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OSTEOARTHRITIS AND EXERCISE--CAUSE OR CURE OF THE  
ARTHRITIC?   
  
  
Peter F. Kelly, D.P.M., F.A.C.F.A.S.  
  
Diplomate, American Board of Podiatric Surgery  
Fellow, American College of Foot and Ankle Surgeons  
  
ABSTRACT  
  
The problem of osteoarthritis (OA) as a debilitating disease is discussed.   
The mechanism of its development is emphasized on a micro-to  
macroscopic scale so that the role of exercise for rehabilitation or  
recreation may be knowledgeable pursued.	Principles and practical  
examples of prevention and rehabilitation are presented.  
  
INTRODUCTION   
  
     Arthritis is largely a problem of the aged, however even a young  
patient with joint disease may be viewed as growing prematurely old.   
When the joints of an individual become less mobile, muscles  
surrounding the joint have decreased activity and circulation.   
Diminished nutrient inflow and compromised immune status of the part  
renders it less resistant to pathologies which may develop more rapidly. 
	Additionally, other body systems are interdependent upon this  
health of the muscoskeletal system, such as the cardiovascular system,  
which uses the messaging action of the large muscle mass of the lower  
extremities to aid in venous return.  
  
     What should be addressed is the theory of exercise in restoring joint  
health, or factors in promoting joint destruction.  In this light the athlete  
would be wise to participate in "joint management" within his own  
exercise program,so that he might become aware of early joint problems,  
and be able to continue longer throughout life obtaining his endorphin  
high.    
  
     Because shock absorption is highly dependent upon the cushioning  
effect of cartilage and synovial fluid, it becomes markedly decreased  
when the lower extremity becomes involved with OA.	This results in  
microtrauma to the rest of the body accumulating damage on  the cellular  
level with every step of the afflicted patient.  Coincident with that, the  
patient guards those joints painful to them, and by this natural  
withdrawal response they restrict their movement.	Contractures and  
extensor atrophy develop.  The resulting decreased mobility causes a  
decreased perfusion to the hyaline cartilage and this forms a vicious  
cycle toward its degeneration to the ankylosed state.(1)  It could be said  
that "the patient's quality of life depends on the quality of their  
movement".  
  
THEORY OF JOINT RESPONSE UNDER STRESS  
  
     Weight bearing exercises produce stress along multiple vectors.   
Repetitious compressive stresses, angulatory, tortional, and tensile  
stress, are all applied in different proportions during athletic activities.   
The cellular and fiber alignment of cartilage, and the associated  
subchondral bone, is designed to optimally dissipate the uniaxial  
(compressive) forces.  Cyclic loading/unloading such as running or  
bicycling is largely uniaxial in nature, and if the extremities are  
adequately aligned to distribute stresses from one body segment to  
another, transmission of uniaxial forces will smoothly radiate through  
cartilage and subchondral bone with a well distributed shock absorption. 
	  
  
     The problem with racketball, basketball and other rapid stop-start  
activities is that they produce a high degree of angulatory and tortional  
loading for which the force distribution patterns of cartilage and bone  
are not well adapted.  Tangiential joint forces are likely to cause  
microtears in the lamina splendins, the outermost layer of articulating  
hyaline cartilage.  Repeated activity can gouge out layers extending to  
subchondral bone.  The limited ability of cartilage to repair itself is  
impossible under these conditions.  
  
     Exercise is also essential for the health of the cartilage.  The periodic  
compression changes the charge within the proteoglycan matrix, causing  
it to perfuse water and its solutes. Cartilage in this respect behaves like  
an electrolytic solution, this uniaxial pressure causing what is known as  
the "electrokinetic effect".  Dependent upon this proper functioning is  
eighty per cent of the total weight of the cartilage--water, the function of  
which is to provide resiliency and frictionless movement.(2)   
  
     Also accommodating stress loads is the subchondral bone plate and  
its cancellous trabeculae, which respond by hypertrophy.  Compression  
stress adaptation may be significant.  It has been demonstrated that even  
in post-menopausal female runners bone density of upper and lower  
extremities will increase compared to age-matched controls.  
  
