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At least 307 records · Page 17Linked to original sources
PubMed1979

Back pain: mechanical or inflammatory?

The majority of patients with a recent onset of back pain that developed rapidly over a few hours have nonspecific spinal disease. The disorder is likely to be self-limited. In contrast, patients presenting with an insidious onset of pain that has lasted for several weeks may have ankylosing spondylitis. Since management differs for the two types of disease, the correct diagnosis is mandatory. The diagnosis of ankylosing spondylitis is confirmed radiologically.

Adolescent↗
PubMedDate not supplied

Importance of apoptotic mechanisms in inflammatory infiltrate of oral lichen planus lesions.

BACKGROUND: Oral lichen planus (OLP) is an autoimmune disease produced by T lymphocyte attack on basal epithelial cells. OLP can undergo malignant transformation that may be linked to an increased proliferative activity and decreased apoptosis rate of the epithelial cells, phenomena that may be influenced by the inflammatory infiltrate. The objectives of this study were to assess the quantitative importance of apoptosis in the inflammatory infiltrate of OLP and to discuss its influence on the persistence of this infiltrate and on the malignant transformation of this disease. MATERIALS AND METHODS: In 32 patients with OLP and 20 controls, apoptosis was studied by TUNEL assay and caspase-3 determination, while cell cycle arrest and senescence were studied by measurement of p21 expression. RESULTS: There was a low frequency of lymphocytic apoptosis according to both TUNEL (34.5% of cases negative, 65.5% with mild expression) and caspase-3 expression (42.9% of cases negative, 50% with mild expression) findings. P21 expression was also negative (9.7% of cases) or mild (80.6% of cases) in most cases. CONCLUSION: The absence or low rate of apoptosis observed in inflammatory cells in OLP appears to contribute to the persistence of the inflammatory infiltrate, potentiating the onset of molecular disorders in epithelial cells and favouring cancer development.

Apoptosis↗
PubMed2006

[Chronic inflammation increases the risk of cardiovascular disease in patients with rheumatoid arthritis].

Rheumatoid arthritis is associated with increased cardiovascular morbidity and mortality due to atherosclerosis. This cannot be explained by an increased presence of traditional risk factors but seems to depend on inflammatory mechanisms. The association of inflammatory pathways with atherosclerosis is complex, and more research is required to optimise preventative measures against cardiovascular complications in inflammatory rheumatic diseases.

Anti-Inflammatory Agents↗
PubMed1991

Heat shock proteins: an autoprotective mechanism for inflammatory cells?

Heat shock/stress proteins are synthesized in all cell types under a variety of stressful conditions. Stress associated with ongoing inflammation relates, at least in part, to toxic products locally generated by cells accumulating in the inflamed tissue and organ. These products include oxygen free radicals, cytokines, proteases, chemotactic factors and, in the particular case of the eosinophil, toxic basic proteins. The heat shock response in inflammatory cells appears to be specifically regulated by their own proinflammatory products (oxygen free radicals, cytokines) generated during physiological functions such as phagocytosis, during differentiation, or in certain pathological states such as inflammatory lung diseases. We suggest that in human monocytes-macrophages heat shock proteins belong to the autoprotective equipment against oxidative stress.

Animals↗
PubMed1990

[Sensory and inflammatory reaction mechanisms in the dental pulp].

Laser-Doppler-flowmetry is used to show whether electrical stimulation of the rats tooth pulp leads to reactions such as neurogenic inflammations. Following electrical stimulation, a flow reduction with a subsequent flow increase can be observed After experimental elimination it can be shown that both sympathetic and nociceptive fibres are involved in this reaction. Thus the neurogenic inflammation of the dental pulp is a mechanism allowing early and localised reactions to noxious stimuli.

Animals↗
PubMed1986

Isolated intervertebral disc resorption. A source of mechanical and inflammatory back pain?

Seven patients underwent anterior interbody spinal fusions to alleviate pain due to resorption of an intervertebral disc. The anterior annulus of the discs at operation was inflamed. The specimens were studied histologically, and the findings are discussed. The demonstration of inflammation in the anterior annulus together with the recent identification of nerve fibres in the anterior annulus now allows a better understanding of discogenic pain and its management.

