What is Osteoarthritis? FAQ

An osteoarthritic joint is a joint in which the process of destruction and production of cartilage is unbalanced. The destruction of cartilage predominates and it ends up affecting the whole joint.

• Cartilage is composed of cells (chondrocytes) lying inside cavities (matrix) filled with a gel consisting of large molecules.
• Chondrocytes produce and destroy the components of the matrix. In normal circumstances there is as much cartilage produced as cartilage destroyed.
• Osteoarthritis settles in when the amount of cartilage destruction is greater than that of cartilage production.
• Over time, the destruction of cartilage affects the whole joint, including the synovial membrane and the portion of the bone beneath the cartilage.

The triggering factor of osteoarthritis is excess pressure on the cartilage. Reactions that follow this excess pressure are of 2 types: mechanical and biological.

• Excessive pressure causes a mechanical rupture of the wall of the matrix. The cartilage cracks, breaks and fragments migrate into the joint.
• The excess pressure activates the chondrocytes that produce more matrix cartilage and then more destruction enzymes (this is the biological response). In the long run, destruction outweighs production and osteoarthritis develops.
• Cartilage is the first component to be affected, but the other components of the joint (the synovium and the bone beneath the cartilage) soon become affected as well. The whole joint has become "osteoarthritic".

The cartilage is not innervated. So it is not that which "hurts". The pain comes from the surrounding tissues that are innervated and are also affected by osteoarthritic lesions: the synovial membrane, the subchondral bone, the ligaments and the tendons.

The pain information starts in the nerve endings present in these tissues. It then travels via the nerves to the spinal cord and up to the brain which triggers the sensation of pain.

Once the cartilage has been damaged, "neo-neurogenesis" may occur. This is the appearance of nerve endings within the cartilage that was initially free from them, because of osteoarthritic disease.

The evolution of osteoarthritis is unpredictable.
Osteoarthritis can develop:

• very slowly, over several decades;
• very quickly with complete loss of cartilage in one or two years;
• over a more or less long period, interspersed with "inflammatory flare-ups" or "acute painful episodes" during which the destruction of the cartilage accelerates.

Osteoarthritis becomes established in two different situations: when excess pressure is applied to normal cartilage, and when pressure (without excess) is exerted on weakened cartilage.

• Excessive pressure on normal cartilage occurs in the event of:
  - being overweight;
  - excess strain on joints of occupational or sports origin (microtrauma);
  - anatomical abnormality (dysplasia) or traumatic sequelae.
• Pressure on the joints is unevenly distributed, thereby creating areas of excess pressure.
• Pressure on weakened cartilage occurs:
  - in diseases of the cartilage such as chondrocalcinosis where calcium is deposited in the cartilage;
  - in diseases of the joint components such as the synovium being affected in rheumatoid arthritis or the bone in osteonecrosis.

Questioning the patient and physical examination of the joint suggest the diagnosis. An x-ray shows the lesion and confirms the diagnosis.

• Examination of the patient analyses two major symptoms of osteoarthritis:
  - mechanical pain accentuated by mobilisation or bearing weight on the joint and relieved by rest;
  - joint stiffness responsible for discomfort on walking (knee, hip) or mobilisation (fingers).
• The physical examination finds:
  - swelling of the joint (knee) in relation to the presence of a large quantity of synovial fluid in the joint (effusion);
  - deformation of the finger joints;
  - decreased joint mobility (knee, hip, fingers).
• Radiographs show images that are characteristic of osteoarthritis:
  - a decrease in the height of the space between the two articular surfaces (joint space narrowing);
  - changes in the structure of the bone beneath the cartilage (sclerosis, geodes);
  - bone spurs at the bone-cartilage junction (osteophytes).

A flare-up of osteoarthritis corresponds to inflammation of the joint.
It is during this flare-up that the destruction of cartilage increases.

• Signs that suggest a flare-up are:
  - a sudden increase in pain (acute painful episode);
  - the inflammatory timeframe of the pain (with nocturnal awakenings);
  - prolonged joint stiffness in the morning (morning stiffness);
  - swelling of the joint (especially noticeable in the knee).
• When possible, puncture of the joint relieves the patient and removes other causes (including infectious) of an acute flare-up.
• A flare-up of osteoarthritis requires:
  - resting the joint;
  - radiographic control of the joint spaced apart from the acute episode to assess the impact of the flare-up on the cartilage (accentuation or not of joint space narrowing).

