leads him to the same location in which Dante has found as the source of V's demon problems. From there, the trio "team up and face the ultimate challenge."
Self described by Capcom as "the latest, craziest and most stylish entry in the series", Devil May Cry 5 begins kicking ass on PC, Xbox One and PlayStation 4 on March 8th.
CapcomGaming NewsPC GamesPS4
Jeff Scott
Growing up a 90's kid, Jeff found his love for gaming during Nintendo's heyday. Because of that, you could (perhaps sadly) call him a "Nintendo Fanboy" to this day.
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redpajama_set_name: RedPajamaCommonCrawl


Welcome to a fun, junk filled post at Beyond The Picket Fence with the Junkers Unite Group. We are a group of bloggers who love JUNK, aka "treasures" that would normally be discarded, passed over, ignored. I am Becky, author and creator at Beyond The Picket Fence. If it is your first time here, welcome!
Today I am bringing you a project made from reclaimed wood--most of it from pallets. My regular readers won't be surprised--I adore reclaimed, salvaged, junky wood.
I started by picking some pallet boards and painting them. I usually use a scrappy chip brush (this is on its last leg). I use one brush for all colors except red, not cleaning it in between.
I start with the lightest color, usually a yellow.
I do not sand the wood before painting. If it is really rough, I use more paint as more will come off when I sand.
After painting my boards, I layed them out how I wanted them and measured their width.
I cut two reclaimed oak boards to put across the top and bottom. The bottom board is wider to leave space for hooks.
I attach the colored pallet boards to these horizontal pieces by screwing in through the back. Be sure to put two screws in each pallet board.
and then rest the box on the bottom horizontal board and screwed down through the bottom of the box into the oak piece. This view is looking down from the top into the box.
Next, secure the short sides of the box with screws from the back of the colored pallet wood.
For the top shelf I randomly cut a rectangular piece of wood at a 45 degree angle to make two brackets. These were secured from the back. Make sure to leave a space for the shelf.
Add a piece of wood for the shelf, screwing it into both the green brackets and the horizontal oak piece. At this point I sanded it and waxed it with a combination of coconut oil and Annie Sloan dark wax.
Some wooden spools added to the bottom make perfect junky hooks.
a place for everything and perfect with a white shower curtain, colorful towels.
Don't need organization in a bathroom, how about in a kitchen?
a bowl with napkins, salt and pepper.
and of course hooks for coats and purses and such.
Do you need extra organization before you start planting this year? Hang this shelf on a fence to add some color, throw a table underneath (this is a pallet we added legs to and metal mesh to sift dirt--work great for a potting bench) and you have the perfect place to pot spring flowers.
I love planting in these tiny, mudy rainboots!
Now that you've got your junk juices flowing, check out all of these fantastic blogs and their projects!
So great Becky! Love your colors!
What a super cool piece, Becky! Your signature colours just make the shelf shine all the more. I know I'd have a tough time deciding where to use it because I think every space can use that happy reclaimed colour goin' on! WANT.
I love how you accessorized your piece in so many different ways. Your paint technique is so awesome!
the paint...and the spool knobs...swoon!
Very nice and versatile too!
Becky, this is absolutely stunning! I love it!
I'd use it on my new screened porch.
So cute - and it really does work in so many places! Great job!
Loving this! it is perfect for any room! but I really do love it for the bathroom! Would love to enter your giveaway! LIKING your FB page! thanks so much!
I love the colors! And you are right this is an incredibly versatile piece. Great job. So sorry I can't win it, I guess I'll have to make one myself, with your instructions I must be able to do that. Thanks!
All of the rooms in my house are painted a nice bright color except the kitchen which is white. I would place this on the kitchen wall for a nice color pop! Love your work BTW!
I would love to use this on my kitchen island. It's so neat!
BTW: The link for MariAnn actually goes to Susan's page.
There are lots of good uses for that shelf and I particularly like it in the bathroom and in the plant potting area. In fact, I need this in my potting area.
Love it Becky!! So many fun ways to use it...and those spools for hooks are so CLEVER :) Fun to party with you again!
Love your project and the variety of ways you showed your readers how it could be used. Don't the board cutting space, but I bet I can find some precut pieces and scraps to adapt the plan. I love the way it's painted. Thanks so much for sharing.
In my office to keep up with all my bills!!
I love the wall shelf...you also use the best colors! I have a playroom it would look awesome in!
The tray is great...thanks for the chance to win it!
Love shelves of any kinds. This one is wonderful!. Especially love the use of spools as hooks!
I have enjoyed every blog I have visited so far, but yours is the perfect up-cycle for me. I'm the Tin Can Diva of my small apt. complex. I cover them with burlap scraps, fill with goodies, and they are my presents for my friends. Now I have something even better to make for everyone. Thanks so much for sharing your talent. Funky Junk Donna is responsible for my visit and introducing all of your ideas for me to "steal".
That tray would match my house--I love COLOR!
I'm a relatively new follower, I love all you creations, and you've inspired me to get working on some old wood I have laying around! If I had this shelf I would use it in the kitchen, the colors match perfectly!
Love the tray. I would use it in the kitchen.
I love the bright colors you used on this adorable reclaimed shelf! It would look great in my beachy themed bathroom! You guys are all amazing with all your wonderful projects,Thanks for the great party yall are so inspiring, and so many great links to check out Pinned for sure!
Well I finally made it over to link up and enter your giveaway. As you already know..I LOVE this shelf!!! I think I would use it in a bathroom or maybe a home office. As always, this is another really awesome item that you have put together.
Love what you have done! I would hang it on my porch.
I LOVE it Becky! I would use it in the bathroom! You are so creative! Thanks!
Love the shelf, Becky! It would be perfect in my son's bedroom. Your tray is awesome, too!
This shelf is so great! Thanks for explaining how you put it together. Your pictures are A-MAZING, and I love that you took the time to stage the shelf in so many ways! I think I would use something like this in our bathroom, since it has so much more character than the boring white shelf I've had in there for years!
Just found you & am loving everything! What a great tray! Would love to be its new owner... serving a frosty pitcher of lemonade or cups of steaming cocoa or tea in the fall - sigh!! Thanks for sharing your creativity!
Love it Becky, I would probably use the shelf in my kitchen. Great colors.
I'd use it either in my kitchen or in my bathroom.
Love this! I would use it in my craft room!
I love it! I would use it in my craft room where I feel free to go a little crazy with color. Thank you for the chance to win.
I love the use of the wooden spools!! I might use it in my bathroom or in my craft nook!
I would use it in the bathroom...would be very helpful in there!!!


