Osteoarthritis (OA) was considered a Degenerative disease when I went to Med School in the late 50s. I am more interested in OA since I have developed it myself.

There is a 40-60% hereditary component. My father’s mother had arthritis badly in her hands, as did my mother’s mother, and so on. A lot of genome-correlation work has shown many different genes involved,

But without a single big contributor, OA appears to be “multifactorial”, similar to a lot of common diseases like Diabetes l. Trauma can be a factor. Old sports injuries, like an ACL tear, that you thought a thing of the past, may come back to haunt you in later years.

INFLAMMATION, the most popular explanatory cause of the decade, may be operating in OA. For instance, you can imagine that OBESITY would contribute to hip and knee OA simply through the traumatic force of gravity. But obesity is also a disease of Inflammation, and increases IL-6 and other cytokines as well.

My own OA involves the classic distal 2 interphalangeal joints (go to the wikipedia manekin for a color-representation of OA classic locations). The base of my thumb, neck and back are also a problem.

Strangely, but wonderfully, my “wheels”, the Hips and Knees, are spared. I have exercised a lot in my life. Clearly, you can’t “wear out” your joints with ordinary exercise.

Our joints have evolved to allow us to move. Since bone has a lot of pain fibres, it would be painful to move the joints, directly bone-on-bone. So we have cartilage on the ends of the bones and discs between the vertebrae. The cartilage is slick to reduce friction.

Cartilage has no blood to supply it with nutrients. Instead, it relies on the joint (synovial) fluid. The cartilage is like a sponge. Walking alternately compresses and relaxes the spongy cartilage, increasing the synovial fluid circulation, thus improving the nutrition of the cartilage. If the Cartilage disappears, there is pain.

I am not a fan of pain medication. My belief was strengthened by the side effects of the study of a medication designed to genetically block pain transmission by injection into the painful joints. The side effect was virtual dissolution of the joints in a fraction of those treated. I felt more comfortable with my pain after reading the article.

Although Acetaminophen helps a little, NSAIDs usually work better, perhaps because of their anti-inflammatory action.

If, like me, you have stomach issues, there are the COX-2 inhibitors like Celebrex. The one dose I recently took was almost magical in its effects. Maybe if you don’t use pain Meds much, they work better.

I do take Glucosamine-Chondroitin, thinking that providing building blocks for cartilage couldn’t hurt. Along this line I also EAT CARTILAGE whenever I eat Chicken or ribs, being careful not to damage my teeth in the act of of exercising my jaws.

I also take Curcumin, hoping to relieve some pain, in spite of the fact that it is poorly absorbed (some brave souls take it by injection). I don’t know if any of this helps, How can you know in such a variable disorder, in the absence of controlled studies.

And pain has no OBJECTIVE markers, and is notoriously hard to study. We literally know more about the surface of mars than we know about Pain.

SLEEP, DIET, and EXERCISE, by minimizing OA factors kike OBESITY and INFLAMMATION are the best bet for preventing and treating OA at present.

–DR. C


Chest pain is a common chief complaint. It may be caused by either benign or life-threatening aetiologies and is usually divided into cardiac and non-cardiac causes. James E. Brown, Professor and Chair, Wright State University Boonshoft School of Medicine, Kettering, Ohio, gives us an overview of assessing chest pain in the emergency setting. 


Dr. James E Brown of the Wright State school Of medicine in Kettering Ohio gave a very interesting discussion of chest pain.

One interesting takeaway is the value of a very experienced clinician dealing with large volumes of emergency room patients. This would make telemedicine with an emergency room hub in a teaching center a very attractive platform.

The consultant doctor in the center has the advantage of his vast experience in rapidly narrowing down the heterogeneous list of different diagnoses that must be considered- the “differential diagnosis”.

Dr. Brown mentioned the “gestalt”, the incorporation of subjective features such as facial and voice cues which add to the objective parameters in patient evaluation. This of course would be amenable to telemedicine although other old-time clinical information like the changes in breath sounds would be more favorable to conventional in-person evaluation.

Ultrasound would More easily be done locally as well.

An interesting take away from this discussion is the value of The patient’s history and past laboratory data, so undervalued by rushed modern doctors. For instance, Electronic medical records (EMR) could provide past history or a previous electrocardiogram for comparison.

Dr. Brown favors the division of chest pain causes into cardiac and non-cardiac. It is easy  to develop tunnel vision and look at the patient only as a possible coronary thrombosis. In fact it is better to Rapidly consider the non-cardiac causes that would demand immediate attention while waiting for the results of the Troponin-T test.

For instance pulmonary embolism, aortic dissection, tension pneumothorax, cardiac Tamponade should be considered.

These considerations should be running through the head of the clinician as the IV,  EKG, and pulse oximetry are being set up.

In addition to the Troponin-T, bedside ultrasound, and Higher “slice count” CAT machines, and higher “Tesla” MRIs  are becoming available major centers which could support small emergency rooms.

If there is One place where “the Flow” would be Appropriate it would be in the mind of the emergency room doctor evaluating acute chest pain.
I have a hard time imagining artificial intelligence endangering her job.

—Dr. C.