Etiology and biochemical mechanisms of development
The exact cause of the disease is currently unknown. The main risk factors include mechanical cartilage overload and impaired congruence (matching of shapes) of articular surfaces. Heredity and a history of previous injuries can also serve as predispositions.
The key link in pathogenesis is chondrocytes. These cells are not only sensitive to biologically active mediators but are also capable of producing them themselves. The biochemical cascade of cartilage destruction is as follows:
- Interleukin-1 (IL-1) acts on chondrocytes.
- In response, chondrocytes begin to actively synthesize matrix proteinases — potent proteolytic enzymes.
- The result is the enzymatic degradation of collagen and proteoglycans, which form the basis of the cartilage matrix.
Following the initial destruction of cartilage, the underlying bone reacts secondarily: marginal bone growths—osteophytes—form on it. As a complication, inflammation (secondary synovitis) frequently joins the process.
Pathophysiology of pain: why does the joint hurt?
One of the most important nuances of the clinical picture is that the articular cartilage itself lacks nerve endings. Pain in osteoarthritis is multi-component, and its sources are the surrounding tissues:
- Subchondral bone: pain arises due to trabecular microcracks (a kind of microfracture beneath the cartilage).
- Synovial membrane: reacts with pain due to a joined inflammatory process (synovitis).
- Osteophytes: growing bone spurs mechanically irritate the nerve endings of the periosteum (periosteum).
- Ligamentous apparatus: pain is formed as a result of ligament overstrain.
- Joint capsule: suffers from inflammation and mechanical stretching.
- Periarticular muscles: respond to the pathology with reflex spasm.
Special forms and spinal involvement
As a rule, significant joint deformations are rare, but when large joints (knee, hip) are involved, prominent pain significantly limits function and leads to disability.
There is a specific hereditary form of the disease. It is characterized by the formation of dense nodules on the hands: Heberden's nodes (on the distal interphalangeal joints) and Bouchard's nodes (on the proximal interphalangeal joints).
When the spine is involved, spondyloarthritis or osteochondrosis develops. The pathology includes:
- Dystrophy of intervertebral discs and joints (including costovertebral joints).
- Formation of osteophytes directly on the vertebral bodies.
If altered structures or osteophytes compress nerve roots, neurological complications develop—radicular syndrome. Clinically, it manifests as pain, paresthesias (sensory disturbances), and decreased reflexes. Neurological symptoms are most pronounced when the cervical spine is affected.
Diagnostic algorithm and therapeutic tactics
The basis for making a diagnosis is a combination of the characteristic clinical picture and radiography data. Laboratory diagnostics (CBC and biochemistry) are indicated only in pronounced synovitis: in this case, leukocytosis, accelerated ESR, as well as elevated levels of fibrin, seromucoid, and sialic acids are detected.
Radiological staging:
- Early signs: uneven joint space narrowing and subchondral sclerosis (compaction and expansion of the epiphyseal bone plate).
- Late signs: sharpening of articular surface edges and formation of large osteophytes.
Principles of treatment:
- Regimen and unloading: it is critically important to limit static loads (e.g., prolonged standing) and walking. In case of obesity, weight correction is mandatory.
- Physical rehabilitation: systematic therapeutic exercise (physical therapy) is indicated. The main principle is a gradual increase in the range of motion without overloading the joint.
- Pharmacotherapy: nonsteroidal anti-inflammatory drugs (NSAIDs) are prescribed to relieve pain and suppress signs of inflammation.
Briefly: answers to topical questions
Which groups of chondroprotectors (SYSADOA) are used for baseline therapy of osteoarthritis?
Sources include the following among symptomatic slow-acting drugs ("chondroprotectors") used for osteoarthritis/gonarthrosis:
- glucosamine sulfate: reduces pain and improves joint function; with long-term use, it slows down joint space narrowing and reduces the need for arthroplasty;
- chondroitin sulfate: at a dose of 1200 mg/day, it significantly reduces the loss of articular cartilage volume in knee osteoarthritis;
- unsaponifiable compounds of avocado and soybean oils: significantly reduce pain syndrome; there is no convincing data on structure-modifying action;
- animal-derived products: bioactive concentrate from small marine fish and glycosaminoglycan-peptide complex preparations; symptomatic efficacy in reducing pain has been proven for gonarthrosis;
- diacerein: classified as a SYSADOA; according to the source, until recently, its efficacy in reducing pain and preventing joint space narrowing was considered questionable.
Sources of pain in osteoarthritis can be remembered using the rule of structures around the cartilage: Bone (microfractures), Membrane (inflammation), Ligaments (overstrain), Muscles (spasm), Osteophytes (periosteal irritation). The main rule: cartilage itself doesn't hurt!
Class and exam questions
What are Heberden's and Bouchard's nodes?
These are characteristic manifestations of the hereditary form of osteoarthritis. They represent nodular formations on the distal (Heberden's) and proximal (Bouchard's) interphalangeal joints of the hands.
Is it mandatory to test blood for inflammatory markers in osteoarthritis?
No, laboratory diagnostics (tests for leukocytes, ESR, fibrin, seromucoid) are indicated only in the presence of clinical signs of secondary synovitis, i.e., when pronounced inflammation joins.
What is the difference between early and late radiological signs?
In early stages, subchondral sclerosis (bone compaction) is detected and the joint space narrows unevenly. In late stages, the edges of the surfaces sharpen and marginal bone growths—osteophytes—form.
What else to study on this topic
- Mechanism of action of interleukin-1 (IL-1) and synthesis of matrix proteinases
- Specifics of the clinical picture of gonarthrosis and coxarthrosis
- Pathogenesis of radicular syndrome in cervical spondyloarthritis
- Diagnostic value of seromucoid and sialic acids in synovitis
- Principles of load dosing in therapeutic exercise (physical therapy)
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