Appearance
5.8 — Joints
Articular cartilage has a coefficient of friction of about 0.005 to 0.02 when lubricated by synovial fluid. Ice on ice is around 0.03 to 0.1. Your knee is several times slipperier than skating, and it manages that while carrying several times your body weight, several thousand times a day, for decades.
It also cannot repair itself. That combination — extraordinary performance, no capacity to heal — is why joint disease is the leading cause of disability worldwide.
Three kinds of joint
Joints are classified by what lies between the bones, and that determines how much movement is possible.
Fibrous joints — bones joined directly by fibrous tissue. Essentially no movement. The skull sutures (Chapter 5.2), the joint holding a tooth in its socket, and the tight binding between the tibia and fibula.
Cartilaginous joints — bones joined by cartilage. Slight movement. The intervertebral discs (Chapter 5.3), the pubic symphysis, and the growth plate in a child, which is a temporary cartilaginous joint.
Synovial joints — bones separated by a fluid-filled cavity. Free movement. These are what people mean by "joint", and every limb joint is one.
The synovial joint
Every synovial joint has the same six components.
Articular cartilage — a layer of hyaline cartilage 2 to 4 millimetres thick covering each bone end. Smooth, slightly compressible, and completely without blood vessels or nerves.
The joint capsule — a fibrous sleeve enclosing the joint, continuous with the periosteum of both bones.
The synovial membrane — the capsule's inner lining, which produces the fluid.
Synovial fluid — a viscous liquid, similar in composition to blood plasma with added hyaluronic acid and a lubricating protein. A knee contains only about 0.5 to 2 millilitres of it.
Ligaments — bands of dense regular connective tissue joining bone to bone, either thickenings within the capsule or separate structures.
A joint cavity — the sealed space containing the fluid.
Some joints add extras: menisci to improve fit, fat pads to cushion, and bursae — small fluid-filled sacs where a tendon rubs over bone. Inflamed bursae cause bursitis, and "housemaid's knee" and "student's elbow" are the traditional names for the two commonest.
What synovial fluid does
Lubrication, by two mechanisms. Hyaluronic acid makes it viscous, and a protein called lubricin coats the cartilage surfaces directly. The fluid is also non-Newtonian: it becomes less viscous when sheared quickly and more viscous when loaded slowly, which means it flows easily during fast movement and resists being squeezed out during sustained load. That is exactly the behaviour a joint needs, and it is why replacing it with any simple liquid does not work.
Nutrition. Cartilage has no blood supply, so everything it needs arrives by diffusion from synovial fluid, and movement is what drives that exchange. Compressing cartilage squeezes fluid out; releasing draws it back in.
This is the physiological reason immobility damages joints. A joint that does not move does not exchange fluid, so its cartilage starves and thins. It is why prolonged immobilisation is avoided after injury wherever possible, why "rest until it stops hurting" is usually the wrong advice for a stiff joint, and why movement is prescribed rather than merely permitted after joint surgery.
And it is the honest basis for evaluating glucosamine and chondroitin supplements, which are cartilage components taken orally. Large well-conducted trials have generally found effects on pain no greater than placebo. They are not dangerous; they are mostly not effective.
Why joints crack
The popping sound when you crack a knuckle was argued about for decades. Real-time MRI imaging published in 2015 showed that the sound coincides with the sudden formation of a gas cavity in the synovial fluid, not its collapse. Pulling the joint apart drops the pressure until dissolved gas comes out of solution abruptly — the same process as opening a fizzy drink.
The joint cannot be cracked again for about 20 minutes, because the gas has to redissolve.
And the long-running claim that it causes arthritis is not supported. The best-known evidence is a physician who cracked the knuckles of one hand only for over sixty years and found no difference between his hands, which is a study with an n of 1 and considerable charm; larger studies have found the same. There is some evidence of reduced grip strength and hand swelling in habitual crackers, so it is not entirely without effect.
The six shapes of synovial joint
Pivot — a rounded end rotating within a ring. One axis. The atlas rotating on the dens (Chapter 5.3); the radius rotating at the elbow.
Hinge — a spool in a groove. One axis. Elbow, knee, ankle, and the finger joints. The knee is a hinge with a twist: it also rotates slightly, and it "locks" in full extension by rotating a few degrees, which lets you stand for long periods with the quadriceps relaxed.
