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Posts Tagged ‘bone erosion’

In an earlier post, I outlined how RA can impact much more than bones including many organs and soft tissues. One group of soft tissues that can be damaged by RA includes those involved with the musculoskeletal system. The musculoskeletal system involves a complex interaction between muscles, bones, joints, and various connective soft tissues – all which can be the target of RA.

Erosion of bone tissues in joints is on of the trademark symptoms of rheumatoid arthritis. Through complex autoimmune biochemical processes, the body’s immune system attacks it’s own tissues like it was a foreign invader. A cascade of signaling chemicals promotes the production of bone cells called osteoclasts that erode bone tissue and surrounding cartilage. This kind of gross damage…

Read more at http://rheumatoidarthritis.net/living/attack-on-connective-tissues/

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Multi-Level: involving more than one.

Anterior: nearer the front, especially situated in the front of the body or nearer to the head.

Cervical: of or relating to the neck.

Discectomy: surgical removal of the whole or a part of an intervertebral disc.

Fusion: the process or result of joining two or more things together to form a single entity.

Osteophytes: bone spurs

Excision: Surgical removal by cutting.

I received an epidural steroid injection into my neck and no relief was felt. Pain levels in my neck, shoulders, and arms got out of hand to the point where sleep was not being had. My fingers were numb, tingling, with small motor function suffering. Work, both professional and at home, was not getting done. Leaving the house was mostly out of the question. Because of these issues, my physical therapist refused to treat me and based on a discussion about various other symptoms, he said that he was running next door to the neurosurgeon’s office to determine if they could see me immediately. He came back shortly and said that they were getting me in 30 minutes. After a long exam and discussion, the doctor indicated that surgery would be the only route that would provide long term relief. After thinking about it and reading the variety of literature provided by the doctor’s office, I finally agree to proceed and it is scheduled for May 15.

The procedure will be a multi-level anterior cervical discectomy, fusion and osteophyte excision. Going in from the front of the neck, two herniated discs between vertebrae C5-C6 and C6-C7 will be removed, bone spurs impinging on nerves and spinal cord cut away, a plastic mesh containing parts of my own bone material inserted into the disc space, and titanium screws will be used to connect the three vertebrae. The entire procedure will take about 3-4 hours and I will stay in the hospital overnight. Recovery is at least 6 weeks. Here’s a nice post from Sandy who described her experiences with a similar procedure.

I’ve had three ankle surgeries and a sinus surgery. Even though the sinus surgery was very close to my brain, this one seems a little more intense. Maybe that’s because they will be putting titanium screws into my neck. Or that a hospital stay is required. Or that there’s so many life necessary parts in that area. But I trust the surgeon as he’s well qualified and trained, board certified, part of a large hospital spine center, and done many of these procedures in the past. The decision to have surgery is never to be taken lightly. But given the long term and increasingly intense pain, coupled with disability of function, it’s clearly time to proceed.

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Rheumatoid_arthritis_jointBone erosion is one of the hallmark symptoms of RA and the biological processes involved in RA often result in the breakdown of bony tissue primarily in joints which are surrounded by a sac called the synovium (see diagram). I have this telltale bone erosion in my fingers documented via x-ray and a dime-sized erosion was found in my heel bone several years ago which caused a sharp bone spur. A surgeon removed the damaged tissue and a pathology report confirmed that it was caused by the erosive processes associated with RA.

But RA can impact other parts of the joint including the surrounding soft tissue – tendons, ligaments, and cartilage. Chronic tenosynovitis, inflammation of the sheath of a tendon is common in rheumatoid arthritis and can result in the permanent damage and tearing of the involved tendons. Such tendon problems caused by RA are well known by the scientific community and are linked to joint deformities (see Sivakumar, et al, 2008; Wakefield, et al, 2007). Tendon problems have even been posited as being one of the most powerful predictors of early RA (Eshed, et al, 2009). Sophisticated imaging techniques developed in the last few decades, such as MRIs and ultrasound, can reveal connective tissue damage in joints caused from RA including tenosynovitis and bursitis (Boutry, et al, 2007). Bursitis, inflammation of the fluid-filled sacs that protect joints (see NIH site), often accompanies tenosynovitis. RA is also implicated as a cause of cartilage damage in knees (see the AAOS site). An MRI taken at the onset of my RA diagnosis revealed cartilage damage in one knee.

