Inflammation

(redirected from periodontal inflammation)
Also found in: Dictionary, Thesaurus, Encyclopedia.

inflammation

 [in″flah-ma´shun]
a localized protective response elicited by injury or destruction of tissues, which serves to destroy, dilute, or wall off both the injurious agent and the injured tissue. adj., adj inflam´matory.  

The inflammatory response can be provoked by physical, chemical, and biologic agents, including mechanical trauma, exposure to excessive amounts of sunlight, x-rays and radioactive materials, corrosive chemicals, extremes of heat and cold, or by infectious agents such as bacteria, viruses, and other pathogenic microorganisms. Although these infectious agents can produce inflammation, infection and inflammation are not synonymous.

The classic signs of inflammation are heat, redness, swelling, pain, and loss of function. These are manifestations of the physiologic changes that occur during the inflammatory process. The three major components of this process are (1) changes in the caliber of blood vessels and the rate of blood flow through them (hemodynamic changes); (2) increased capillary permeability; and (3) leukocytic exudation.

Hemodynamic changes begin soon after injury and progress at varying rates, according to the extent of injury. They start with dilation of the arterioles and the opening of new capillaries and venular beds in the area. This causes an accelerated flow of blood, accounting for the signs of heat and redness. Next follows increased permeability of the microcirculation, which permits leakage of protein-rich fluid out of small blood vessels and into the extravascular fluid compartment, accounting for the inflammatory edema.

Leukocytic exudation occurs in the following sequence. First, the leukocytes move to the endothelial lining of the small blood vessels (margination) and line the endothelium in a tightly packed formation (pavementing). Eventually, these leukocytes move through the endothelial spaces and escape into the extravascular space (emigration). Once they are outside the blood vessels they are free to move and, by chemotaxis, are drawn to the site of injury. Accumulations of neutrophils and macrophages at the area of inflammation act to neutralize foreign particles by phagocytosis.

Chemical mediators of the inflammatory process include a variety of substances originating in the plasma and the cells of uninjured tissue, and possibly from the damaged tissue. The major kinds of mediators are (1) vasoactive amines, such as histamine and serotonin; (2) plasma endopeptidases that comprise three interrelated systems, the kinin system that produces bradykinin, the complement system that produces proteins that interact with antigen--antibody complexes and mediate immunologic injury and inflammation, and the clotting system that increases vascular permeability and chemotactic activity for the leukocytes; (3) prostaglandins, which can reproduce several aspects of the inflammatory process; (4) neutrophil products; (5) lymphocyte factors; and (6) other mediators, such as slow-reacting substance of anaphylaxis and endogenous pyrogen.

Hormonal Response. Some hormones, such as cortisol, have an antiinflammatory action that limits inflammation to a local reaction while others are proinflammatory. Thus, the endocrine system has a regulatory effect on the process of inflammation so that it can be balanced and beneficial in the body's attempts to recover from injury.
Cellular changes in inflammation. 1, Margination of neutrophils brings these inflammatory cells in close contact with the endothelium. 2, Adhesion of platelets results in the release of mediators of inflammation and coagulation. Fibrin strands are the first signs of clot formation. 3, Pavementing of leukocytes is mediated by adhesion molecules activated by the mediators of inflammation released from platelets and leukocytes. RBC, red blood cells. From Damjanov, 2000.
acute inflammation inflammation, usually of sudden onset, marked by the classical signs of heat, redness, swelling, pain, and loss of function, and in which vascular and exudative processes predominate.
catarrhal inflammation a form affecting mainly a mucous surface, marked by a copious discharge of mucus and epithelial debris.
chronic inflammation prolonged and persistent inflammation marked chiefly by new connective tissue formation; it may be a continuation of an acute form or a prolonged low-grade form.
exudative inflammation one in which the prominent feature is an exudate.
fibrinous inflammation one marked by an exudate of coagulated fibrin.
granulomatous inflammation a form, usually chronic, attended by formation of granulomas.
interstitial inflammation inflammation affecting chiefly the stroma of an organ.
parenchymatous inflammation inflammation affecting chiefly the essential tissue elements of an organ.
productive inflammation (proliferative inflammation) one leading to the production of new connective tissue fibers.
pseudomembranous inflammation an acute inflammatory response to a powerful necrotizing toxin (such asdiphtheria toxin), characterized by formation on a mucosal surface of a false membrane composed of precipitated fibrin, necrotic epithelium, and inflammatory leukocytes.
purulent inflammation suppurative inflammation.
serous inflammation one producing a serous exudate.
subacute inflammation a condition intermediate between chronic and acute inflammation, exhibiting some of the characteristics of each.
suppurative inflammation one marked by pus formation.
toxic inflammation one due to a poison, e.g., a bacterial product.
traumatic inflammation one that follows a wound or injury.
ulcerative inflammation that in which necrosis on or near the surface leads to loss of tissue and creation of a local defect (ulcer).