ROSEBURG — Three Douglas County Sheriff's Office employees were honored Friday, Feb. 22, at the Roseburg Optimist Club's annual Respect for Law Banquet.
The annual banquet was hosted at the Douglas County Fairgrounds where the organization honored law enforcement professionals from various agencies in the County.
Corporal Jon Dorland received the Patrol Deputy of the Year award for his overall commitment and dedication to the agency. Dorland, who has been assigned to the patrol division for nearly 12 years, was selected in 2013 fill the role of K-9 handler. He exceeded the expectations of the position and "set the bar" for the future of DCSO's K-9 program. Dorland and his K-9 partner Grim received several accolades, including Springfield Police Department's 'Top Dog' award, two years in a row. Promoted to the rank of Corporal in 2018, Dorland continues to serve the agency as a front line supervisor who is respected by his peers, subordinates and supervisors.
911 Dispatcher of the Year went to Communications Officer Heather Gray who has been with the agency for 7 years. Gray is described by her peers as dependable, caring and "the consummate dispatcher". Gray often serves the agency in other ways by assisting in community outreach events and as a training officer and lead dispatcher. Sheriff Hanlin said Gray is "honest and reliable in every aspect of her position".
Deputy Larissa May was honored as Corrections Deputy of the Year. May started her career by volunteering with the Sheriff's Office Search and Rescue program when she was 14 years old. Even after being hired full-time as a Correction Deputy, May continues to serve as a SAR volunteer. Deputy May was commended for her positive attitude and work ethic. She has assumed additional duties to include being a member of the Corrections Emergency Response Team and Inmate Services Coordinator. Her supervisors describe her as a reliable employee who represents the Sheriff's Office in a positive manner.
"I am extremely proud of these employees who demonstrate their commitment to the agency and the community we serve on a daily basis.", said Sheriff Hanlin.
The club also honored law enforcement professionals from Roseburg PD, Sutherlin PD, Winston PD, Myrtle Creek PD and Oregon State Police.


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NVT PHYBRIDGE NEWS
How to Effectively Support A Cloud-Based Communication Solution - Part 2/2
In this second episode, Richard Kasslack and Doug Green discuss the trends and challenges that organizations face as they plan to modernize to a Cloud-based communication solution. Richard talks about the gap between what customers expect…
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In part one of this two-part series, Richard Kasslack and Doug Green discuss the challenges that organizations face as they plan to modernize to a Cloud-based communication solution. Richard shares the infrastructure strategy that best supports…
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Overcome Infrastructure Barriers and Easily Upgrade From Your End-of-Life CS1000
Is your company one of the thousands still relying on a Nortel CS1000 (CS1K) or another outdated analog phone system? Even as these systems become end-of-life, many organizations feel as though they cannot upgrade to the latest IP voice solution…
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Large Institute of Technology Modernizes from UniPhyer to PoLRE While Deploying A New Cloud-Based Communication Solution
Modern LAN Pioneer Upgrades to the Next Generation of NVT Phybridge Innovation One of the top U.S. universities, located in the southeastern region, has modernized its communication capabilities to provide industry-leading education. Offering…
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Podcast: Applying Modern LAN in Healthcare & Hospitality
In this podcast, we examine how NVT Phybridge simplifies IP modernization requirements for healthcare organizations. Julian Kennedy, Healthcare, Hospitality and Retail Vertical Specialist, discusses the many challenges that healthcare organizations…
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Paul Taggar Named EMEA Managing Director at NVT Phybridge
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Luxurious Resort in Cozumel, Mexico Simplifies Deployment of IP Surveillance System Using Modern LAN Principles
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Crusher Rentals rents, Equipment for Sale; Projects; Contact; Crushing and Screening Equipment Hire.
Crushers Cone For Sale New and Used. Home / Heavy Construction Equipment For Sale For sale or rent. QS331 cone crusher. Excellent reduction capabilities.


The 2016 edition of the Code_Saturne User Meeting was held at EDF Lab Chatou (France) on April the 1st.
This edition was the ninth User Meeting since the code was made open source. More than 130 participants attended the conference. The list of posters and presentations is given below. Most of them can be downloaded by clicking on their reference.
Foreword: Code_Saturne has been open-sourced 10 years ago!
Study of rotating stall in a centrifugal compressor in the effort to study its inception and behaviour, and methods to suppress it.
The best poster of 2016 Code_Saturne user meeting was presented by Pierre Cantin.


Who will attend the birth?
Every birth is attended by a Licensed Midwife. Every birth is also attended by at least one additional highly qualified assistant, who may be a licensed midwife or an apprentice/student midwife. The apprentices and assistants are involved in the prenatal care, so you will be familiar with all of the staff present at the birth. In the extremely unlikely event that more than two moms are in labor at the same time, we have excellent back up midwives available. In that case, an apprentice or assistant who you knows well will also attend your birth, so you will still have a familiar presence at the birth.
Who can be with me when I give birth?
We encourage you to invite whomever you would like to attend your birth, including your children if you desire. Some moms choose privacy while others choose to have many people at their births. We ask that you have a designated adult present to care for your small children if they will be at your birth.
Planned home birth usually creates a bit of clutter around your house, consisting of towels for getting in and out of the birth tub, half eaten snacks for the birthing mom, the birth supplies, baby things and the midwives' bags and equipment. The 'mess' at the time of birth is well contained and we've never ruined a carpet or a comforter!
We are able to take some private insurance PPO plans. No HMOs cover us at this time. Unfortunately we are not covered by Medi-Cal, AIM, or military insurance. Midwives across the country are working to get Certified Professional Midwives recognized federally as providers.
We are committed to providing accessible home birth midwifery care for all women who desire it, regardless of their insurance. We have created a sliding scale to make our services as affordable as possible. We do not turn anyone away for lack of funds.
Labor is usually very hard work, and often painful. Not all women experience pain in labor, but most do, so we are glad you are asking this question and seriously considering your options.
We encourage women to prepare themselves during the pregnancy for the realities of labor. We recommend families take a childbirth preparation class, such as Birthing From Within, for women to prepare physically and emotionally for the experience of labor. Many other classes are available in the community as well, such as Bradley, Hypnobabies, Hypnobirthing and others, each with different ways of preparing women for the experience of childbirth. Prenatal yoga and other exercise and relaxation classes can be very beneficial as well.
During labor, we offer a variety of means to help cope with the intensity of labor. We offer freedom of movement, the use of water, both the shower and immersion in a deep tub, massage, emotional support and many other non-pharmaceutical techniques. At our birth center we have 3 rooms with tubs available for comfort, and we offer portable tubs for rent for home births.