The pain of osteoarthritic joints is best evaluated by a visual analogue scale.

• A visual analogue scale has two advantages:
  - it gives the patient (not the doctor) the task of assessing the pain him or herself;
  - it is a monitoring tool of the analgesic treatment prescribed by the doctor.
• The visual analogue scale is a ruler that on one side (that of the patient) is a continuous strip of which one end is "no pain" and the opposite end is "worst pain imaginable".
  The side of the ruler visible to the doctor is graduated from 0 to 10
• The patient moves a cursor along the "strip" until his estimate of the intensity of pain (between the 2 marks "no pain" and "maximum tolerable pain").
  On his side, the doctor notes the corresponding rating (between 0 and 10).

Obesity is a risk factor for osteoarthritis in joints that bear the weight of the body (knee, hip). Mechanical overload is not the only cause because obesity is also a risk factor for localised osteoarthritis of the fingers.

• The responsibility of obesity in the development and worsening of osteoarthritis has been demonstrated for the knee.
• In relation to a subject of normal weight, the obese subject has a higher risk:
  - of suffering from osteoarthritis of the knee,
  - and more quickly aggravating pre-existing osteoarthritis of the knee.
  
• Obesity does not just promote or accelerate the development of osteoarthritis of weight bearing joints. Because of the metabolic disorders it leads to, it is a risk factor for all osteoarthritis sites (in particular, osteoarthritis of the fingers).

Joint fractures, severe sprains and "small" repeated trauma to a joint are risk factors for osteoarthritis.

• Joint fractures injure the cartilage because the fracture goes through the joint surface. In general, the bone consolidates, but the evolution of cartilage damage can develop into osteoarthritis.
• When sprains are severe (with torn ligaments) they can destabilise the joint. This instability promotes the development of osteoarthritis.
  The complete removal of a meniscus has the same effect.
• Occupational activities and sporting activities that involve repetitive movements causing repeated "microtrauma" are risk factors for osteoarthritis.

The doctor assesses the mobility of the joint and the condition of the muscles surrounding the joint. He looks for the presence of fluid in the joint and the presence of inflammatory signs.

• Joint mobility reflects joint stiffness.
  Muscle wasting (atrophy) is a consequence of stiffness because less mobility leads to less activity.
  Muscular stiffness and atrophy should receive treatment (rehabilitation exercises with or without the assistance of a physiotherapist).
• Looking for the first "inflammatory" signs (fluid in the joint, peri-articular heat) is essential for the early management of any "flare-up" of osteoarthritis.

During the development of osteoarthritis, radiographs have a twofold interest: diagnosis (what damage is there after a "flare-up"?) and prognosis (how fast will the disease evolve?).

• A flare-up of osteoarthritis (acute painful episode) is usually accompanied by an accentuation of cartilage degradation. The x-ray taken at the end of the flare-up is used to evaluate the consequences of the latter on the joint (has it decreased in height?).
  The risk of accelerated degradation is an argument for identifying a flare-up of osteoarthritis as early as possible and treat it immediately.
• Radiological monitoring of osteoarthritic joints predicts the "development rate" of the disease from the evolution in the height of the joint space (or joint space narrowing).
  Hence, the accelerated evolution of this joint space narrowing associated with a severe disability is an argument for the need to place a prosthesis (knee - hip).

Anatomical abnormalities may be the cause of osteoarthritis if it is localised in the hip, knee or foot. Treatment aims to prevent the onset of osteoarthritis.

• In the hip, congenital anomalies (dysplasia) concern either the pelvis (the part of the hip called the acetabulum) or the femur (at the neck).
• The misalignment of the leg relative to the thigh deforms knees: either knock-kneed or bow-legged. These deformations create mechanical overload localised in the outer part or the inner part of the knee.
• Abnormalities of the arch of the foot (flat feet and hollow feet or high arches) may have an impact on osteoarthritis of the knees.

