My shoulders crack alot as well, especially during incline bench and dips. I was told it is due to a lack of cartillage in the joint.
RHEUMATOLOGY IN A NUTSHELL
Rheumatology is mostly about joints. Most problems with joints improve with time rather than treatment, so the doctor’s main job is to explain what is wrong with joints in a way that people can understand. When treatment works it also helps if the doctor knows why!
Unfortunately, current jargon is unhelpful. Any change in a joint, however slight or transient, is called arthritis. For the last hundred years doctors have divided arthritis into "diseases" like osteoarthritis and rheumatoid arthritis. While these terms have had their value they often obscure what is really happening inside joints. Telling someone they have such and such sort of arthritis is often both meaningless and demoralising. In the last ten years mechanisms have finally began to become clear. Clarity has allowed simplification and for arbitrary Latin names to be replaced by common sense concepts.
The commonest factor contributing to bone and joint pain is probably the remodelling of bone that occurs with age. Remodelling leads to net loss, and if severe, osteoporosis, but at the same time it produces a gradual change in shape. Bones thicken around joints and ligament attachments. In almost everybody after the age of 40 this bony overgrowth leads to friction on other tissues, such as the rotator cuff tendon in the shoulder or nerve roots in the spine. In many people visible bony ridges appear around small joints, as typified by Heberden’s nodes.
The reason for this change in bone shape is not known, but it can be seen as a bit like the thickening of an ageing hollow tree or of a man-made object repeatedly repaired or repainted. There is a tendency for things that are weakened inside to be restored on the outside.
Less often, but commonly enough to cause significant problems for at least a quarter of the population, joint pain is caused to by disintegration of articular cartilage. The obvious examples are the hip and knee, in which complete loss of the weightbearing cartilage is a common reason for joint replacement. Cartilage loss is also common in the first MTP (bunion) joint and in the first carpometacarpal joint at the thumb base.
The causes of cartilage disintegration are sometimes obvious — abnormal development, inflammation or trauma, but in most cases they are less clear. Cartilage does not wear out just with use. In most joints the same collagen molecules stay at the tissue surface for a lifetime. A number of clues suggest that a major cause of cartilage disintegration is the changing shape of nearby bone. This has been difficult to establish with certainty because cartilage disintegration in itself leads to remodelling of bone, stimulated by the abnormal forces transmitted to bone once cartilage has failed.
Because cartilage disintegration and bone growth often go together they have been lumped together as osteoarthritis. However, this has made people think there is a disease called osteoarthritis in which one thing follows another in a standard sequence, which there clearly is not. The solution is to consider cartilage loss and bone growth on their own merits, which is necessary anyway, because the management of each is different.
Joint pain may also be due to inflammation of the synovial lining (synovitis). Because this may occur in many joints and last lifelong, it is a major cause of loss of quality of life. Acute episodes of synovitis tend to be due to infection, which is uncommon, but important, or crystals, as in gout and pseudogout. Chronic synovitis is usually due to abnormal regulation of the immune system, as in rheumatoid arthritis.
Immune disorders leading to synovitis can be divided into those involving antibodies - true autoimmunity - and those associated with MHC Class I, which probably involve cytotoxic cells.
Autoantibodies probably cause widespread small joint arthritis through an interaction between small IgG-based immune complexes and the IgG Fc receptor FcgRIIIa. This mechanism probably also accounts for associated problems such as pericarditis and subcutaneous nodules. It is likely to be responsible for most of the features of rheumatoid arthritis and those that overlap in lupus.
Problems in many other tissues due to other autoantibody-mediated mechanisms often fall under the rheumatologist, simply because joint pain is often part of multisystem problems.
Inflammation associated with Class I histocompatibility antigens, especially HLA-B27, affects entheses (ligament and tendon attachments) as much as synovium and may be associated with skin (psoriasis), gut (inflammatory bowel disease) or mucosal (Reiter's) problems. The synovitis, may be secondary to enthesitis. Inflammation probably arises from abnormal regulation of cytotoxic cells, which may be CD8+ T cells, but may be other types of cell capable of killing. Class I interacts with receptors on all types of leucocyte as well as binding to CD8.
Treatment of joint disease was rudimentary until a revolution occurred in the mid twentieth century with the development of treatments for tuberculosis and the design of a reliable total hip replacement by Charnley. Corticosteroids also had a dramatic impact, but at major cost in terms of toxicity. Cyclo-oxygenase inhibitors alternative to aspirin and slow acting anti-rheumatic agents have, in comparison been mixed blessings, but have provided the potential to reduce morbidity significantly. Physical therapies, developed at a time when a safe placebo was better than the risks of a general anaesthetic or toxic drugs, are still widely used despite the fact that there is little evidence for their value.
A second revolution is likely to occur very soon in the treatment of immunological and inflammatory disease with the development of means of manipulating specific elements of the immune response. Management of cartilage failure will continue to improve with better integration of artificial joints in to bone. The new issue is the management of bone remodelling as the population ages. Osteoporosis is already a major target for treatment. Whether other aspects of bone remodelling are amenable to treatment remains to be seen.