Pharmaceutical anesthesia and analgesia are not available at the birth center or at a home birth. WE DO NOT OFFER EPIDURALS. Epidural anesthesia is not safe for use outside of a hospital, and we find nearly all women who desire an unmedicated birth with our practice can do so without anesthesia. In case the woman requires or desires an epidural, we will accompany her to the hospital.
What do you do if there is a complication or an emergency?
Most complications are not emergencies. Midwives are experts in the pregnancy and birth process, and are able to recognize slight deviations from normal, and usually get them back on track with minimal, at-home intervention (such as diet changes, position changes, feeding mom, herbs, medicines, etc). If a complication does not resolve, we will transfer the mom's or baby's care to a hospital provider, in pregnancy, labor, or postpartum.
In the case of a true emergency, we are qualified to stabilize mom or baby while the Emergency Medical Service is called and we transport by ambulance. We are certified in CPR and Neonatal Resuscitation and have oxygen, IV fluids and medicines to control postpartum bleeding.
What happens if we have to transfer to the hospital?
In an emergency, we call EMS and transfer by ambulance. In an unrushed transfer, we go by private vehicle to the most appropriate hospital. Some women prefer a specific hospital if they are receiving concurrent care, or due to insurance.
For women giving birth at the birth center, we will transfer to the nearest hospital in a true emergency. In a non-emergent situation, we transfer to the hospital of your choice.
If you have been seeing a doctor or hospital midwife, the doctor or midwife on call for that group will be your primary caregiver when you arrive at the hospital. If you have not had concurrent care, the ob/gyn doctor on call at the hospital will take over your care. Every hospital has a doctor on call for 'walk in' patients, and you will never be turned away in labor or postpartum. We will give the nurses and doctor or midwife report on your situation in labor, and then we will remain as labor support for you until your baby is born and/or you or your baby are stable. However if you transfer to a hospital outside of San Diego county, we will not be able to accompany you to the hospital.
If I give birth in the birth center or at home, how do I get a birth certificate and social security number?
We are happy to assist you with the registration of your baby's birth. As soon as your baby is born, we schedule an appointment at the San Diego County Office of Vital Records to register the birth. This appointment is usually 2-4 weeks after your baby is born. The midwife, mother and baby will attend this appointment together, and the father is welcome as well. You will be able to leave this appointment with a certified copy of your baby's birth certificate. For registration of the birth, the mother must provide current valid identification, as well as a visa or permanent resident card if she is not a US citizen.
If you need a verification of your baby's birth prior to the birth certificate appointment, we will provide you a formal letter verifying the birth. This will allow you to cross the border with the baby, register the baby with some insurance companies and the military, etc.
After you receive your baby's birth certificate, you can apply for your baby's social security number. You can do this in person at any social security office or by mail. We will provide you with an additional verification of your baby's birth for use with the social security office.


Abstract : The high performance Digital Signal Processors (DSP) currently manufactured by Texas Instruments are heterogeneous multiprocessor architectures. Programming these architectures is a complex task often reserved to specialized engineers because the bottlenecks of both the algorithm and the architecture need to be deeply understood in order to obtain a fairly parallel execution. The PREESM framework objective is to simplify the programming of multicore DSP systems by building on dataflow programming methods. The current functionalities of this scalable framework cover memory and time analysis, as well as automatic deadlock-free code generation. Several tutorials are provided with the tool for fast initiation of C programmers to multicore DSP programming. This paper demonstrates PREESM capabilities by comparing simulation and execution performances on a stereo matching algorithm prototyped on the TMS320C6678 8-core DSP device.


Amber gold with a faint raw sienna cast. Fairly viscous 'tears' on the side of the glass.
A fresh and inviting fragrance encompassing scents of orange, brown sugar and baking spices, mead, oxidized apples, cedar chest, lemon oil, Melba toast and ginger tea. With a drop of water, a hint of almonds emerges.
Sweet at the outset, with the corn influence momentarily taking the lead. Caramel fudge, apple butter, citrus and honey. Then an explosion of baking spices and cascading vanilla imbued oak along with a dash of cayenne heat. The balance between the sweetness and the palpable rye snap is well gauged. And the whiskey is succulent, yet not too heavy, in its mouth-feel. A drop of water softens the fireworks a tad.
More oak driven, as the caramel and honey fade gently behind a drier, warming, spirited glow.
Wild Turkey 101 has long been a staple in my liquor cabinet. And while more recent issues are perhaps not quite as texturally voluptuous as the once available 8-year old release, they are still classic essays in the art of Bourbon making. In short, subtlety and power superbly intertwined.
Drink WT101 neat or with just a single drop of water.


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Developments in the clinical understanding of osteoarthritis
David T Felson1
With the recognition that osteoarthritis is a disease of the whole joint, attention has focused increasingly on features in the joint environment which cause ongoing joint damage and are likely sources of pain. This article reviews current ways of assessing osteoarthritis progression and what factors potentiate it, structural abnormalities that probably produce pain, new understandings of the genetics of osteoarthritis, and evaluations of new and old treatments.
Osteoarthritis (OA) is the most common form of arthritis and remains one of the few chronic diseases of aging for which there is little, if any, effective treatment. It accounts for more mobility disability in the elderly than any other disease. Symptomatic knee OA affects roughly 12% of persons 60 years old or older and, despite medical advances, remains for many a major source of pain and function limitation. Hip OA, though less prevalent than disease in the knee, is common and frequently disabling, and hand OA causes pain and function loss in a large percentage of the elderly. Given the aging of the population and the increasing occurrence of obesity in our population, a major risk factor for disease, estimates suggest a doubling in prevalence from 2000 to 2020 [1].
We will focus on developments in our clinical understanding of OA in the last 10 years. This period has seen major changes in our conceptualization of the disease, the widespread introduction of magnetic resonance imaging (MRI) in clinical studies (a tool that has permitted us to better visualize structural changes within OA joints), and the emergence of large-scale clinical studies investigating mechanical and loading abnormalities as risk factors for disease. The results of these studies have led to changes in our approach to treatment. The discussion will target knee OA, which has been the best studied of all joints affected. Advances in the medical understanding of hip and hand OA will also be reviewed.
