By H. Kirk Watson, MD

Human tissues “speak” to and influence one another.  This communication expresses itself eloquently in the pathology of the hand.  The upper extremity has numerous areas of mechanized motion one tissue on another and the excursions are large for the size of the structures e.g. 7 cm of sliding for the adult flexor digitorum profundus.  There are many joints with large excursions and heavy loads.  All of these motion planes require the minimal degree of coefficient of friction and this achieved by synovium.

Synovium “speaks” to the collagen to which it’s attached.  Inflammation, whether traumatic or secondary to the body physiology, will cause hypertrophy of the support collagen.  A simple example is stenosing tenosynovitis.  If activity exceeds what the A1 pulley is used to then synovitis and the A1 pulley thickens.  As collagen thickens clinical entities develop; including the trigger fingers, median nerve compression of carpal tunnel syndrome, de Quervain’s, extensor compartment tenosynovitis, and PIP joint contractures.  This last one is a unique phenomenon where joint synovium lines the inside of the check rein capsule while fibro osseous tunnel synovium lines the outside.  Both layers enhance check rein fibrosis.  Very complex tendon anatomy dorsally, is not synovial lined and there are no collagen hypertrophy clinical etiologies of a similar nature.  Systemic changes can change the hyaluronic acid to water ratio and excess water decreases the coefficient of friction producing a palpable rub or “wet leather sign” common with de Quervain’s.

Similarly in joints bone collagen hypertrophies in response to synovial inflammation.  Malaligned joint surfaces wear cartilage beyond the ability of the synovium to “clean up”.  Chronically inflamed synovium hypertrophies bone collagen at synovial attachments and osteophytes occur e.g. the ridge on the dorsum of the scaphoid occurs from chronic low grade synovitis secondary to dynamic rotary subluxation.  Contrary to expectations the excision of the ridge removes the synovial intimacy with the bone.  The clinical symptoms do not recur, and despite no surgery to restabilize the scaphoid the patient remains clinically well for decades.

Elbow surgeons experience similar results from simple osteophyte excision.  This is also true of the distal radioulnar joint.  Osteophytes form circumferentially at the proximal cartilage surface.  Some distal joint cartilage is often preserved and resection of this osteophyte ridge detaches synovium and gives excellent long term clinical results.  How synovium speaks to collagen remains to be sorted out.  Contrary views solicited.