     When maintained in proper alignment, and subjected to the  
repetitious compressive forces of jogging, the joint will show few  
serious injuries.  Periarticular symptoms, however, will develop due to  
chronic repeated activities of ligamentous straining.  At the  points of  
ligamentous insertion mild osteophytes occur, but no narrowing of the  
joint space should be noted.  Common sites are the tibial spiking  
(Felsenreich's Sign) where the cruciate ligaments insert, and "footballer's  
ankle" on the distal anteroinferior tibia due to repeated kicking of the  
ball in an equinus position (see figure 1.).  
  
     Weight-bearing excercises should avoid being taken to the end of the  
range of motion of the joint.  Not only is the cartilage thinner at the edge  
of the convex side, but the amount of articulation decreases  
exponentially thus making subchondral bone fractures more likely,  
resulting in sclerosed or brittle bone.  Therefore, as long as the joint is  
functioning throughout its normal range of motion with periodic  
normative compressive stress and is in a normal alignment, with  
cartilage undamaged, regular exercise although producing periarticular  
symptoms, will not contribute toward the distructive and degenerative  
change of osteoarthritis (O.A.).(1,3)  
  
THE DAMAGED JOINT AND EXTRACAPSULAR COMPONENTS  
  
     Periodic compression and release is essential for normal hyaline  
cartilage nutrient perfusion.  The nutrient and mineral concentration is  
nearly the same in the cartilage as it is in the synovial fluid.  Dependency  
on this equilibrium makes it very susceptible to trauma, and  
degeneration (as in O.A.), also prolonged hemarthrosis (blood in the  
joint), and changes from metabolic disorders.  
  
     Malalignment of joints, soft tissue imbalances, or chronically applied  
outside forces, will not allow normal perfusion to occur to the  
chondrocytes, resulting in predictable effects on the cartilage substance. 
	Joint adaptation lends itself to soft tissue and muscular  
imbalances, increasing instability of that joint.  Ligamentous structures  
become lax and incompetent.  Asymmetrical loading in addition to  
increased wear, will not allow metabolic products to escape into the  
synovial fluid.  Nutrients are not forced into the cartilage on the lightly  
articulated areas.  Changes in the synovium may also be observed.         
Before chronic injury can be substantial enough to be classified as "post  
traumatic synovitis" (or arthritis) more subtle damage has already  
occurred.  The primary change in O.A. (Kellgren's Arthritis) is in the  
yellow, scored, and denuded articular cartilage.  When cartilage is  
denuded blood vessels reach the surface from the bone beneath, and  
there is a localized advance in the line of ossification causing marginal  
exostosis to develop around the periphery.  These impose upon the nerve  
endings of the synovium, causing pain and a reactive hyperplasia due to  
the irritation.  Foci of fibrous tissues develop in the subchondral bone  
which then go on to degenerate as a cystic softening visible as  
rarefaction on X-rays if large enough.    
  
     Subchondral bone may become more sclerotic (seen radiologically as   
eburnation) rather than demineralized and eroded as osteophytes  
develop.  Should the pain be debilitating, lack of muscle use results in  
atrophy which causes the joint to become progressively less stable.(4)  
  
     Start-stop sports and those applying violent tortional and tangiential  
forces to the lower extremity contribute greatly to ligamentous instability  
and tearing.  The amount of stress that must be dissipated increases with  
body weight, gravity, and the acceleration moment. The surrounding  
fibrous tissue will absorb certain amounts over a brief time interval, and  
by this contributes to the stability and alignment of the joint.  Because of  
the golgi tendon organ flexor-extensor reflex, the surrounding tendonous  
insertions will seek a balanced muscular redistribution.	If  
subjected to excessive loads this fibrous and tendonous reenforcement  
may undergo gradual distortion and thus may actually contribute to joint  
malalignment and articular damage.  
  
     For example, a torn anterior cruciate ligament has been referred to as  
"the beginning of the end of the knee".  Rapidly following is a  
deterioration of the menisci and articular cartilage.  Rotational and  
anterior joint laxity result in high surface stresses and friction.  Without  
proper and complete rehabilitation this knee will result in absolute  
destruction.  
  