New conceptualizations of osteoarthritis
While the signature pathologic feature of OA is hyaline articular cartilage loss, it is increasingly recognized that OA is a disease of the whole joint and that all structures are affected [2]. Not only is hyaline cartilage lost, but bone remodeling and attrition occur relatively early in the disease process [3]. Fibrocartilage degeneration including the meniscus and labrum (in the hip) is integral to disease, and changes in the load-distributing function of this fibrocartilage may induce injury to adjacent hyaline cartilage. Chondro-osteophytes, protrusions of new cartilage which subsequently ossify, form both at the joint margin and centrally at areas where cartilage has eroded. The synovium often develops lining cell hyperplasia and in some cases becomes infiltrated with subsynovial inflammatory cells [4]. Activated synovium secretes excess synovial fluid, leading to capsular swelling. This swelling, through a spinal reflex, inhibits complete activation of muscles bridging the joint (arthrogenous inhibition) and this, combined with lack of use, leads to muscle weakness and atrophy. The inflammation present in the synovium triggers changes in the peripheral nervous system, affecting the afferent processing of nociceptive signals from the joint and surrounding tissues. Thus, OA pathologically affects all structures of the joint and understanding the process of disease and its progression necessitates an appreciation for how changes in one of these structures (for example, the meniscus) may affect others.
A major driver of the development of disease and its progression is aberrant loading, or mechanopathology (both microscopic and macroscopic). When the joint is young and healthy, complex and overlapping systems protect it from injury. These include the muscles across the joint which contract in a smooth coordinated fashion through the excursion of the joint, coordination informed by nervous system inputs. Also included are the frictionless lubrication of surfaces during movement and competent ligaments that provide limits to joint excursion. Normal anatomy means that the distances between the bones produce loading that is distributed physiologically across the joint during movement. When cartilage erosion occurs or a knee ligament becomes injured and fails to limit physiologic motion, loading becomes unevenly distributed. This localized excess loading leads to further damage and malalignment within the joint during movement. Either malalignment or local stepoffs within the joint subject the cartilage (both fibro and hyaline) to excess focal loading, producing progressive damage. The joint becomes grossly malaligned during movement, and at the site of malalignment, focal loading is excessive, accelerating damage. Muscles may no longer work in a smooth coordinated fashion, and inflammation within the joint may cause further nervous system and muscle changes. This picture of mechanopathology contributing to pathology in multiple joint tissues that interact with one another to accelerate that pathology represents the picture of fully developed disease. Hyaline articular cartilage loss, a defining feature of disease, is only a small part of this picture.
A new insight into the pathology of OA has been the recognition that modest enthesitis is a common feature. In early hand OA, there is inflammation at the boney insertion of the collateral ligaments [5] and histological examination shows synovitis investing the ligament insertion sites [6]. In knees, similar bone lesions are seen on MRI near the insertion sites of intact anterior and posterior cruciate ligaments in OA knees [7].
The focus on cartilage loss may have served as a distraction from the main clinical feature of OA: pain. Cartilage is aneural, and longitudinal studies have suggested that cartilage loss and pain relief are poorly, if at all, correlated [8, 9]. Investigations of the nature of pain in OA and of the relation of pain with specific structural features have provided new insights into how OA may be successfully managed.
The symptoms of osteoarthritis: pain and instability
The pain of OA is activity-related, with pain coming on generally only when a person does specific activities that induce it. For example, in persons with knee OA, walking up and down stairs often produces pain whereas lying in bed frequently does not. However, recent work suggests that this simple description of activity pain in OA is inadequate. In a qualitative study in which large numbers of persons with knee and hip OA were interviewed, Hawker and colleagues [10] identified two different types of pain experienced by patients. The first was a chronic and constant dull aching that for most patients was expected and did not affect their lifestyle or inhibit their activities. The second was a much more stressful and anxiety-provoking flare of pain that in end-stage disease often occurred unexpectedly and without an obvious trigger. Early in disease, pain was only episodic and its precipitants were known and pain episodes were self-limited. By the time one got severe disease, pain became chronic and superimposed on that chronic pain were unanticipated episodes of severe pain.
There are other elements to the pain in OA which may have implications for treatment. First [11], depressive symptoms are far more common in patients with painful OA than previously recognized, and sleep disorders may occur in these patients which may magnify their pain. Furthermore, many of these patients use descriptors for pain (for example, burning) which suggest that their pain has neuropathic elements.
Functional pain occurs when a person alters behavior to avoid pain that injures a part of the body (for example, removing a finger from a burning stove). All pain in OA is probably not functional. Synovitis-induced inflammatory changes within the joint may, in turn, have effects on peripheral nervous system inputs at the spinal cord level, inducing both peripheral and ultimately central changes in pain processing. Kosek and Ordeberg [12] were intrigued by the often widespread pain experienced by patients with hip OA, suggesting that more than just the receptor area for the hip is involved in nociception. They tested patients with hip OA for the presence of central nervous system sensitization. Sensitization is tested by evaluating whether another noxious stimulus inhibits the pain produced by a painful stimulus like hip OA. These investigators tested 15 patients with unilateral painful hip OA versus age- and gender-matched controls and found that noxious stimulation (in this case, a blood pressure cuff overinflated to produce ischemia) did not reduce pain sensitivity in the non-OA leg in patients, whereas it did so normally in controls. This provides strong evidence of central sensitization in patients with hip OA. Intriguingly, after these patients underwent hip replacement surgery, they were retested and their noxious inhibitory control had returned to normal. These findings of dysfunctional pain in patients with OA leave room for treatment that focuses solely on pain relief, including potent analgesics and molecules that block nervous system transmission of pain. Pain can also serve as a protective mechanism for a person to avoid activities that lead to more joint damage. Thus, there is a theoretical risk to pure analgesic treatment which will need to be studied.
As noted by Hawker and colleagues [10], constant pain becomes a feature of OA later in the disease. If pain does not abate (even if it is relatively mild), a person is more likely to need a knee or hip replacement than if pain is severe but intermittent. Consistent pain tends to occur when structural disease is advanced and when the patient has co-existing depressive symptoms that are more depressive [13].
Pain is not the only symptom of OA experienced by patients with knee and hip OA. They also frequently experience a sensation of instability or buckling. The most common symptom is one of shifting or instability without actually falling or giving way. However, giving way or buckling is also common and leads to a high rate of falls in persons with knee OA. Of adults in middle and elderly years from the Framingham study [14], 12% experienced one episode of knee buckling in the previous 3 months and, in many of these, buckling led to falls. Most persons with buckling had both knee pain and more than one episode of buckling. Persons with knee buckling were more functionally disabled than those without it, even adjusting for the severity of their knee pain. Buckling in the knee may reflect weakness of muscles such as the quadriceps, which stabilize the joint during activities like stair climbing. Strengthening exercises and balance training may be therapeutic [15]. If buckling occurs with activities involving switching direction when walking, a tear of the anterior cruciate ligament needs to be investigated, but most people who are middle-aged or older who have knee buckling have no such tear. Buckling also tends to be more common in persons who have pain in multiple joints in their legs, not just the knee.