Saddle — each surface concave in one direction and convex in the other, like two saddles at right angles. Two axes plus some rotation. The only true example in the body is the thumb's base joint, and it is what makes opposition possible (Chapter 5.5).
Plane (gliding) — flat surfaces sliding on each other. Small movements, but many joints acting together produce a lot. The joints between carpal bones, between tarsal bones, and the facet joints of the spine.
Condyloid (ellipsoid) — an oval end in an oval socket. Two axes, no rotation. The wrist joint, and the knuckles.
Ball-and-socket — three axes. The shoulder and the hip, which sit at opposite ends of the stability-versus-mobility trade (Chapters 5.4 and 5.6).
Articular cartilage, and why it does not heal
Cartilage is roughly 70 to 80 percent water, held in a mesh of type II collagen and large molecules called proteoglycans.
The proteoglycans are the key to how it works. They carry large numbers of negative charges, which attract water strongly. So the cartilage is a swollen gel held in check by the collagen mesh, and it behaves like a water-filled sponge in a net. When you load it, water is forced out slowly through the tiny pores of the mesh, and that resistance to flow is what carries the load. Release the load and the charges draw the water back in.
This mechanism is why cartilage handles slow sustained loads far better than sudden ones. It also means the properties depend on hydration, and on the collagen mesh being intact.
Cartilage cannot repair itself, for three reasons stacked together.
No blood supply, so no inflammatory cells, no platelets and no growth factors arrive at an injury — the normal healing sequence never starts.
Very few cells. Chondrocytes make up only about 1 to 5 percent of the tissue volume, and they are trapped in matrix, unable to migrate to a defect.
No nerve supply, so cartilage damage is painless until it becomes deep enough to expose bone, which does have nerves. This is why joint damage is silent for years and then suddenly symptomatic — and why osteoarthritis is often well advanced before anyone notices it.
Attempts to repair it are an active field and the results are honest but modest. Microfracture drills into the bone beneath a defect so that marrow cells can enter, and it produces fibrocartilage rather than the original type — mechanically inferior and prone to breaking down within a few years. Cell transplantation grows a patient's own chondrocytes and reimplants them. Both help some patients with small isolated defects and neither restores a worn joint.
Ligaments and tendons
Ligament joins bone to bone. Tendon joins muscle to bone. Both are dense regular connective tissue — collagen fibres in parallel — and both are enormously strong along their line of pull and weak across it.
Both heal slowly, because their blood supply is poor. A ligament takes weeks to months, and the healed tissue never quite regains its original strength or its original stiffness.
Sprain versus strain is a distinction that gets confused constantly. A sprain is a ligament injury. A strain is a muscle or tendon injury.
Sprains are graded, and the grade determines the treatment.
- Grade 1 — stretched, fibres intact. Pain, minimal swelling, no instability.
- Grade 2 — partially torn. More pain and swelling, some instability.
- Grade 3 — complete rupture. Often less pain than grade 2 once the initial injury has passed, because the torn fibres are no longer being stretched, and clear instability. The paradox that a complete tear can hurt less than a partial one catches people out and leads to serious injuries being underestimated.
Ankle sprains are the commonest of all sports injuries, and about 85 percent are inversion injuries — the sole turning inward — tearing the ligaments on the outer side. The reason is geometric: the outer ankle bone extends further down than the inner one, physically blocking eversion, so the ankle turns much more easily inward. And the ligament on the inner side is far stronger.
Treatment has changed and the old advice is now wrong in one respect. The current approach is protection, optimal loading, ice, compression and elevation — with early controlled movement rather than prolonged rest, because immobility weakens ligament and starves cartilage. And routine anti-inflammatory drugs in the first days are now questioned, since inflammation is part of the repair process; they are used for pain rather than prescribed automatically.
The single most important part of ankle sprain rehabilitation is balance training, because the injury damages the position sensors in the ligament as well as the ligament itself. Without retraining that sense, the ankle re-sprains — and recurrent ankle sprain is overwhelmingly a proprioception problem, not a strength problem.
What the next page fixes
Everything so far has been the normal skeleton. Chapter 5.9 covers what goes wrong with it: how a fracture actually heals week by week, what osteoporosis is and who should be treated for it, and the difference between the two arthritis types that are confused more often than almost any other pair of diagnoses in medicine.