Occlusal injury

There are two types of human bite injuries. Occlusal injuries are inflicted by actual biting, whereas clenched-fist injuries are sustained when a person s closed fist hits another s teeth. Of the two, clenched-fist injuries typically are more prone to infectious complications.43,44... 

Thrombolytic Enzymes. Although atherosclerosis and the accompanying vascular wall defects are ultimately responsible for such diseases as acute pulmonary embolism, arterial occlusion, and myocardial infarction, the lack of blood flow caused by a fibrin clot directly results in tissue injury and in the clinical symptoms of these devastating diseases (54). Thrombolytic enzyme therapy removes the fibrin clot by dissolution, and has shown promise in the treatment of a number of thrombo-occlusive diseases (60). 

In general, arterial thrombi are platelet-rich ( white clots ) and form at ruptured atherosclerotic plaques, leading to intraluminal occlusion of arteries that can result in end-organ injury (e.g., myocardial infarction, stroke). In contrast, venous thrombi consist mainly of fibrin and red blood cells ( red clots ), and usually form in low-flow veins of the limbs, producing deep vein thrombosis (DVT) the major threat to life results when lower extremity (and, occasionally, upper extremity) venous thrombi embolize via the right heart chambers into the pulmonary arteries, i.e., pulmonary embolism (PE). 

Coagulation summarizes the mechanisms involved in stopping bleeding due to an injured or defective vessel wall. Coagulation is characterized by procoagulatory and anticoagulatory factors that are in balance under normal conditions. Vessel injuries are occluded by the coagulation system and spontaneous vessel occlusions dissolved by the fibrinolytic cascade. 

N-Nitro-L-arginine methyl ester (L-NAME) is an inhibitor of NOS L-NAME reportedly reduces the volume of cortical and striatal infarct after middle cerebral artery occlusion in the rat. This protection can be reversed by co-injection of L-arginine. L-NAME also reduced the excitotoxic damage induced by NMDA injection. Finally, the authors showed that L-NAME reduced glutamate efflux produced by ischaemic injury in rats. The authors concluded that NOS induced by NMDA receptor overstimulation is a key event in the neuronal injury cascade (Buisson eta/., 1993). 

The NO donor, C87-3754, reportedly attenuates the injury induced in cats by splanchnic artery occlusion of the coeliac, superior mesenteric and inferior mesenteric... 

Ohnishi (Sakamoto etal., 1991) has described an oligomeric derivative of prostaglandin Bi (PGB2) and ascorbic acid. In a rat bilateral carotid occlusion-reperfiision injury complicated by haemorrhagic hypotension, this compound reduced a-phenyl-r-butyl nitrone (PBN) spin-trapped radicals and thiobarbituric acid-reactive products (TBARs) (a measure of lipid peroxidation) in isolated... 

In experimental animals the respiratory system is a primary target of acrolein exposure after inhalation, and there is an inverse relationship between the exposure concentration and the time it takes for death to occur." Inhalation LCso values of 327ppm for 10 minutes and 130ppm for 30 minutes have been reported in rats." Of 57 male rats, 32 died after exposure to 4 ppm for 6 hours/day for up to 62 days. Desquamation of the respiratory epithelium followed by airway occlusion and asphyxiation is the primary mechanism for acrolein-induced mortality in animals." Sublethal acrolein exposure in mice at 3 and 6 ppm suppressed pulmonary antibacterial defense mechanisms. A combination of epithelial cell injury and inhibition of macrophage function may be responsible for acrolein-induced suppression of pulmonary host defense. ... 

Many pathological conditions, including ischemia/reperfusion, inflammation, and sepsis may induce tissues to simultaneously produce both superoxide and nitric oxide. For example, ischemia allows intracellular calcium to accumulate in endothelium (Fig. 20). If the tissue is reperfused, the readmission of oxygen will allow nitric oxide as well as superoxide to be produced (Beckman, 1990). For each 10-fold increase in the concentration of nitric oxide and superoxide, the rate of peroxynitrite formation will increase by 100-fold. Sepsis causes the induction of a second nitric oxide synthase in many tissues, which can produce a thousand times more nitric oxide than the normal levels of the constitutive enzyme (Moncada et al., 1991). Nitric oxide and indirectly peroxynitrite have been implicated in several important disease states. Blockade of nitric oxide synthesis with N-methyl or N-nitroarginine reduces glutamate-induced neuronal degeneration in primary cortical cultures (Dawson et al., 1991). Nitroarginine also decreases cortical infarct volume by 70% in mice subjected to middle cerebral artery occlusion (Nowicki et al., 1991). Myocardial injury from a combined hy-... 

Fibrosis resulting in the loss of normal organ structures is the hallmark of chronic rejection. The fibrosis may be due to wound healing, which is then followed by the cellular necrosis of acute rejection. However, it must be pointed out that chronic rejection develops many times in the absence of acute rejection. Fibrosis may be a result of several diverse factors such as equation of chronic rejection with chronic delayed-type hypersensitivity reaction, injury to blood vessels and resulting response to chronic ischemia, the proliferation of smooth muscle cells in the intima of arterial walls producing vascular occlusion, or persistent viral infections that will induce cellular immune response. 

Noninvasive detection of vascular abnormalities is of the utmost importance in clinical imaging. Indeed, a lot of injuries and diseases manifest themselves through modifications of the vasculature [1,2]. For example, abnormal angiogenesis (blood vessel growth) is observed in the development of most tumors. Embolism and atherosclerosis also manifest themselves through alterations of the blood vessels, namely through occlusions. Hemorrhage could also be detected noninvasively, which is crucial in injuries or in diseases such as ulcers [1]. 

The usual definition of a neuroprotectant is an agent that aims to prevent neuronal death by inhibiting one or more of the pathophysiological steps in the processes that follow injury to the central nervous system (CNS) or ischemia due to occlusion of an artery or hypoxia due to any cause. This definition has now been extended to include protection against neurodegeneration and neurotoxins. The extended definition includes interventions that slows or halts the progression of neuronal degeneration. 

Two types of circulatory perturbations contribute to different types of ischemic injury to the brain (reviewed by Lipton 1999) (1) stroke (a complete occlusion of a cerebral artery) irreversibly kills the neurons in its core region and severely damages others in the penumbral region and (2) reversible circulatory arrest, with a transient total stop of cerebral blood flow, selectively kills vulnerable cell populations. These clinical conditions can be studied in animals, with focal ischemic models replicating stroke and global ischemic models replicating cardiac arrest. 

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