Soft tissue damage became apparent after dealing with a persistently cranky elbow that was only getting worse to the point that major pain killers were needed one evening. I learned from an orthopedic doctor this week that I now have tendon tears in my elbow. The good news is that the bones and joint spaces are in good shape and appear to be undamaged from RA. While in non-RA patients the tendons commonly tear due to overuse, the doctor was unsure about the relative contributions of RA and overuse to the tearing. But since I don’t tend to overuse my elbow, except when fishing a couple of times this summer, I can’t help but think that RA is the major contributor – especially in light of previous history. Tendon problems have been a hallmark of my struggles with RA. One of the first symptoms I experienced, even before official diagnosis, was Achilles tendon tearing in both ankles which resulted in two surgeries. This bilateral problem, coupled with other symptoms, ultimately led to seeing a rheumatologist and receiving a diagnosis of RA. Several years later the tendon tearing continued and a third surgery was needed on the right ankle to repair the tendon, remove a bursa sac, and remove damaged bone tissue. Even after those procedures, my Achilles tendons continue to speak rather loudly everyday.

At this point, conservative treatments to the elbow will begin and include use of braces, topical NSAIDs (Voltaren gel), and physical therapy. Cortisone injections may be used if conservative treatments don’t work with surgical repair being the last line of treatment. So we wait and see if the most recent RA treatment (Rituxan) and the newly prescribed elbow treatments can slow down soft tissue damage enough to allow the tendons to heal on their own.

Photo attribution: By Wouterstomp at en.wikipedia [Public domain], from Wikimedia Commons

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450px-Walking_ManThe other day I walked into the kitchen and my wife laughingly said to me, “You’re walking like Frankenstein”. I laughed back because I knew that I was like the “living dead” for many reasons but mostly because of changes in my joints. I have bursitis in both hips which radiates pain down the thigh and in the buttocks (I got two cortisone shots recently and they did nothing – but that’s another story), cartilage damage in both knees, and three surgeries on my ankles. Add to that, I could barely get out of bed and walk around this morning due to sharp pain in the same area of the right ankle that’s had two surgeries. I’ve felt that pain before which was from erosion in the heel bone causing spurs to dig into the Achilles tendon. Yep, I was walking stiffly and probably looked like a monster from a movie.

It’s a natural tendency to make adjustments due to pain or joints that aren’t working as designed. Joint changes from rheumatoid arthritis seem to be inevitable As bone and soft tissues are attacked, damaged, and eroded, the joints can no longer work as they should. Fortunately, disease modifying medications can slow down the damaging biochemical processes. In spite of being on medications, changes are still affecting my movement and activity.

When the term arthritis is mentioned, the first thing that comes to most people’s mind is probably bone damage. With the more common osteoarthritis (OA), there may be damaged cartilage causing bone to rub together. But with rheumatoid arthritis (RA), the immune system attacks the body’s own tissue. The capsule surrounding the joint, called the synovium, becomes enlarged due to an increase of immune cells. Eventually an overproduction of bone eroding cells and enzymes begins to erode bone tissue and soft tissues.[i] The soft tissues that hold the joint together including tendons, ligaments, and cartilage are also damaged.[ii] [iii] When all of these tissues become affected, the entire skeletal structure designed for movement cannot work properly. Add to that stiffness caused by RA, and the result is walking like Frankenstein!

