Steroid Injections Accelerate Damage To Joint Surfaces

Picture from Ortho Arizona

Many patients with knee osteoarthritis (OA) who come to see us in our clinics often tell us that they were given intra articular (inside the joint) corticosteroid injections (IACS). ICAS is a common treatment choice that is considered minimally invasive to delay knee replacements for patients with severe OA. 

Other than providing brief pain relief, the pain often comes back. I wrote earlier this year that steroid/ cortisone injections significantly increases the risk of tendon tears.

Perhaps it's time to think more than twice before you allow anyone to inject into you knee joint. Make it any other joint for that matter as latest published research shows that individuals who got IACS were twice as likely to have harmful effects on knee articular cartilage structure than those who received no or placebo treatment.

Different stages of articular cartilage damage

A group of researchers investigated the effect of IACS on articular cartilage structure in patients with knee OA using joint space width on x-ray and articular cartilage thickness with MRI.

They found 6 studies consisting of a total pf 1437 participants. The estimated effect of IACS on articular cartilage structure showed significant odds of it worsening as measured by joint space narrowing and articular cartilage thickness. The authors concluded that their meta- analysis showed that IACS increases the likelihood of knee joint deterioration.

Other than increasing the risk of tendon tears, steroid/ cortisone  injections into knee joints may be doing more harm than good by accelerating joint surfaces degeneration. The short lasting pain relief is definitely not worth the long term consequences of your articular cartilage degenerating. 

Reference

Ibad HA, Kasaeian A, Ghotbi G et al (2023). Longitudinal MRI-defined Cartilage Loss And Radiographic Joint Space Narrowing Following Intra-articular Corticosteroid Injection For Knee Osteoarthritis: A Systematic Review And Meta-analysis. Osteo Imaging. DOI: 10.1016/j.ostima.2023.100157

PS Sim Summits K2

Summit of K2

Yes, it was last month that many of you would have read about PS Sim reaching the top of K2 - the second highest mountain in the world after Everest.

Straits Times article on 240823

Well, she came by our clinic today and both MJ and Kaylee were both ecstatic to meet her. In fact, they have been asking about her ever since they have seen her pictures in our clinic. The 2 fan girls got to ask her whatever questions they wanted. And of course they wanted pictures with her (below).

Kaylee asked her to compare Everest to K2. In her words, "Everest is a walk in the park compared to K2". To which I replied that it's not a walk in the park definitely.

We are all inspired by you PS!! Please put up an exihibition/ show and tell of all your pictures/ videos from Everest, K2 and the rest of 7 summits, we will definitely come.

Hip Adductor Related Groin Pain

If you follow Aussie Rules Football (or AFL), yesterday was the 2nd second semi final with GWS Giants defeating Port Adelaide 93-70. Aized and I had to help Aussie Rules football players back when we were  doing our post graduate physiotherapy studies in 2003. I still follow the AFL league from time to time. AFL footballers often suffer from groin pain.

Other than AFL footballers, soccer (also known as football), rugby players and those who play badminton and squash etc are involved in rapid acceleration, deceleration and sudden changes in direction are all more prone to groin injuries.

Athletes with a previous groin injury are at a greater risk than those with no previous injury. This can be up to 2.4 times greater over consecutive seasons with football players (Haglund et al, 2006).

The hip adductors

Football players have a yearly incidence of adductor related groin pain of 10-18 percent. 53 percent of theses cases are from overuse. Groin injuries in male club footballers accounted for 4-19 percent of all injuries and 2-14 percent in women club footballers.

Different types or groin pain

It can be difficult to diagnose groin injuries since there can be many different complex causes. Hip adductor related groin pain is defined as hip adductor tenderness and pain with resisted hip adduction testing. It is also the more common causes of groin pain. Other than hip adductor groin pain, the iliopsoas, inguinal and pubic symphysis are other causes of groin pain (pictured above).

Exercise therapy is commonly prescribed for groin pain although there is no specific exercise protocol. Exercises, particularly adductor eccentric strengthening seems to be beneficial for pain reduction and return to sports at 16 week follow up in comparison to stretching, electrotherapy (ultrasound, interferential currents) and transverse friction massage.

We do see many patients with groin pain in our clinics. However, our approach to treatment is different. We do not get our patients to do the strengthening exercises when they are in the clinic. We prefer to treat them using mostly our hands instead. For example, for a patient with groin pain, they may also have a higher hip on one side (pictured below).

R hip lower

We can treat the hip with respect to the shorter side. Short in terms of length. It also depends on what our assessments show. The patients can do the strengthening exercises they need on their own. We treat what they cannot do themselves in the time they have with us. Come see us in our clinics if you have groin or hip pain.

References

Haglund M, Walden M and Ekstrand J (2006). Previous Injury As A Risk Factor For Injury In Elite Football: A Prospective Study Over Two Consecutive Seasons. BJSM. 40: 767-772. DOI: 10.1136/bjsm.2006.026609

Weir A, Brukner P, Delahunt E et al (2015). Doha Agreement Meeting On Terminology And Definitions in Groin Pain In Athletes. BJSM. 49: 768-774. DOI: 10.1136/bjsports-2015-09486

Yosefzadeh A, Shadmehr A, Olyaei GR et al (2018). Effect Of Holmich Protocol Exercise Therapy On Long-standing Adductor-related Groin Pain In Athletes. BMJ Open Sp Ex Med. 4: e000343. DOI: 10.1136/bmjsem-2018-000343

Avascular Necrosis

Picture by Frank Gillard from Radiopaedia

Seeing this x-ray reminds me of what I was suspected of having when I started having persistent knee pain back in early 2002, which then led me to having 3 knee surgeries. A doctor I consulted suspected I had early avascular necrosis in my lateral femoral condyle. 