The relation of pain to structural pathology in osteoarthritis
Since cartilage is aneural, other structures within the joint must be the source of pain in OA. Historical and anatomical studies suggested that pain fibers can be identified in the synovium, in ligaments especially near their insertions, in bone, in muscle, and in the outer third of the meniscus in the knee. In an unusual study in which the lead investigator became the study subject and underwent an awake unanesthetized arthroscopy, Dye and colleagues [16] probed different knee structures and found that, whereas articular cartilage was not tender, ligament insertion sites and the synovium were.
A series of studies has focused on features that appear abnormal on knee MRI in those with and without pain. The majority of the studies have been conducted among persons who have radiographic knee OA and have compared those with and without knee pain with the idea that MRI can identify pathology in pain-sensitive structures such as the synovium, the meniscus, the bone, and capsular distension with fluid.
Patients with knee OA often have poorly circumscribed lesions in the bone marrow on MRI. Painful knees are more likely to demonstrate these lesions than non-painful knees. For example, Felson and colleagues [17] showed that, of persons with x-ray OA and chronic pain, 37% had large bone marrow lesions (BMLs) in their knees on MRI versus only 2% of OA knees that were not painful (for comparison of BMLs in painful versus non-painful knees, P < 0.001). The relation of large BMLs with pain was confirmed by Sowers and colleagues [18] but not by Kornaat and colleagues [19]. To the extent that we can assess cartilage loss, studies suggest that BMLs [20] are strongly related to risk of loss, especially overlying the lesion.
BMLs are not the only bone feature related to pain in OA. Attrition of bone is more common in persons with knee pain and OA than OA persons without knee pain [21]. The truth is that, by the time a knee has severe pain and shows evidence of OA on MRI, many pathologic features coexist, making it difficult to identify the single feature that causes pain (Figure 1). Because of the coexistence of these lesions, investigators increasingly have looked at whether change in specific MRI features over time correlates with change in pain. In a report from the Multicenter Osteoarthritis Study (MOST) looking at compartment-specific BMLs in knees of persons with no knee pain at baseline followed for 15 months with repeated MRIs, Felson and colleagues [22] reported that new-onset knee pain was related to an increase in size of BMLs on MRI. Of 110 cases with new-onset knee pain, 49.1% demonstrated an increase in compartmental BML scores compared with 26.8% of controls (n = 220, P < 0.001). Most people with increasing size of BMLs had BMLs at baseline. Of those with no BMLs at baseline, new BMLs occurred in 32.4% of cases compared with 10.8% of controls.
Gadolinium-enhanced magnetic resonance image (sagittal view) of a knee with multiple structural features typical of osteoarthritis. There are bone marrow lesions, cysts, and synovial thickening.
Other features linked to pain in knee OA are synovitis and effusions. Using non-contrast-enhanced MRI, which yields an incomplete view of synovitis, Hill and colleagues [23] reported that change in synovitis on MRI was positively correlated with change in severity of knee pain in 270 persons with symptomatic knee OA who had undergone serial MRIs. The correlation, though significant, was only modest (r = 0.21, P = 0.0003), translating into an increase in pain visual-analogue scale score (on a 0 to 100 scale) of 3.15 [23] per one-grade increase in synovitis (0 to 9 scale). This longitudinal study suggested that a diminution in synovitis would reduce pain. The findings of Hill and colleagues have been corroborated by Zhang and colleagues [24], who used data from serial MRIs in the MOST study and found that change in synovitis score was strongly related to change in pain – a decrease in score being associated with a lower pain score. The presence of a knee effusion and its size are also correlated with the occurrence of pain in the knee, and change in effusion size relates directly (bigger effusion, more pain) to change in pain [22].
Lastly, patients sometimes have knee pain that originates outside the joint. Hill and colleagues [25] demonstrated that periarticular MRI findings (including semimembranosustibial collateral ligament bursitis, anserine bursitis, iliotibial band syndrome, or tibiofibular cyst) were more common in those with knee pain (15%) than in those without it (4%, P = 0.004). The frequency of peripatellar lesions was not significantly different between participants with and without pain (12% versus 21%, respectively).
Structural progression of osteoarthritis
Even as MRI has become increasingly used to study disease, methods of x-ray imaging have been refined so that x-ray acquisition is now standardized with scoring and measurements that permit accurate and reproducible characterization of disease progression. Joint space loss in the medial compartment can be assessed as a proxy for medial cartilage loss. Some methods require fluoroscopic positioning, which is hard to standardize across centers [26]. Other methods using fixed knee flexion are easier to standardize. One of these uses a positioning frame that permits a highly reproducible assessment of the joint space [27]; this method is widely used in longitudinal studies. While joint space loss has been recommended as a way to track knee OA progression [28], there are inherent problems with measuring joint space loss on x-ray over time. First, this measurement focuses on the medial joint but approximately 20% of patients with knee OA sustain lateral compartment progression that leads to pseudowidening of the medial joint. Second, much of the joint space is filled by the meniscus, especially at its periphery, and meniscal extrusion frequently can lead to joint space loss [29]. Lastly, even tiny differences in the beam angle of the x-ray from baseline to follow-up lead to substantial differences in joint space width, producing spurious estimates of loss or gain. Different strategies have been adopted to overcome these problems with the x-ray. One is the addition of lateral weight-bearing views [30]. On the lateral view, the tibiofemoral joint can provide complementary information on the tibiofemoral joint to that imaged by the posteroanterior or anteroposterior view. In addition, semiquantitative scoring can provide information on lateral, medial, and patellofemoral joint progression, and experienced x-ray readers are sometimes more accurate in characterizing joint space loss than ruler-based measurements, especially when tiny beam angle changes that they can discount have occurred. In persons at high risk of progression, such as older persons who are obese, progression rates on the radiograph can reach 50% or more over the course of 30 months [31]. In the hip, joint space loss much more accurately represents cartilage loss than in the knee. The hip is rounder, making it easier to acquire images straight through the joint. Plus, there is no intervening soft tissue like the meniscus that confounds the measurement of cartilage thickness.
In many studies, the MRI image has supplanted knee x-rays as a way of evaluating cartilage loss. Amin and colleagues [32] showed that knee x-rays have a sensitivity of only about 25% for cartilage loss seen on MRI. The x-ray underestimates cartilage loss occurring in the posterior sweep of the femur and often in the upslope of the medial and lateral compartments near the cruciate ligaments. Unfortunately, although early estimates suggested that cartilage loss would occur at a rate of about 5% per year [33] among OA knees, recent large-scale work from the OA Initiative suggests that, among OA knees, the rate of cartilage loss is far less than this, only about 2% per year [34]. Such a low rate of loss coupled with variability of measurement makes studies evaluating factors that might affect cartilage loss highly challenging and also makes drug development work difficult. Current efforts focus on identifying a subgroup at high risk of loss in which new treatments might be tested. Further measurement work in cartilage loss may be necessary before it can be optimized. There may be subregions where loss in rapid and can be measured reproducibly. Semiquantitative scoring of cartilage continues to play an important role because focal erosions are present early in disease and are not well detected by quantitative measurements that summarize cartilage across a larger region [3]. Semiquantitative scoring also incorporates scores for knee joint features outside cartilage such as the meniscus and bone marrow.