My joints used for walking are changing and the effects are becoming noticeable not just to me, but to those around me. Add to that the fact that any hope for strenuous physical activity is pretty much gone for now. My daughter wants to go snow skiing but the best I could do is drive her there and sit in the lodge drinking cocoa. The hope is that treatments can keep the process at bay long enough so I can avoid more surgeries and using assistive devices just to carry out that common, everyday task we take for granted – walking.

Photo Credit: By Stefan Eggert (User:Berreu) (Own work) [GFDL (http://www.gnu.org/copyleft/fdl.html) or CC-BY-SA-3.0 (http://creativecommons.org/licenses/by-sa/3.0/)], via Wikimedia Commons

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 Definition of TWINGE
transitive verb
1 dialect : pluck, tweak
2: to affect with a sharp pain or pang[i]

A typical day with RA includes gentle reminders such as stiff and tender fingers while typing, difficulty getting up out of a chair if sitting more than 30 minutes, a knee that pops loudly while flexing, elbows that ache, and then there’s the ubiquitous fight with fatigue. After three ankle surgeries on torn Achilles tendons, tendon insertion tears, and bone erosion in the heel, these areas are omnipresent reminders of RA. Most days it’s tolerable and doesn’t impact walking – although strenuous exercise is out of the question. But every once in a while when going up or down stairs a sharp pain comes out of nowhere to scream a very loud reminder. This twinge catches me by surprise. Many times the pain is so bad that I must stop on the stairs and change the way I walk. Many have seen me limp away from the stairs. The sharp pain usually lasts for a few hours before subsiding. Once the major pain is gone, I usually forget it and move on. But the little voice in my head always asks if there is more RA-induced damage that will result in another surgical procedure someday. Ignoring that voice is helpful as there’s nothing to do about it now.

Recovery from sinus surgery seems to be going well. It’s been 10 days and the bleeding is almost gone, breathing is better, headaches are less intense, and energy levels are slowly returning yet with peaks and valleys. The best news is that today was the last dose of the antibiotic Cephalexin. This is the last of four antibiotics taken over the past 3 months. These strong antibiotics impact the GI system in very uncomfortable ways which won’t be missed. Arava will be added back to the RA treatment regimen tomorrow. Of course, Arava brings its own set of GI side effects which aren’t too bad at the 10mg per day level. The next Orencia infusion is Tuesday and I’m glad that I didn’t have to miss a dose during this entire sinus situation. Hopefully sinus infections will be a thing of the past.

Early next week I plan to write a post about the role of cell death in rheumatoid arthritis, genetic links, possible treatments, and how this is connected to cancer. Have a good weekend!


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I’ve been absent from this blog for almost 1 ½ years, I decided to jump back and start writing again. And much has transpired since the last post. After stringing it out as long as possible, I had my third ankle surgery in late November 2011. The orthopedic surgeon cleaned up bone erosion on the top side of the heel bone, removed a bone spur poking into my Achilles tendon, removed a bursa sac, and repaired mores tears in the Achilles tendon. Tissues samples were sent to pathology and the lab results noted bone erosion and inflammation caused by rheumatoid arthritis.

Stopping Humira injections in early November 2011 was necessitated by the pending ankle surgery but also by the fact that it just wasn’t helping that much anymore. In addition, a 3 cm swollen lymph node in my armpit needed to be checked out. Short story – saw a great oncologist and after many blood tests, an ultrasound, and a CT scan with iodine contrast, everything came back negative with no lymphoma! One interesting blood test result was that I had a positive Rheumatoid Factor test for the first time. I was finally seropositive and felt like I was no longer the seronegative stepchild of RA. Although I know that upwards of 30% of folk don’t have positive RA blood tests.

I was started on Orcenia infusions in January 2012. I was done with TNF blockers after using Enbrel, Cimzia, and Humira. After insurance approval, I had three loading doses every two weeks before moving to a regular schedule of once a month. Having a nurse administered infusion at a clinic was a new experience compared to self-injections of Enbrel and Humira. It was a rough few months but I began to get back some energy and have less joint pain and stiffness.