in·flam·ma·tion

(in'flă-mā'shŭn), Avoid the misspelling inflamation.
A fundamental pathologic process consisting of a dynamic complex of histologically apparent cytologic changes, cellular infiltration, and mediator release that occurs in the affected blood vessels and adjacent tissues in response to an injury or abnormal stimulation caused by a physical, chemical, or biologic agent, including the local reactions and resulting morphologic changes; the destruction or removal of the injurious material; and the responses that lead to repair and healing. The so-called cardinal signs of inflammation are rubor, redness; calor, heat (or warmth); tumor, swelling; and dolor, pain; a fifth sign, functio laesa, inhibited or lost function, is sometimes added. All these signs may be observed in certain instances, but none is necessarily always present.
[L. inflammo, pp. -atus, fr. in, in, + flamma, flame]

inflammation

(ĭn′flə-mā′shən)
n.
1. The act of inflaming or the state of being inflamed.
2. A localized protective reaction of tissue to irritation, injury, or infection, characterized by pain, redness, swelling, and sometimes loss of function.

inflammation

A response to injury which is characterized by pain, swelling, heat, redness, and/or loss of function. See Round cellinflammation.

in·flam·ma·tion

(in'flă-mā'shŭn)
A fundamental, stereotyped complex of cytologic and chemical reactions that occur in affected blood vessels and adjacent tissues in response to an injury or abnormal stimulation caused by a physical, chemical, or biologic agent. Redness (rubor), heat (calor), swelling (tumor), and pain (dolor) are signs generally associated with inflammation.
[L. inflammo, pp. -atus, fr. in, in, + flamma, flame]

inflammation

The response of living tissue to injury, featuring widening of blood vessels, with redness, heat, swelling and pain-the cardinal signs ‘rubor’, ‘calor’, ‘tumor’ and ‘dolor’ of the first century physician Celsus. Inflammation also involves loss of function and is the commonest of all the disease processes. It is expressed by the ending ‘-itis’. Inflammation involves release of PROSTAGLANDINS which strongly stimulate pain nerve endings. It is, in general, protective and assists the immune system to restore normality, but persistent (chronic) inflammation may lead to the formation of undesirable scar tissue.

inflammation

a local response to injury or damage, by which HISTAMINES are released that trigger a number of effects including dilation of blood vessels, and the invasion of blood proteins, blood fluid and LEUCOCYTES into the tissues to combat invading bacteria.

Inflammation

The body's immune reaction to presumed foreign substances like germs. Inflammation is characterized by increased blood supply and activation of defense mechanisms. It produces redness, swelling, heat, and pain.

inflammation

A complex reaction that occurs in response to injury, infection, irritation, toxicity or hypersensitivity. The reaction is characterized by redness, heat, pain and swelling to different degrees. Treatment depends on the cause. See antiinflammatory drug; infection.

in·flam·ma·tion

(in'flă-mā'shŭn) Avoid the misspelling inflamation.
Fundamental pathologic process consisting of a dynamic complex of histologically apparent cytologic changes, cellular infiltration, and mediator release that occurs in the affected blood vessels and adjacent tissues in response to an injury or abnormal stimulation caused by a physical, chemical, or biologic agent.
[L. inflammo, pp. -atus, fr. in, in, + flamma, flame]

Patient discussion about Inflammation

Q. What causes inflammation of the knee joint?

A. It depends on many things - the age of the person, other diseases he or she may have, whether he experienced any trauma to the joint, drugs or other substances he or she uses. Generally speaking, it may be caused by an infection (usually after trauma, very painful and abrupt inflammation, necessitates rapid treatment), rheumatologic diseases (such as rheumatoid arthritis or others, reaction to drugs or as a feature of other diseases.