Risk factors for disease progression: understanding why the structure of the joint deteriorates
With the advent of standardized radiographs and the introduction of MRI into clinical research in OA, several new natural history studies of persons with OA have been carried out, looking at factors that affect the likelihood of structural progression that in x-ray studies is defined as joint space loss and in MRI studies as cartilage loss. These studies cannot be summarized easily since they use different techniques for examining structural progression and test different risk factors. X-ray studies generally do not evaluate MRI-assessed risk factors such as meniscal tears or extrusion. MRI studies are complicated by their tendency to evaluate risk factors for cartilage loss at each of multiple anatomic sites.
In studies using MRI examining mechanical risk factors, there are three risk factors that are consistently and strongly related to cartilage loss: malalignment of the tibiofemoral joint, BMLs, and meniscal disease manifested either as a tear or as extrusion. Sharma and colleagues [35] reported that mal-alignment based on mechanical axis measurement was strongly related to joint space loss on x-ray, and subsequent studies [20, 36] have reported that malalignment strongly predicts the likelihood of cartilage loss on MRI too. If the knee is varus, cartilage loss will be medial, and if valgus, lateral compartment loss will occur.
BMLs markedly increase the risk of later cartilage loss, especially loss in a region of the joint superficial to the lesion [20]. These lesions are strongly related to malalignment [37], with medial BMLs occurring when the knee is varus and lateral lesions when the knee is valgus. Adjusting for malalignment attenuates the relationship of BMLs with progression, suggesting that malalignment explains much of the relation of BMLs with disease progression. Interestingly, Pelletier and colleagues [38] followed 107 patients with knee OA, a smaller number than in the other studies, and reported that medial compartment cartilage volume loss was correlated with lateral BMLs more significantly than it was with medial lesions, a finding that requires further investigation.
The last factor consistently related to cartilage loss or joint space loss is meniscal disease manifested either as tears or as meniscal extrusion. The latter phenomenon occurs when enough substance of the meniscus has been torn, especially at the meniscal root posterior to the knee, that the meniscus is no longer tethered to its attachments and can float freely outside the knee. When such extrusion occurs, it narrows the joint on x-ray [39] and also increases the risk of cartilage loss [36] since extrusion is functionally equivalent to having no meniscus at all, a major known risk factor for cartilage loss. Meniscal tears, because they may alter the load-distributing function of the meniscus, even when there is no extrusion, also increase the risk of cartilage loss [36, 38]. Just as tibiofemoral malalignment predisposes to cartilage loss in the tibiofemoral compartments of the knee, so patellar malalignment, either medial or lateral, predisposes to cartilage loss in the respective patellar compartment [40].
The risk factors for new-onset OA may differ from those associated with increased risk of progression in those who already have disease. The presence of hand OA, probably a proxy for generalized OA, appears to increase the risk that a person will get new-onset knee and hip OA [41]. Hand OA has also been noted to increase the risk of knee OA in those with meniscal tears who are at high risk of developing knee OA [42].
The focus of most progression studies had been on cartilage loss, and too little attention has been paid to change in pain or function in persons with knee OA. Roos and colleagues [43] reported a 7-year follow-up of persons undergoing meniscectomy, many of whom had OA at baseline. Older age at time of operation and higher body mass index were factors that accelerated the loss in function. Interestingly, a high body mass index has been tied in multiple studies to worse pain and function but not necessarily to greater structural progression.
The course of OA varies from person to person. Some with knee OA experience little change in pain or function and little structural progression. Others note a rapid downhill course.
Changes in pain and function appear to have little relation to the trajectory of structural progression. What produces this variety in disease trajectory is not clear. Identifying sources of heterogeneity might permit the identification of factors that keep disease stable and therefore could be tested as treatments. Those with malalignment at the knee experience both rapid structural progression and functional deterioration [35]. In fact, malalignment is such a potent risk factor for tibiofemoral progression that, especially among those with severe varus malalignment, other risk factors such as obesity appear to have little effect on the disease course [44]. Thus, some of the heterogeneity of the disease path is likely to be due to the presence or absence of malalignment across the joint.
Genetics of osteoarthritis
The proportion of OA due to genetic contributions varies by joint. Upwards of 50% of the occurrence of hip and hand OA may be due, in part, to genetic inheritance, whereas the percentage of knee OA varies in different population studies from non-detectably low values to up to 40%. In the general population, little knee OA is heritable, but among middle-aged women with bilateral disease occurring at an early age, heritability reaches 40%.
Large-scale studies using the genome-wide association approach are under way worldwide, and individual cohort studies are reporting that particular genes or polymorphisms within genetic regions predispose to high rates of OA. In general, many reported genetic associations reported by one group are not replicated by other cohorts and turn out to be chance findings. However, in OA, some associations have been replicated, suggesting that there really are genes that confer high rates of disease in these chromosomal regions. The most consistently confirmed genetic association is for a gene coding secreted frizzled-related protein-3 (usually called FRZB), an association reported especially in relation to the risk of hip OA in women [45]. The function of this gene is to serve as an antagonist to Wnt signaling proteins that play roles in the development of cartilage during growth and control chondrocyte maturation [46]. A mutation associated with OA does not inhibit Wnt signaling as well as the wild-type, resulting in more beta-catenin translocation to the nucleus and activation of transcription factors that increase metalloproteinase production or cartilage destruction.
Interleukin-1 (IL-1) has a multitude of functions in cartilage and in synovium within the joint. In most activities, the net effect of IL-1 is to promote cartilage degradation. Genome-wide scans have suggested that a gene conferring increased risk of OA lies within the IL-1 cluster on chromosome 2q. While confirmed in several different cohorts, the specific gene conferring risk could be IL-1, an antagonist to IL-1, a different interleukin, or even another gene close by [47].
Other genes have been reported as related to OA risk but independent replication of these associations has not been clear-cut. Undoubtedly, as meta-analyses are performed combining cohorts and providing more power to detect associations, other genes will be uncovered that increase OA risk. This will provide new understandings of how OA can develop and what treatments might be designed.