By this point, I decided to pursue a new rheumatologist. I had been with my original rheumatologist from the beginning and he made the initial diagnosis. But over time I began to realize that it was time for a change. I sought out a new rheumy by asking around, checking out published lists of top doctors in the region, and looking at patient reviews online. A choice was made and an appointment with a new rheumy scheduled. As an added advantage, her clinic just relocated to a brand new, clean, and cheery building. I had all medical records sent to her.

The first appointment was a pleasant experience from the beginning with smiling staff, caring nurses, and the fact that I didn’t have to wait. The first thing the doctor told me was that she spent considerable time reading all of my medical records. That was a refreshing to know – she already had an idea about my case before I arrived. She then asked me to tell my story in my own words. Given my history, my new rheumy suspects that I may have a combination of RA and ankylosing spondylitis – an autoimmune condition which commonly affects ankles, hips, and backs. She joked that I would be a good subject for genetic testing! We discussed how Orencia was working and she felt like I would benefit from the addition of a disease modifying drug (DMARD). Since methotrexate and I didn’t have a good relationship a few years ago, she wanted to try leflunomide (Arava). In fact, she suspects that one reason that TNF blockers stopped working was that I wasn’t on combination therapy resulting in the building up of antibodies to Enbrel and Humira. I appreciated her optimism about being able to help and compassion about my experiences.

New adventures lie ahead with a new doctor, new medicines, and new possible side effects. But hope springs eternal just like the sun finally coming out in Seattle.

Photo taken by my daughter on a sunny day in Puget Sound.

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Rheumatoid arthritis

MRI and Ultrasound of RA damaged joints Image via Wikipedia

When people hear the general term arthritis, they typically think of an older person with joint pain. This concept misses the mark when describing rheumatoid arthritis (RA). When people think about RA, they might picture someone with grossly disfigured hands or feet. One of the symptoms of RA that doctors often examine is bone erosion – typically in the fingers.

But as an autoimmune disease, RA can impact much more than the bones. It can damage a variety of soft tissues including the eyes (iritis), lungs (fibrosis), heart, blood vessels (vasculitis), nerves (carpel tunnel), and skin (nodules, ulcers), and connective tissue (cartilage, tendons, ligaments).[i] Often-times, the soft tissue damage occurs long before bone erosion is visible or even before an official RA diagnosis comes.

Two symptoms which I personally experienced before an official diagnosis of RA were iritis – inflammation in the eyes, and torn Achilles tendons (an ongoing problem with me). Chronic tenosynovitis (inflammation of the sheath of a tendon), such as that found in rheumatoid arthritis, can result in the permanent damage and tearing of the involved tendon. Such tendon problems caused by RA are well known by the scientific community and are linked to joint deformities.[ii] Tendon problems have even been posited as being one of the most powerful predictors of early RA.[iii] Sophisticated imaging techniques developed in the last few decades, such as MRIs and ultrasound, can reveal connective tissue damage in joints caused from RA including tenosynovitis and bursitis.[iv] Bursitis, inflammation of the fluid-filled sacs that protect joints[v], often accompanies tenosynovitis. RA is also implicated as a cause of soft tissue damage in shoulders[vi] and cartilage damage in knees.[vii]

It is interesting to note that the diagnostic criteria[viii] used to diagnose RA, while including general joint synovitis as indicated by pain, swelling, and tenderness, don’t include other soft tissue problems. These criteria are in place in spite of the fact that some of the soft-tissue problems occur long before the presence so-called hallmark symptoms like bone erosion. It could be that such a wide variety of symptoms across patients occur and the criteria are based on those symptoms that tend to be universal. However, a quick read of patient blogs (see my list) reveals that many RA patients suffer profusely from soft tissue damage. From a patient perspective, it would be beneficial if soft-tissue damage from RA would be given increased attention in the general literature (it’s difficult to find information) and in diagnostic criteria.

