PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 1961323

[Allergy in dentistry].

P van Cauwenberge·N Masy
View original source ↗Export metadata ↓

Abstract

In the dental office chiefly two kinds of (the four) allergic reactions are encountered. Type I is provoked mainly by local anesthetics and drugs and causes immediate, general symptoms among which the dramatic anaphylactic shock. Type IV ('delayed reaction') is provoked by metals ( in particular nickel) and synthetic prosthetic materials, sometimes by drugs, and gives rise to local pathological changes in and around the mouth. In case of a suspected allergy several diagnostic tests are available. First of all one has to prevent allergic reactions, for instance by looking for alternative materials. In case of serious anaphylactic reactions one must know how to treat these.

Explore related subjects

AnaphylaxisAnesthetics, LocalDental MaterialsHumansHypersensitivityNickelEnglish AbstractJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

P van Cauwenberge, N Masy. 1991. [Allergy in dentistry].. https://pubmed.ncbi.nlm.nih.gov/1961323/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2025

Magnesium protects against anaphylactic shock and cardiac myolysis in guinea-pigs.

The pathophysiological responses to immune stress (IS) include activation of several processes which are dependent on cytosolic Ca2+ elevation. Magnesium frequently acts as a natural Ca2+ antagonist. In this study we have observed that Mg2+ can protect guinea-pigs against IS. Antigen-sensitized guinea-pigs, which had been fed a magnesium-deficient diet, were given a single dose (15 mg) of MgCl2 intraperitoneally 1 h before antigen challenge. The development of anaphylactic shock (AS) was observed during the next 2 h, and the hearts were subsequently examined histologically for signs of cardiac myolysis (CM). Magnesium (i) reduced the incidence of CM from 40% to 10% (p < 0.05); (ii) reduced the incidence of AS from 61% to 35% (p < 0.05); (iii) attenuated the severity of the AS; and (iv) lowered mortality from 39% in the control to 19% in the Mg(2+)-treated group (p = 0.1). Serum and tissue total [Mg2+] were not affected by the administration of MgCl2. Also, the serum and heart Mg2+ levels were the same whether or not the guinea-pigs developed AS or CM. In cell culture we demonstrated that by elevating the [Mg2+] in the medium bathing sensitized rat basophilic leukemia (RBL) cells, the increase in cytosolic [Ca2+] subsequent to antigen challenge was reduced from 174 +/- 23.28% (1 mM) to 82.74 +/- 13.22% (3 mM). We conclude that a single treatment with Mg2+ can considerably diminish damage induced by immune stress, probably by its altering the Ca2+: Mg2+ ratio. Since the physiological reaction to different types of stress is similar, Mg2+ could prove beneficial in preventing stress-induced shock in general. Studies examining the mechanisms by which Mg2+ exerts its effects thus provide a scientific basis for the current clinical use of Mg2+ in acute myocardial infarction (AMI) and asthma.

Anaphylaxis↗
PubMed2007

Enhanced mast cell activation in mice deficient in the A2b adenosine receptor.

Antigen-mediated cross-linking of IgE bound to mast cells via the high affinity receptor for IgE triggers a signaling cascade that results in the release of intracellular calcium stores, followed by an influx of extracellular calcium. The collective increase in intracellular calcium is critical to the release of the granular contents of the mast cell, which include the mediators of acute anaphylaxis. We show that the sensitivity of the mast cell to antigen-mediated degranulation through this pathway can be dramatically influenced by the A2b adenosine receptor. Loss of this Gs-coupled receptor on mouse bone marrow-derived mast cells results in decreased basal levels of cyclic AMP and an excessive influx of extracellular calcium through store-operated calcium channels following antigen activation. Mice lacking the A2b receptor display increased sensitivity to IgE-mediated anaphylaxis. Collectively, these findings show that the A2b adenosine receptor functions as a critical regulator of signaling pathways within the mast cell, which act in concert to limit the magnitude of mast cell responsiveness when antigen is encountered.

Anaphylaxis↗