Non-surgical treatments of osteoarthritis
While recent studies have tested new treatments for OA, many have failed to identify treatments that successfully modify the structural pathology of OA or prevent joint deterioration. Successful approaches have included those targeting pain and inflammation and others focused on rehabilitation strategies. Those will be reviewed here.
Non-steroidal inflammatory drugs and cyclooxygenase-2 inhibitors
For many years, on the basis of small older trials, it was felt that anti-inflammatory drugs and analgesics such as paracetamol were equipotent for OA treatment. A series of large multi-center trials has disproved this notion, showing unequivocally that both anti-inflammatory drugs and cyclooxygenase-2 (COX-2) inhibitors are more efficacious for the treatment of pain and functional limitation than paracetamol is. In a meta-analysis of five OA trials, Wegman and colleagues [48] showed a standardized mean difference favoring non-steroidal anti-inflammatory drugs (NSAIDs) over paracetamol for pain of 0.33 (95% confidence interval 0.15 to 0.51), indicating a small effect. Pincus and colleagues [49] reported not only that celecoxib was more effective than acetaminophen but that 53% of patients preferred celecoxib and only 24% preferred acetaminophen, with the remainder not expressing a preference. Even low-dose ibuprofen (400 mg/day) was found to be significantly more efficacious than high-dose acetaminophen in one large-scale trial [50]. In a large crossover trial Pincus and colleagues [49] showed that, once patients had received NSAIDs, their chances of responding to acetaminophen, when switched to it later, were extremely low. That informed current guidelines for OA treatment, which advise that acetaminophen be used only early in treatment of OA and report that once patients have been tried on NSAIDs they are very unlikely to experience benefits should they be switched back to acetaminophen.
While anti-inflammatory therapies are more efficacious than acetaminophen for OA, their relative efficacy is not much greater and this creates difficult treatment decisions because of the high toxicity rates of many NSAIDs and COX-2 inhibitors. In fact, because of the increased rates of cardiovascular events associated with COX-2 inhibitors and with some conventional NSAIDs [51], many of these drugs are not appropriate long-term treatment choices for older persons with OA, especially those at high risk of heart disease or stroke. The American Heart Association and a meta-analysis of trials [52] have identified rofecoxib and all other COX-2 inhibitors as putting patients at high risk [51], although low doses of celecoxib, such as 200 mg/day, may not be associated with risk. One widely used NSAID, diclofenac, has predominant COX-2-inhibiting actions and its use is associated with elevated risks of cardiovascular disease, making it similar in risk to COX-2 inhibitors. Diclofenac should be avoided for most long-term uses in OA. The only safe drug from the perspective of cardiovascular risk is naproxen, and the risk is not elevated compared with non-users or with acetaminophen users. For some NSAIDs such as nabumetone and non-acetylated salicylates, there are insufficient data to characterize cardiovascular risk. This includes such drugs as ibuprofen, whose use may or may not be associated with an increase in risk. Ibuprofen may interact with low-dose aspirin, negating the cardioprotective effects of the latter, especially if the two drugs are taken at the same time.
NSAIDs also cause an increased risk of gastrointestinal toxicity, and the switch from COX-2 inhibitor use back to conventional NSAIDs may be accompanied by a temporal increase in gastrointestinal events attributable to NSAID use without use of gastroprotective drugs. Strategies to avoid the high risk of NSAID-related gastrointestinal side effects (Table 1) include the use of low doses of NSAID or use on an as-needed basis. Other tactics include the selection of NSAIDs with a lower risk of gastrointestinal side effects, the concurrent use of gastroprotective drugs, and the selection of patients who are at low risk, including those who have no coexistent Helicobacter pylori infection, and other high-risk patients. A composite of meta-analyses of large observational studies [53–56], which have evaluated the comparative gastrointestinal side effects of NSAIDs, is shown in Table 2, in which drugs are ranked according to their gastrointestinal risk. For many patients with OA, choosing a safe NSAID and keeping the dose low can help to avoid side effects. For those at higher gastrointestinal risk, adding a proton pump inhibitor, misoprostol, or a double dose of H2 blocker [57] can minimize gastrointestinal risk.
Table 1 Strategies to decrease the gastrointestinal risk of non-steroidal anti-inflammatory drugs
Table 2 Gastrointestinal risk of non-steroidal anti-inflammatory drugs/cyclooxygenase-2 from safest to riskiest
Topical non-steroidal anti-inflammatory drugs
With the 2007 approval by the US Food and Drug Administration of topical diclofenac and the availability of these agents in Europe, clinicians have a choice of administration modality for anti-inflammatory drugs. NSAIDs are placed into a gel or topical solution with another chemical moiety that enhances penetration of the skin barrier. When NSAIDs are absorbed through the skin, plasma concentrations are an order of magnitude lower than with the same amount of drug administered orally or parenterally. However, when these drugs are administered topically in proximity to a joint (for example, on top of the knee), the drug can be found in joint tissues such as the synovium and cartilage [58].
Clinical trials of topical NSAIDs versus placebo have not all been positive, and there is a troubling tendency for all published trials to be industry-funded. There may be publication bias of topical NSAID trials, the failure of small trials that show no effect to be published [59]. This publication bias suggests that readers may not have access to all evidence collected on topical NSAIDs, and should be skeptical of published trial information. Compared with placebo in three published trials, topical diclofenac led to a 1.6-unit improvement in WOMAC (Western Ontario and McMaster Universities Osteoarthritis Index) pain score (which has a range of 0 to 20) [60]. Results of trials comparing the efficacies of topical with oral NSAIDs have generally found that topical NSAIDs are slightly less efficacious than oral agents [61, 62]. In a large trial based on general practices in England, for patients given topical versus oral ibuprofen, pain improvement in the oral ibuprofen group was superior, especially at 12 and 24 months after starting treatment, and discontinuation for inadequate pain relief occurred in 23% of patients on topical drug versus only 13% in those on oral drug [63]. The major advantage of topical therapy is that it has fewer gastrointestinal side effects and renal and blood pressure-related side effects [59, 60, 62] than oral NSAIDs. Unfortunately, topical NSAIDs often cause local skin irritation where the medication is applied, inducing redness, burning, or itching in up to 40% of patients (Table 3).
Table 3 Comparison of oral and topical non-steroidal anti-inflammatory drugs for osteoarthritis
Rehabilitative approaches to osteoarthritis treatment
a. Bracing or taping
Taping or bracing a joint can immobilize it. This can relieve pain in a joint that is painful when used or can realign a joint that has become malaligned. Taping or bracing may also improve impaired neurosensory input around the joint and, by doing so, improve motor function. Treatments with taping or bracing have been tested in knee OA, especially for patients with disease affecting either the patellofemoral or medial tibiofemoral compartments.