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Towards the end of a whirlwind of recent travels, a never ending headache set in. Many factors historically caused me headaches including migraines, stress, and reaction to medications (see earlier post re. Humira). When I was driving home from work yesterday, I began to connect together a set of other symptoms…constantly clogged left side of nose, pressure around my left eye, pain on the molars on the left side, and a recent spate of colds that made the rounds with my children. A sinus infection seemed to be the culprit. By Friday afternoon, the medical options are pretty slim but I swung into the local urgent care. Surprisingly they were not busy and within a few moments I was diagnosed with a sinus infection. I was prescribed the fast acting antibiotic Azithromycin and I coupled that with a decongestant and a neti pot to cleanse the sinuses. Upon waking this morning, the headache and pressure was gone and it remained that way all day!

As an autoimmune disease, RA is treated by medicines that suppress the immune system. If the immune system can be suppressed, then it will be less likely to attack itself and the symptoms of RA can be controlled. Drugs used to treat RA like methotrexate and the biologicals are immunosuppressant drugs. I’ve been on an immunosuppressant for the past 1 ½ years…Enbrel, Cimzia, and now Humira. According to Humira’s website,

HUMIRA is a TNF-blocker medicine that can lower the ability of your immune system to fight infections.” [i]

Before starting on a biological, a negative tuberculosis test is required. Upper respiratory infections, including sinus infections, are first on the list for common side effects for Humira.[ii] This isn’t my first infection while being on a biological medicine. I had a urinary tract infection about 8 months ago and had a couple months of swollen lymph glands around my neck which was attributed to some unknown infection (likely viral). Lower on the list of side effects are cancers like lymphomas. Although it’s easy to get freaked out by such statements and decide not to take a biological treatment for RA, the chances for this occurring are very low and the benefits outweigh the risks for most people.

On one hand, I’m thankful for Humira and its impact on treating my RA. I’ve had pretty decent energy and bone erosion in the fingers seems to be halted (see earlier post). (Although I’m starting to debate Humira’s effectiveness because of ongoing problems with my ankles. It’s just impossible to tell what things would be like without Humira). On the other hand, I don’t like the fights with infections that are likely caused by having an suppressed immune system. There always seems to be a set of tradeoffs when it comes to the imperfect science of medical treatments.

 

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Humira - sunday week 12

Image by pollyalida via Flickr

Things are pretty hectic these days and that typically brings an increase in fatigue and joint symptoms. It doesn’t help that my Humira injection is due tomorrow but I’m itching to take it today with the notion that it may help me feel better. Of course, today I read of a study demonstrating that stress increases the release of inflammatory proteins like TNF alpha.[i] But I was more intrigued by the Arthritis Foundation article about how long it takes for rheumatic diseases to be diagnosed.[ii] Average time to diagnosis varies (see table below) but it is clear that folks with these diseases suffer for a long time before getting proper treatments. The article states, “Many rheumatic diseases have symptoms that overlap, and blood tests are rarely conclusive.”

Rheumatoid arthritis 6 to 9 months
Juvenile arthritis             5 months
Fibromyalgia                    2 to 5 years
Sjögren’s syndrome         3 to 7 years
Ankylosing spondylitis    6 to 9 years

Such was the case with me. After being referred by my general practitioner (an internist), my rheumatologist first suspected ankylosing spondylitis since my primary symptoms at the time were uveitis (inflammation of the iris) and achilles tendon problems. But my blood test for HLA-B27, the common genetic marker for this disease, was negative. About the same time, other tell-tale symptoms of RA began appearing…middle finger joints, wrists, elbows, knees – all occurring symmetrically on both sides. Bone erosion was noted via x-rays. Morning stiffness (what’s that? I’m stiff all day long!) and overwhelming fatigue (the truck running over you type) wrapped it up for the rheumy and he diagnosed me with RA.

