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At least 883 records · Page 49Linked to original sources
PubMed1989

Pulpal hemodynamics and interstitial fluid pressure: balance of transmicrovascular fluid transport.

The net rate of fluid movement across the microvascular endothelium is governed by hydrostatic and protein osmotic pressures operating on each side of the vessel wall. These basic forces regulating the pulpal transmicrovascular fluid exchange are the same as in other tissues. However, the pulp is special in regard to its enclosement between rigid dentin walls, implying low interstitial compliance. In addition, the pulp has a relatively low perfusion pressure. In the low compliant pulpal interstitium, even a modest rise in net filtration will favor a relatively large increase in interstitial fluid pressure (IFP) which opposes further filtration. This will result in a minimal increase in interstitial fluid volume and, theoretically, any dilution of interstitial protein concentration is not possible. Thus, an increase in vessels' permeability to protein in this low compliant system must be balanced by a further rise in IFP, unless a washout of proteins takes place by raised lymph flow. However, a significant increase in IFP may seriously impede pulpal blood flow both by raising venous vascular resistance and secondarily by reducing pulpal perfusion pressure. The most important edema-preventing mechanisms in tissues with low compliance, as the dental pulp, seems to be a rise in IFP which initiates increased lymph flow and washout of proteins.

Animals↗
PubMed1989

Trigeminal neuralgia in a patient with multiple sclerosis.

The incidence of trigeminal neuralgia in patients with multiple sclerosis is low; however, the association of the two can present a difficult diagnostic problem to the unsuspecting practitioner. Certain characteristics of trigeminal neuralgia in patients with undiagnosed multiple sclerosis can lead to a diagnosis of the disease.

Female↗
PubMed1989

Experimental bacterial anachoresis in dog dental pulps capped with calcium hydroxide.

The pulps of 36 permanent dog teeth were mechanically exposed and capped with Dycal, calcium hydroxide powder mixed with saline, or Teflon. At 2, 14, and 28 days postoperatively, nine teeth treated with the materials were extracted (treated control teeth): A suspension of streptococci was then injected intravenously. Twenty-four h later the dogs were killed and both the 27 treated teeth (experimental group) and 6 unoperated control teeth were removed in tissue blocks. Tissue sections were examined for the presence of bacteria, hard tissue formation, inflammatory cell response and necrosis. Bacteria were not observed in the unoperated and treated control teeth or in three of four teeth capped with Teflon for 29 days. In all the remaining specimens colonies of gram-positive cocci were found.

Animals↗
PubMed1996

Immunohistochemical demonstration of prostaglandins E2, F2 alpha, and 6-keto-prostaglandin F1 alpha in rat dental pulp with experimentally induced inflammation.

Using formalin-fixed and EDTA-decalcified cryostat sections, the immunohistochemical localization of prostaglandin (PG) E2, PGF2 alpha, and 6-keto-PGF1 alpha (a stable metabolite of PGI2) was examined in normal rat and inflamed dental pulp. Inflammation was induced by opening the pulp chamber. There was no immunoreactivity for prostaglandins in normal dental pulp, whereas positivities for PGE2, PGF2 alpha, and 6-keto-PGF1 alpha were demonstrated in the cytoplasm of macrophages and endothelial cells in the inflamed dental pulp. In addition to these cells, numerous pulp cells and odontoblasts existing in the inflamed pulp and its apical noninflamed area also were intensely stained for PGF2 alpha. Such an area with positive cells gradually extended in an apical direction with the progression of inflammation. These findings suggested that PG production from these host cells is involved in development of inflammation of rat dental pulp.

6-Ketoprostaglandin F1 alpha↗