One of the most efficacious treatments has been patellar taping, which shows impressive effects on pain relief in patients with patellar pain and patellofemoral OA and perhaps even those with knee pain in general [64, 65]. The exact mechanism by which adhesive tape placed over the superior aspect of the patella works to relieve pain is not clear. There is conflicting evidence as to whether it actually alters patellar malalignment. Even so, trials have strongly suggested that this treatment relieves pain [64–66]. The limitations may be that it is not easy to educate patients on how to apply tape themselves and that the adhesive tape that one applies may irritate the skin. As a consequence of limitations of taping, brace studies for the patella are currently ongoing. The effects of patellar braces on patellar malalignment are also unclear, but braces may push the patella into the trochlear groove [67], thereby increasing the contact area of the patella and decreasing focal stress.
Tibiofemoral bracing has also been shown to be efficacious [68]. In a randomized trial of patients with medial disease, Kirkley and colleagues [68] tested a brace versus neoprene sleeve versus no treatment at all and found that the neoprene sleeve relieved pain better than nothing but that the brace relieved pain better than either of the other two treatments as measured by the WOMAC, a survey that asks persons about knee pain during five different activities and produces a score reflecting pain severity. In those with varus OA, tibiofemoral braces straighten the knee slightly [69], decreasing varus malalignment. Braces are an underused treatment for medial OA, in part because adherence with them in the long term is not high, especially among older persons with disease.
b. Orthotics/shoes
Adduction moment (AM) is the largest moment arm across the knee during gait and represents the dynamic equivalent of static varus alignment. Persons with painful medial knee OA often adapt their gaits in ways that are presumed to lessen pain because the adaptations lower AM. For example, when off analgesics, persons with medial knee OA walk with their toes out, decreasing the AM, but when on effective analgesics and in little pain, they walk with toes in, allowing their AMs to increase [70]. AM has been shown in those without knee pain to predict those at high risk of getting it [71]. AM is the most powerful risk factor yet described for medial joint progression [72]. Lowering AM has become a major goal of biomechanical treatments of medial knee OA.
Certain shoes and insoles have been designed so that, when worn or inserted, they lower knee AM. However, in trials, use of these shoes and insoles has not translated consistently to improved pain in knee OA patients [73–75]. The reasons may include insufficient decrease in AM (only 6% on average) with great variability in AM change from patient to patient [76], failure of short-term effects to translate to longer term gait effects, and failure to identify patients who would be most likely to benefit (for example, some have patellofemoral pain). Shoes and insoles remain a promising treatment for medial knee OA, but one in which the ultimate goal of pain relief has not been realized.
c. Exercise
Multiple trials testing different types of exercise regimens are consistent in showing that exercise alleviates pain from knee OA. Even aquatic exercise appears to be modestly effective and may be better tolerated than land-based exercise. However, there are a number of substantial concerns about exercise as a treatment option for patients. First, the effect is (on average) only modest, with a number of patients not experiencing any pain benefit (and some even getting worse). Second, adherence to exercise over the long term in this chronic illness is poor. For example, in one large randomized trial [77], roughly 50% of people stopped exercising entirely by the 16-month follow-up, and in many trials adherence rates are worse than that.
How can adherence be improved? Hurley and colleagues [78], who achieved a high rate of adherence at 6 months (82%), suggested that elements explaining this success included individualizing treatment, instilling confidence that exercise would not be harmful, reassuring patients that initial positive effects were likely to continue, and teaching coping strategies. Rejeski and colleagues [79], who carried out an 18-month exercise intervention, reported that the only people who had high adherence at the end were those who had high adherence to exercise soon after it was prescribed. Campbell and colleagues [80] conducted an interview study and found that patients would exercise over the long term only if they felt that exercise improved their OA symptoms. Since all types of exercise appear to be effective, it may be best to prescribe the type of exercise most acceptable to the patient as this may be one most likely to encourage adherence.
Exercise is also a necessary component of a weight loss intervention for obese patients with knee OA. Unfortunately, the only large-scale intervention examining weight loss and exercise, the Arthritis, Diet, and Activity Promotion Trial (ADAPT) [77], suggested that, for knee OA patients, weight loss itself had only a modest and non-significant effect on pain and function. Exercise by itself did not significantly improve symptoms (the modest effect of exercise on pain in this trial was similar to its effect in other trials [81]). The combination of exercise and weight loss treatment in the ADAPT trial had an especially large effect that reached significance compared with an attention control group. Results of this study emphasize the modest effect of exercise, the necessity of coupling weight loss with exercise, and the impressive effect of combined treatment. For hip OA, individual studies have not consistently reported that exercise is efficacious. However, a recent meta-analysis pulling together data from all of the individual hip OA trials has strongly supported the notion that exercise is efficacious versus attention control [82]. Unfortunately, as in knee OA, exercise for hip OA has only modest efficacy.
Over the last 10 years, major advances in our understanding of clinical OA have occurred in areas as diverse and fundamental as a change in conceptualization of disease, our understanding of factors that affect its progression, our appreciation for the breadth and complexity of symptoms, and our approach to treatment. Among changes has been our recognition of the central role of clinical mechanopathology, including malalignment and factors in the local joint environment such as muscle and meniscal pathology in the knee. Also, we have a new appreciation for structural abnormalities in the joint such as BMLs and synovitis that probably cause pain. Lastly, new approaches to treatment, including topical NSAIDs, knee bracing and patellar taping along with exercise regimens, have offered new options to our patients with disease.
The Scientific Basis of Rheumatology: A Decade of Progress
This article is part of a special collection of reviews, The Scientific Basis of Rheumatology: A Decade of Progress, published to mark Arthritis Research & Therapy's 10th anniversary.
Other articles in this series can be found at: http://arthritis-research.com/sbr
ADAPT:
Arthritis, Diet, and Activity Promotion Trial
adduction moment
BML:
bone marrow lesion
COX-2:
cyclooxygenase-2
IL-1:
Multicenter Osteoarthritis Study
MRI:
non-steroidal anti-inflammatory drug
WOMAC:
Western Ontario and McMaster Universities Osteoarthritis Index.
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I am indebted to Frank Roemer for help with MRI images. This review was supported by NIH AR47785.
Boston University School of Medicine, Suite 200, 650 Albany Street, Boston, MA, 02118, USA
David T Felson
Correspondence to David T Felson.
Felson, D.T. Developments in the clinical understanding of osteoarthritis. Arthritis Res Ther 11, 203 (2009). https://doi.org/10.1186/ar2531
Cartilage Loss
Topical NSAID
Meniscal Extrusion


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