     In the knee, normally 30-60% of the force transmitted through the  
lower extremity is absorbed by the menisci.  A torn meniscus interrupts  
the circumferential development of "hoop stress" patterns resulting in a  
two- to three-fold increase of force across the cartilage.  The force  
abnormally distributed to the joint surface results in intrinsic instability.	   
Degenerative joint disease results from the increased fatigue and  
wear.(1,8)	Joint bodies result from the formation of detached  
pieces of articular cartilage, small osteoarticular fracture fragments, or  
marginal osteophytes.  When they are nourished by the synovial fluid  
they grow slowly by the accretion of layers of cartilage on their surface.   
Fibrocartilagenous changes and calcification occurs on the cartilage  
component, but will not become bone as it still lacks a blood supply.  
  
     The presence of blood also interferes with adequate nutrition of  
cartilage.  Injury to the joint from chronic hemarthrosis is demonstrated   
by iron-containing bodies in the chondrocytes and in subchondral  
trabecular degeneration.   The synovial membrane proliferates in  
discolored brown folds of a villous hypertrophy and covers over the joint  
surface.  
  
     Subjecting a malaligned joint to repeated use not only makes it  
unable to distribute forces of stress loading, but it affects the soft tissues  
otherwise maintaining its functional position.  This contributes to  
predictable sprains, instability, and progression of the arthritis.(5,6,7)  
  
ESSENTIAL GOALS OF THERAPY  
  
     In the conservative management of joint disease an exercise plan is  
essential.  In the surgical management of arthrodesis (joint  
replacements), arthroplasties, and joint destructive procedures, physical  
therapy exercise benefits joint health by stabilizing and balancing the  
soft tissue structures.  This is to help in the absorbtion of additional  
shock so that it might be more uniformly directed through the more  
appropriate, stronger portions of the joint.    
  
     When multiple joints are involved, such as in advanced cases of  
crippling rheumatoid arthritis, and joint prosthesis are thus implanted,  
the range of motion will still be limited, but the endoprosthesis will  
allow the patient to be more ambulatory than previously.   
Postoperational exercises, as discussed below, can be modified to keep  
the joints flexible.    
  
     An important aspect of post-op therapy is passive range of motion  
exercises and conditioning the soft tissue structures to give support and  
strength to that joint.  While exercise therapy cannot be expected to be a  
cure-all, by applying the principles discussed here, it is not hard to  
imagine that joint prosthesis longevity would be correspondingly  
increased.  
  
THE KNEE  
  
     For patients having severe degenerative joint disease (DJD) of the  
knee, but more than half of the articular joint space present, treatment is  
nonoperative and consists of nonsteroidal anti-inflammatory drugs  
(NSADs), isometric exercises, and rest during the acute term.   
Progressive isometric exercises to increase quadriceps and hamstring  
strength will allow the patient to avoid minor translatory shifts of the  
knee joint and better distribute weight.  These are generally performed  
within twenty per cent of full extension using progressive weights.	  
  
     Substitution using muscular reenforcement for nonfunctioning  
ligaments is the principle, but at the same time it is important to  
minimize the transarticular force of the exercise.  Swimming is  
beneficial, as is bicycling with the seat adjusted to keep the knee flexed  
at all times  as well as adjusted to a low gear.  Bicycling is  
contraindicated if the patient has chondomalacia.(1,8)  
  
     A long term study would be appropriate in the evaluation of runners  
as compared to healthy non-runners in this area.  Long term (five years  
or greater) radiological and clinical evaluation would be most welcome.   
The radiological evaluation should document joint space narrowing,  
joint symmetry, subchondral bone integrity, and conditions of  
hyperostosis.  The clinical exam might include range of motion and  
hypermobility measurements, stressing of the surrounding capsular  
structures, and notations concerning the exact location of pain and,  
distention about the joint, and the degree and frequency of exercises  
applied.   
  
THE ANKLE  
  
     Cycling and swimming is also highly recommended for ankle  
degeneration.  In the acute phase, passive range of motion of the joint  
and stretching exercises of the achilles tendon through a painfree range  
of movement should be used.  The leg may be supported in a sling cast  
and manipulated or,if possible, exercised if not painful.  A hydrotherapy  
pool warmed to 34= centigrade, large enough to provide buoyancy and  
simulated walking will speed earlier ambulation, while relieving muscle  
spasm.    
  