During an acute painful episode, resting the joint limits cartilage degradation and is associated with an anti-inflammatory treatment for the inflammation and pain.

• During an acute painful episode, cartilage degradation is accelerated.
• To limit it, it is necessary to:
  - rest the joint that is suffering without discontinuing any physical activity; if the painful joint is the knee or hip, it is sufficient to stop bearing weight on it by using forearm crutches;
  - take an anti-inflammatory treatment for several days.

Rehabilitation for osteoarthritis has 3 objectives: maintain mobility of the joint, fight against deformation and strengthen the muscles around the joint.

• Stiffness, disability affecting the quality of life of osteoarthritic patients, is combated by exercises to maintain good joint mobility.
• Deformations are the result of the wrong positions taken to relieve pain (flexion of the knee and / or hip). In the long run, these wrong positions become permanent and, in turn, a disability (discomfort on walking).
• Strengthening the muscles around the joint has a dual action: analgesic and stabilising.

To assess the risk of osteoarthritis associated with sports activity, you need to take into account the type of sport and the level of practice.

• Sports such as football or rugby lead to a lot of trauma. These injuries (sprains, joint fractures) may leave sequelae (instability, cartilage damage), which, in the long run, promote the development of osteoarthritis.
• Sports people practising a competitive team sport (especially as professionals) are more exposed than those practising a leisure time sport because their sporting activity is more intense, more frequent and more prolonged.
• The risk of osteoarthritis is higher if, beside the risk of trauma, the sports person has other risk factors such as a discrete morphological abnormality of the limbs or is slightly overweight.

In the treatment of osteoarthritis, surgery may be considered as a preventive measure (surgical treatment of an anatomical abnormality) or curative measure (placing a prosthesis to replace a partially destroyed joint).

• Preventive surgery is considered in two circumstances:
  - ltreatment of a congenital abnormality (dysplasia) of the hip, before the first signs of osteoarthritis;
  - realignment of the leg bone in the event of incipient osteoarthritis of the knee localised on one side of the knee.
• Placing a prosthesis is reserved for:
  - patients with intense pain and severe disability despite the correct treatment (sufficient dose for a long time) and well-monitored,
  - provided that the x-ray shows advanced osteoarthritis.
• A joint prosthesis is usually for the hip or knee.

Medication for osteoarthritis can include drugs administered orally (by mouth) and others for local use (on the skin or by injection into the joint).

• Oral medications are:
  - analgesics that act on pain;
  - anti-inflammatory drugs that act on inflammation and pain;
  - symptomatic slow-acting drugs whose goal is to reduce the symptoms. The effects appear only after several weeks of administration, but persist for several weeks after stopping the treatment.
• Topical medications are:
  - anti-inflammatory ointments applied locally and in the form of a solution injected into the joint;
  - lubricants (hyaluronic acid), close to synovial fluid, injected into the knee joint.

The World Health Organisation classifies analgesics (painkillers) according to 3 levels of strength. Those of the first level are preferred in the treatment of osteoarthritis.

• Analgesics of level 1 are the most commonly prescribed.
• Analgesics of level 2 are less well tolerated and are prescribed only when the level 1 analgesics are ineffective.
• Analgesics of level 3 are used only in exceptional cases (severe pain, severe disability in a non-operable patient) because of their adverse effects.
• Note: most often it is the elderly who suffer from osteoarthritis and they are also the patients who are the most vulnerable to adverse side effects from the drugs.

Local applications of anti-inflammatory drugs are reserved for superficial joints (fingers, knees) are less effective and generally well tolerated.

• Anti-inflammatory drugs applied topically on the skin are available in two forms: gels and ointments.
• They are less effective than oral anti-inflammatory drugs but their overall tolerance is much better.
  Tolerance of local applications is not always perfect and they should be suspended in the event of a skin reaction.

Symptomatic slow-acting drugs are well tolerated.

• These are drugs used specifically in osteoarthritis. They have the ability to reduce the intensity of pain. Their effectiveness on painful symptoms has been proven in osteoarthritis of the hip and knee.
• The analgesic effect of these drugs occurs after a period of a few weeks (4-8) and persists for several weeks after stopping the treatment.