In turn, the term temporomandibular disorder is defined as "musculoskeletal disorders affecting the temporomandibular joints and their associated musculature. It is a collective term which represents a diverse group of pathologies involving the temporomandibular joint, the muscles of mastication, or both". Another definition of temporomandibular disorders is "a group of conditions with similar signs and symptoms that affect the temporomandibular joints, the muscles of mastication, or both." Temporomandibular disorder is a term that creates confusion since it refers to a group of similarly symptomatic conditions, whilst many sources use the term temporomandibular disorders as a vague description, rather than a specific syndrome, and refer to any condition which may affect the temporomandibular joints (see table). The temporomandibular joint is susceptible to a huge range of diseases, some rarer than others, and there is no implication that all of these will cause any symptoms or limitation in function at all.The preferred terms in medical publications is to an extent influenced by geographic location. For example, in the United Kingdom, the term pain dysfunction syndrome is in common use. In the United States, the term temporomandibular disorder is generally favored. The American Academy of Orofacial Pain uses temporomandibular disorder, whilst the National Institute of Dental and Craniofacial Research uses temporomandibular joint disorder. A more complete list of synonyms for this topic is extensive, with some being more commonly used than others.
This makes aspirin different from other NSAIDs (such as diclofenac and ibuprofen), which are reversible inhibitors. Low-dose aspirin use irreversibly blocks the formation of thromboxane A2 in platelets, producing an inhibitory effect on platelet aggregation during the lifetime of the affected platelet (8–9 days). This antithrombotic property makes aspirin useful for reducing the incidence of heart attacks in people who have had a heart attack, unstable angina, ischemic stroke or transient ischemic attack. 40 mg of aspirin a day is able to inhibit a large proportion of maximum thromboxane A2 release provoked acutely, with the prostaglandin I2 synthesis being little affected; however, higher doses of aspirin are required to attain further inhibition.Prostaglandins, local hormones produced in the body, have diverse effects, including the transmission of pain information to the brain, modulation of the hypothalamic thermostat, and inflammation. Thromboxanes are responsible for the aggregation of platelets that form blood clots. Heart attacks are caused primarily by blood clots, and low doses of aspirin are seen as an effective medical intervention to prevent a second acute myocardial infarction. COX-1 and COX-2 inhibition
At least two different types of cyclooxygenases, COX-1 and COX-2, are acted on by aspirin. Aspirin irreversibly inhibits COX-1 and modifies the enzymatic activity of COX-2. COX-2 normally produces prostanoids, most of which are proinflammatory. Aspirin-modified PTGS2 (prostaglandin-endoperoxide synthase 2) produces lipoxins, most of which are anti-inflammatory.