This diagnosis was made in spite of negative RA factor blood tests. My RA factor tests have always been “borderline”…it’s not a black and white test. Another antibody test, anti-cyclic citrullinated peptide (anti-CCP) is another one used to determine RA. So far, I’ve been negative on that one as well. Therefore, I have what is called “seronegative RA.” I met the criteria using the now outdated diagnostic criteria.[iii] The diagnosis criteria were recently updated[iv] and according this new system, I still meet the diagnostic critieria without having positive blood tests. My rheumy regularly mentions that seronegative RA patients tend to fare better with symptoms over the long run and this is borne out by research.[v] Some seronegative RA patients “convert” over time…they end up with positive tests. Interestingly, a large proportion of folks diagnosed with RA are seronegative…up to 30% in some studies.[vi]

Being seronegative makes me feel somewhat like the stepchild to those who are seropositive. Maybe I’m not “official enough”. But then I have to step back and remember that my symptoms are real, I have permanent joint damage, and I’m forking out upwards of $20,000 a year for biological treatments (well ok, my insurance covers most of it). Perhaps I will seroconvert someday. But in the meantime I’ll hang onto the research that says that us seronegative RA types have a better long term prognosis.


[i] http://www.arthritistoday.org/news/social-rejection-stress-inflammation080.php

[ii] http://www.arthritistoday.org/daily-living/relationships/you-and-your-doctor/rheumatic-diseases-misdiagnosed.php

[iii] http://www.hopkins-arthritis.org/physician-corner/education/acr/acr.html

[iv] http://www.rheumatology.org/practice/clinical/classification/ra/2010_revised_criteria_classification_ra.pdf

[v] http://www.ncbi.nlm.nih.gov/pubmed/3855618

[vi] http://onlinelibrary.wiley.com/doi/10.1111/j.0105-2896.2009.00856.x/full

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About two years ago was the first time I began to notice swelling and pain in my proximal interphalangeal (PIP) joints in both hands. The PIP joints are the middle knuckle in each finger (not including the thumb). Although I had other symptoms, this was really the reason for seeing my primary care physician ultimately leading to a visit to a rheumatologist and a RA diagnosis. Early on, my rheumy ordered x-rays and the radiology report indicated some bone erosion in these joints. In spite of being seronegative for RA factor, this finding was enough for my rheumy to quickly begin disease modifying medications eventually leading to the use of TNF blockers (Enbrel, Cimzia, now Humira). Since then, inflammation has spread to the some of my metacarpophalangeal joints (MCP) at the bottom of each finger and to the wrist (and elbow, and knees, and feet…).

Inflammation of the PIP joints is typical in RA patients and can lead to permanent deformities in the fingers.[i] Joint damage can come on rapidly if RA is not treated. I vividly recall my first encounter with RA about 20 years ago. In the days before major disease modifying medicines, my neighbor had severe RA and his hands, fingers, and feet were deformed beyond use. He was such a gentleman and upon shaking my hand, quickly explained why his fingers were so deformed. Surgery scars were prominent on each finger. Surgeons went in and clipped the ligaments in a futile attempt to slow the deformity.

Because of this, I’ve kept an eye on my fingers. A few months back, my rheumy ordered another round of x-rays and the good news was that the radiologist noticed no additional bone erosion. But since I live with my fingers every day, it’s easy for me to notice slight changes. Several fingers began to bend towards the outside (called ulnar drift) and some are no longer straight but are twisting/rotating (see photos).

I can certainly rejoice in the fact that bone erosion in my fingers seems halted at this time. And I can’t complain because many RA patients have dramatic joint damage and deformity. I suspect that the use of TNF blockers has something to do with my case. Never the less, I can see the changes over time.


[i] http://www.hopkins-arthritis.org/arthritis-info/rheumatoid-arthritis/rheum_clin_pres.html

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