Adult↗
PubMed1986

Immunopathologic mechanisms of inflammatory vascular disease in primary Sjögren's syndrome--a model.

Our laboratory has been studying the immunopathogenesis of inflammatory vascular disease (IVD) in patients with Sjögren's syndrome (SS). In parallel, we have developed the autoimmune strain of MRL/Mp mice as a model of IVD. Sjögren's syndrome patients and MRL/Mp mice both develop two main histopathologic types of IVD (i.e. mononuclear and neutrophilic) which have differential serologic associations with respect to serum autoantibodies and complement levels. We present evidence that mononuclear (lymphocytic) vasculitis may exist as a distinct form of vascular inflammation and also may transition into neutrophilic vasculitis. On the basis of these studies we propose a new model of lymphocyte initiated vascular inflammation as an alternative to classical immune complex mediated vasculitis.

Animals↗
PubMed1994

Antinociceptive actions of dexmedetomidine and the kappa-opioid agonist U-50,488H against noxious thermal, mechanical and inflammatory stimuli.

The antinociceptive efficacies of both intrathecally (i.t.) and systemically administered dexmedetomidine (a selective alpha-2 adrenoceptor agonist) and U-50,488H [trans(+/-)-3,4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl)-cyclohexyl]- benzene-acetamide] (a kappa-opioid receptor agonist) were studied during peripheral inflammation induced by carrageenan. The antinociceptive tests were the hot plate (HP), the tail flick (TF) and the paw pressure tests (PP). The motor incoordination, if any, produced by both i.t. and s.c. dexmedetomidine were evaluated with the rotarod. The interaction between dexmedetomidine and U-50,488H and between atipamezole (a selective alpha-2 adrenoceptor antagonist) and U-50,488H were also assessed. The carrageenan injection induced not only peripheral hyperalgesia but also central sensitization, as assessed by decreased PP and TF latencies, respectively. The i.t. dexmedetomidine (0.15, 0.45, 1.35, 4.05) micrograms) resulted in dose-dependent increases in the PP thresholds and TF latencies in both the control rats and the rats with unilateral inflammation, without causing changes in motor coordination, whereas on s.c. administration of dexmedetomidine (3-100 micrograms/kg), antinociception was produced in PP only at doses (30 micrograms/kg) that already interfered with rotarod performance. U-50,488H was ineffective i.t. (5-200 micrograms) but, on s.c. administration (2.5-22.5 mg/kg), dose-dependent increases were found in the PP thresholds and TF latencies of the rats with unilateral inflammation. Atipamezole, in a dose (3 mg/kg) that has been shown to block the antinociceptive effects of dexmedetomidine, did not modify the antinociceptive effects of U-50,488H.(ABSTRACT TRUNCATED AT 250 WORDS)

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1995

[Molecular and cellular mechanisms in inflammatory reactions].

Inflammation is a complex stereotypical reaction of the body expressing the response to damage of its cells and/or vascularized tissues. It is the body's reaction to invasion by an infectious agent, antigen challenge or even just physical, chemical, or traumatic damage. The development of inflammatory reactions is controlled by a number of cellular and molecular components. Leukocytes (namely neutrophils and macrophages) belong to the key inflammatory cells. Their accumulation in inflamed tissue results from adhesive interactions between leukocytes and endothelial cells within the microcirculation. The nature and magnitude of the adhesive interactions that take place within postcapillary venules are determined by a variety of factors, of which the contribution of different adhesion molecules (selectins, integrins, members of immunoglobulin superfamily) to leukocyte rolling, adherence, and emigration in venules is discussed. The main purpose of inflammation seems to be to bring fluids, proteins and cells from the blood into the damaged tissues for the elimination of injuring agent and triggering the healing and repairing processes. This is under the control of inflammation mediators which include vasoactive substances, proinflammatory and antiinflammatory cytokines, chemokines, acute phase reactants, bioactive lipids (prostanoids, platelet activating factor--PAF) and products of the plasma enzyme systems (complement, the coagulation clothing, kinin and fibrinolytic pathways) which are shortly reviewed. Several neuroendocrine hormones, neuropeptides, neurotransmitters and mainly glucocorticoids also play an important role of endogenous regulators of any inflammatory process. (Tab. 4, Fig. 1, Ref. 52.).

Animals↗