Avascular necrosis (also know as osteonecrosis) is the dying of bone tissue due to lack of blood supply. Depending on where it is, it can lead to tiny breaks in the bone and cause the bone to collapse. This process can take years to occur.

A dislocated joint or a fracture in parts of the bone can also hinder or stop blood flow to a section of the remaining bone. This commonly occurs at the epiphysis (end part) of long bones at weight bearing joints. Some common sites include the femoral head, talus, humeral head, knee and the scaphoid bone (in the wrist).

Avascular necrosis is associated with long term use of steroid medications and injections and too much alcohol. Anyone can be affected. It tends to be most common in people between the ages of 30 and 50.

Repetitive trauma can also cause avascular necrosis. This is not as commonly discussed in the medical journals. This form of avascular necrosis is most common in athletes. Rafael Nadal has a chronic left foot ailment, Mueller-Weiss syndrome where there is avasular necrosis in his navicular bone. Young gymnasts that I have previously treated are also prone to this in the wrist, knee and hips.

The doctor I consulted for my persistent knee pain back then felt that my super high mileage  (I was training for the 100 km Trailwalker event in Hong kong and the full Ironman) caused my knee pain.

The cause of avascular necrosis brought on by trauma (or repetitive stress like running and jumping) is not fully understood. Genetics combined with certain medication (like corticisteroids), excessive alcohol intake and other diseases like sickle cell anemia and Gaucher's disease can play a role as well.

Fatty deposits (or lipids) in blood vessels can block blood vessels and reduce blood flow to bone as well. There are suggestions that long term and high doses of corticisteroids (like prednisone) can increase lipid levels in blood, reducing blood flow to the bones.

Some people have no pain or symptoms at all in the early stages of avascular necrosis. As it worsens, the affected joints may hurt when weight bearing. Eventually there may be pain even at rest. Pain can be mild or severe and develops gradually. 

Having too many alcoholic drinks over several years can also cause fatty deposits to form in blood vessels.

Certain medical treatments like radiation therapy for cancer can also weaken bone. Kidney transplant patients have also been known to be associated with avascular necrosis.

To reduce the risk of avascular necrosis, please limit your alcohol intake since heavy drinking is one of the top risk factors for developing avascular necrosis. 

Keep your cholesterol levels low as tiny bits of fats (lipids) are the most common substance blocking blood supply to bones. Stop smoking as smoking narrows blood vessels which will reduce blood flow.

For those doing repetitive sports, I always suggest running on softer surfaces like grass or sand. Do not be in a hurry to increase your mileage, your bones and joints need time to get used to the load.

Lessen the junk miles or better still ride the stationary bike or use the elliptical trainer to target different areas. Strength training is very important for your bone health.

Reference

Shah KN, Racine J, Jones LC et al (2015). Pathophysiology And Risk Factors For Osteonecrosis. Curr Rev Muscu Med. 8(3): 201-209. DOI: 10.1007/s12178-015-9277-8

Best Vehicle Seat Position For Driving

Picture from the European Spine Journal

The laundry (towels, bed covers, pillowcases) in our clinics get picked up twice a week for the past 16 years by a husband and wife team - Ray and Elaine. Elaine does the driving while Ray does the pickup and delivery of the huge laundry bags. I spoke to them and Elaine was complaining about her back pain after all that driving and I told her it's probably linked to her lumbar (lower back) load from all the driving and sitting in their van.

Picture from the European Spine Journal

A recently published study used a Christophy spine model (inclusive of head, neck and limbs, pictured above) and compared calculated lower back loads and muscle forces while driving to experimental data from previous studies. 

Using data from previous radiology studies, this Christophy spine model was tested in different driving positions with different back supports. The load on the lower back was then calculated with the various back supports and backrest inclination angles.

0 cm, 2 cm and 4 cm lumbar supports were used along with inclinations of the backrest from 23 degrees to 33 degrees (by 2 degrees intervals).  

Ready for the results? Especially for those of you who drive a lot.

The overall lower back spinal loads and muscular forces at the L3-L4, L4-L5 and L5-S1 decreased very obviously with the 4 cm back support, with the seat inclination angle set to 10 degrees. With the 4 cm back support, the overall lower back spinal load decreased by 11.3 percent while  muscular forces were reduced by 26.24 percent.

The recommended backrest inclination angles are between 29 to 33 degrees with a 10 degrees seat cushion to the horizontal. 

This is a useful study to explain the association of drivers' sitting postion and the change in lower back load. It helps provide a reference for the prevention of low back pain.

Now if someone can send these recommendations to car manufacturers to improve the design of vehicle seats, that would be great.

References

Christophy M,  Faruk Senan NA, Lotz JC et al (2012). A Musculoskeletal Model For the Lumbar Spine. Biomech Model Mechanobiol. 11: 19-34. DOI: 10.1007/s10237-011-0290-6

Gao K, Du J, Ding R et al (2023). Lumbar Spinal Loads And Lumbar Muscle Forces Evaluation With Various Lumbar Supports And Backrest Inclination Angles In Driving Posture. Eur Spine J. 32: 408-419. DOI: 10.1007/s00586-022-07446-x.