Abstract
The most prevalent form of arthritis is osteoarthritis (OA) of the knee, which is characterized by a degeneration of articular cartilage resulting in the development of osteophytes, or bone spurs. Main goals of OA treatment are to reduce pain, slow the disease progression, and improve joint function and the quality of life. The purpose of this study was to verify all the therapies recommended by the European Society for Clinical and Economic Aspects of Osteoporosis and Osteoarthritis (ESCEO) from the biochemical point of view. Nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit the synthesis of eicosanoids, whereas paracetamol prevents the production of prostaglandin (PG) by interacting with peroxidase (POX) site of the prostaglandin H2 synthase complex. Tramadol is an opioid that has a dual mechanism of action: It binds to the μ-opioid receptor and it inhibits serotonin and adrenaline. Corticosteroids, which are also prescribed for OA pain, inhibit the activity of phospholipase A2 and block the synthesis of arachidonate-derived eicosanoids. Symptomatic slow-acting drugs for osteoarthritis (SYSADOA) are drugs that are well tolerated by patients and help to restore proteoglycan matrix of the cartilage. These drugs include compounds that naturally build articular cartilage. The articular cartilage, as well as the bone located around the cartilage, is destroyed as osteoarthritis progresses. Thus, bisphosphonates, commonly used in the treatment of osteoporosis, were evaluated as potential therapy. However, there is no official recommendation for their use in therapy. The aim of the study was to analyze the biochemical mechanisms of principal drugs used for the treatment of knee OA. Therefore, a narrative review summarizing the current knowledge regarding the applied therapies was prepared.
Highlights
Osteoarthritis (OA), the most common form of arthritis worldwide, is a degenerative arthropathy affecting all synovial joints, mainly cartilage and subchondral bone
American College of Rheumatology (ACR) guidelines do not recommend the usage of chondroitin sulfate, glucosamine, and combination products including two of them for knee OA, but they are recommended for hand OA [26]
The best known drugs are Nonsteroidal anti-inflammatory drugs (NSAIDs), which inhibit the synthesis of eicosanoids, and paracetamol, which prevents the production of prostaglandins by interacting with POX
Summary
Osteoarthritis (OA), the most common form of arthritis worldwide, is a degenerative arthropathy affecting all synovial joints, mainly cartilage and subchondral bone. The European Medicine Agency (EMA) recommended chondroitin sulfate as a biologically active molecule [49] It is anti-inflammatory agent, able to stimulate the synthesis of proteoglycan and hyaluronic acid, as well as inhibit the synthesis of proteolytic enzymes and NF-κB contributing to the cartilage damage [18]. Mechanism of action of fast-acting symptom modifying drugs including analgesics (e.g., paracetamol and tramadol), nonsteroidal anti-inflammatory drugs (NSAIDs) (e.g., ibuprofen, naproxen, and ketoprofen), coxibs and corticosteroids. Intraarticular corticosteroids (IACS) (e.g., triamcinolone) are shortterm pain relief drugs which decrease the synthesis of pro-inflammatory mediators such as prostaglandins and leukotrienes, neutrophil superoxide, and MMPs. CS inhibit the activity of PLA2, and as a result, the synthesis of arachidonate-derived eicosanoids is blocked [64]. BPs are widely used for the treatment of hypercalcemia, multiple myeloma, post-menopausal osteoporosis as oral, intravenous (i.v.), and intramuscular (i.m.) formulations [67,72,75]
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