     For normal walking (full weight bearing) ankle joint movement  
should be reduced to a minimum using an elevated heel with a soft sole  
material to reduce shock.  Orthosis such as a  molded ankle foot orthosis  
(AFO) may be necessary as the osteoarthritis progresses.(9)  
  
THE MAJOR JOINTS OF THE FOOT  
  
     The subtalar joint (STJ) is located directly beneath the ankle bone  
(sub-talus).  Its motion is in a screw-like manner with the calcaneus (heel  
bone) riding underneath it in an inversion-eversion movement.   
Symptoms of OA in the STJ are essentially a diffuse pain in the hindfoot  
area which is aggravated by walking over uneven surfaces and relieved  
by rest.  As with the above arthropathies physical exam may reveal  
warmth in the respective joint area.  When there is the complaint of  
persistent pain, but X-rays are unremarkable characteristic of early OA,  
a bone scan would be beneficial to demonstrate increased metabolic  
arthritic bone degeneration and regeneration.  
  
     Treatment would be the same as OA of the ankle joint, with NSADs  
and initial passive range of motion exercise in hydrotherapy baths.  The  
peroneal muscles may become spastic due to irritation and  
hypersensitivity of the nerves in the sinus tarsi and a peroneal flatfoot  
may result.	The addition of intra-articular steroid and anesthetic  
injections will halt inflammation and possibly break the pain cycle.   
After the acute phase has passed, inversion-eversion exercises should be  
started.	To lessen the aggravation of STJ movement a polypropylene  
AFO with a rocker bottom shoe will hold the joint rigid and lessen the  
otherwise higher energy required for propulsion.(1)  
  
     The midtarsal joint (MTJ) is the main joint of  the midfoot.  Its major  
role is in the conversion of internal and external movement of the leg to  
a triplanar movement of the foot.  Because of this conversion, it serves  
to absorb torque and shock from the upper torso in a closed kinetic  
chain.  It is probably the most poorly understood of the major joints,  
which is unfortunate because of its important torque conversion role.  
  
     The MTJ actually consists of two joints, the talo-navicular joint on  
the medial side 1;s  0;s , which connects the ankle bone to the midfoot,  
and the calcaneo-cuboid joint on the lateral side, which connects the  
rearfoot to the midfoot.  These two joints function synergistically to  
create two independently functioning axes not directly related to the  
joints' original movements.  The difficulty in understanding the absolute  
aspects of STJ function rests on the two axes' complex mechanical  
interactions with each other as well as with their high degree of  
variability among normal individuals.      
  
     For example, an abnormal forward tilt of the longitudinal axis of the  
MTJ can produce excessive torque translation from the upper body in  
the transverse plane, to the midfoot in largely the frontal plane.  This  
results in excessive movement of the lower vertebrae (usually L5-S1),  
and results in common lower back pain.  The second axis, the oblique  
axis, is oftentimes compensatory to other leg and foot dysfunctions,  
resulting in a type of flatfoot.  These are only two examples to describe  
the two MTJ axes, and they may even occur concurrently.  With time,  
misorientation of these axes results in an undetected arthritis, which may  
progress respectively, in herniation of a disc which could necessitate  
spinal fusion, or in severe and painful foot dysfunction, necessitating a  
triple arthrodesis.  
  
     In dealing with the joints of the foot, a general rule regarding the  
prognosis of joints restoration is   
that the results of nonoperative therapy become increasingly poor when  
proceeding distally from the subtalar joint.  Orthotics as a supportive  
measure may maintain the deformity temporarily, however the  
discomfort increases as the bones continue in their subluxation and  
protrusion onto the orthotic.    
  
PRACTICAL GOALS OF THERAPY  
  
     The goals of an exercise program should be to maintain or improve  
function by preserving range of motion and improving muscle strength.   
The latter is important to help stabilize the joint, and by maintaining soft  
tissues' conditioning, they will thus reduce the stress applied to the joint.   
Gradual conditioning is important so that muscle pain and soreness is  
not aggravated.   
  