You may read more here: http://en.wikipedia.org/wiki/Arthritis

Q. what is fragments of endocervical glandular mucosa with inflammation and squamous metaplasia fragments of endocervical glandular mucosa

A. It means that part of the mucose on the cervix area has changes from a certain kind of mucose cells to another, and that there is a bit of an inflammation around it. This should be brought to the knowledge of a gynecologist and be monitored by him/her.

Q. Does anyone know how to relieve chronic back pain due to inflammation and arthritis? I have tried OTC arthritis pain meds they don't offer much relief for me. I have had surgery for herniated disc. My doctor says that there is a lot of inflammation and arthritis in my back. You can't get Vioxx anymore. Is there an alternative?

A. there also is a drug called diclofenac(cataflam) ask your DR.

More discussions about Inflammation
References in periodicals archive ?
DBP is the main transport protein of vitamin D in the circulation, and plasma 25(OH)D levels have been reported to be increased in patients with GAgP, as well as being associated with periodontal inflammation [4, 5].
researched IL-1 gene polymorphisms in periodontitis patients by linking previous findings regarding the association of IL-1 polymorphisms and severity of adult periodontitis with microbial species found in IL-1 genotype-negative versus IL-1 genotype-positive patients and hence concluded that "those who were IL-1 genotype positive tended to have higher levels of the more damaging microbial species (red and orange complex organisms) associated with periodontal inflammation [90]"
The researchers found that compounds belonging to the two categories showed similar results in resolving periodontal inflammation and tissue regeneration.
Papillon-Lefevre syndrome (PLS) is a rare autosomal recessive disorder presented with diffuse transgradient palmoplantar hyperkeratosis, and an aggressive periodontal inflammation leading to premature loss of primary and permanent teeth.
A large number of distinct types of bacteria with different pathogenicity increase periodontal inflammation. ROS are related to PMN action in the destruction of periodontal pathogens.
These findings therefore suggest that, due to the downregulation of the GHS-R1a by long-term exposure to periodontal bacteria, the anti-inflammatory actions of GHRL may be reduced in chronic periodontal infections, which could lead to an enhanced periodontal inflammation and destruction.
In this review, we will discuss the possible roles of the most highly expressed members of the PAR family in the periodontium, [PAR.sub.1] and [PAR.sub.2], as important molecules that mediate mammalian and bacterial enzyme's effects on cells in the regulation of periodontal inflammation and repair.
Abstract: Recent studies investigating protease-activated receptor type 2 (PAR-2) suggest an association between the receptor and periodontal inflammation. It is known that gingipain, a bacterial protease secreted by the important periodontopathogen Porphyromonas gingivalis can activate PAR-2.
The efficacy of oral irrigation in addition to a toothbrush on the plaque and clinical parameters of periodontal inflammation. A systematic review.
Focused Question: What is the adjunctive effect of a diode laser (DL) following non-surgical periodontal debridement (SRP) during the initial phase of periodontal therapy on the clinical parameters of periodontal inflammation?
The aim of the study was to investigate whether the substance P and neurokinin A were present in gingival crevicular fluid in both periodontal health and disease and to study the relationship with periodontal inflammation. In subjects with periodontitis, there were significant increases in the levels of SP and NKA in both sites with periodontal disease in comparison to healthy sites.
An NYU nursing--dental research team has found that oral blood samples drawn from deep pockets of periodontal inflammation can be used to measure hemoglobin A1c, an important gauge of a patient's diabetes status.