     Physical conditioning may retard a loss of mobility and therefore a  
program which balances the soft tissues stabilizing the joint should be  
encouraged according to the level of conditioning and the physiological  
age of the joint.  This is appropriate whether it be in the elderly patient,  
or in the athlete who persists in prematurely aging his joints.    
  
     In the elderly patient, light "sports" are often recommended to keep  
these joints in motion.  It is interesting to note that in the realm of the  
debilitated, the therapy of light sports starts out on the level of poker  
playing and progresses through several levels to ping-pong, then perhaps  
ultimately to badminton, which is considered a fairly considerable  
attainment.  The significance is not of course in the level of sports  
achievement, but in joint restoration (9).    
  
SUMMARY   
  
     Osteoarthritis is a widespread problem in our society.  Not only does  
it debilitate the aged and the traumatized, but it also attacks in those  
pursuing optimal health.  Because its origins and prevention are largely  
similar, the underlying development of OA had been presented and  
emphasized.  
  
     It is evident that repetitive stresses, especially of the tangiential  
"jamming" type and those placing the force on the perimetry of cartilage  
during the extremes of flexion and extension, can induce intense  
applications of strain.  Whether it be in quantity or vectorial relation, this  
is a strong predisposing factor to osteoarthritis.	At first the effects  
are on an undetectable biochemical level.	Cartilage might, under the  
proper conditions, be able to undergo a partial regeneration.  However,  
with chronic abuse, the soft tissue surrounding the joint tends to lose  
mobility and such stresses result in increasing the impact of these same  
forces on the joint.  This seems to occur normally with advancing age  
under conditions of decreased mobility.(10)    
  
     Should the athletically inclined keep a sharp watch on the prevention  
of excessive joint stressfullness, especially during the extremes in range  
of motion, their ability to exhibit increased performance without pain  
will enable them to remain effectively younger throughout their natural  
life.  
  
FIGURES  
  
Fig. 1	Lateral view of the ankle of an international foot-baller.  Note  
the bony  spur on the front of the tibia and the irregularity  of the  
capsular attachment of the talus. This is due to  repeated strain of the  
capsule from kicking with the foot fully plantarflexed.  From Watson- 
Jones Fractures and Joint Injuries.  
  
REFERENCES  
  
1.  Moskowitz, R.W., Howell, D.S., Goldberg, V.M., Mankin, H.J.:   
Osteoarthritis Diagnosis and Management.  W.B. Saunders Co., 29-36,  
390-409, 407-8, 561-66, 1984.  
  
2.  Brighton, T.B., Black, B., Pollack, S.R., Lee, R.C., Grodzinski, A.J.,  
Glimcher, M.J.:  "The Electromechanics  0;385;t of Normal and  
Chemically Modified Articular Cartilage".  Electrical Properties of Bone  
and Cartilage, Experimental Effects and Clinical Applications, Grune  
and Stratton, 47-55, 1982.  
  
3.  Salter, R.B., Bell, R.S., Keeley, F.W.:  The Protective Effect of  
Continuous Passive Motion on Living Articular Cartilage in Acute  
Septic Arthritis.  Clinical Orthopedics and Related Research, 159:223- 
47, 1981.  
  
4.  Forrester, D.M., Brown, J.C.:  Clinics in Rheumatic Diseases. W.B.  
Saunders Co., 9:2, 297-9, 1983.  
  
5.  Lichtenstien, L., Diseases of Bone and Joints.  C.V. Mosby Co., 186- 
200, 1970.  
  
6.  Wagner, H., "Principles of Corective Osteotomies in Osteoarthrosis  
of the Knee", Progress in Orthopedic Surgery, Vol. II, U.H. Weil, 75-79,  
1980.  
  
7.  Ross, C.F., Schuster, R.U.:  "A Preliminary Report on Predicting  
Injuries in Distance Runners".  J.A.P.A.0;s , 73:275-7, 1983.  
  
8.  Wilson, J.N.:  Watson-Jones Fractures and Joint Injuries.  Churchill  
Livingston, 67-8, 82-6, 1982.  
  
9.  Barker, R.L., Burton, J.R., Zeive, P.D.:  Principles of Ambulatory  
Medicine, Williams and Wilkins, 640-1, 1982.