Role of substance P in neurogenic inflammation in the rat incisor pulp and the lower lip

Ohkubo, Tsuyako; Shibata, Manabu; Yamaguchi, Yasuo; Kaya, Hidehiro; Takahashi, Hiroshi

doi:10.1016/0003-9969(93)90200-6

Cited by 34 publications

(10 citation statements)

References 41 publications

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“…In addition, in dental pulp several pharmacological and immunohistochemical studies have demonstrated that sensory nerves and sensory neuropeptides (CGRP and SP) are involved in inflammation (Fristad et al, 1995;Ohkubo et al, 1993) and that sympathetic nerves inhibit sensory nerve-induced vasodilation and plasma extravasation (Kerezoudis et al, 1993a,b). The vascular endothelium of apparently healthy human dental pulp expresses a variety of adhesion molecules that promote leukocyte emigration, although their activities are lower than those in inflamed pulp (Sawa et al, 1998).…”

Section: Venule Permeabilitymentioning

confidence: 98%

Three‐dimensional wall structure and the innervation of dental pulp blood vessels

Iijima

Zhang

2002

Microscopy Res & Technique

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The involvement of neural components in plasma extravasation and blood flow in the dental pulp has been established by pharmacological and physiological studies. We review here the segmental constitution of pulp vessels and the possible involvement of neural components in both the contractility and permeability of the pulp vessels from a morphological viewpoint. Six vascular segments can be identified based on the morphology of peri-endothelial cells, such as smooth muscle cells and pericytes. These are: muscular arterioles, terminal arterioles, precapillary arterioles, capillaries, postcapillary venules, and collecting or muscular venules. The perivascular nerve forms a mesh with numerous terminal varicosities, some of which attach directly to arteriolar smooth muscle cells. This mesh can be seen by scanning electron microscopy, and indicates the important role of neural components in regulating the pulpal circulation. After administering norepinephrine (0.2 mg/kg/dog), the surface texture of the smooth muscle cells of pulp arterioles reveals marked irregularities, which are correlated with arteriolar contraction. The pericytes in larger postcapillary venules (diameter 20 microm or larger) also show irregularities, whereas no changes are seen in the pericytes of either smaller postcapillary venules or capillaries. The intercellular spaces of pericytes in the postcapillary venules are wide enough for leukocytes to pass through, and the occasional extravasation of leukocytes through venule walls can be seen under electron microscopy. The microvessels of healthy human dental pulp react weakly to selectins, indicating that apparently healthy dental pulp may be weakly inflamed. In rat dental pulp, CGRP-immunoreactive nerves and nerve terminals containing many granular vesicles supply the postcapillary venules more densely than the arterioles, which suggests the involvement of postcapillary venules in neurogenic inflammation in the dental pulp.

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Section: Venule Permeabilitymentioning

confidence: 98%

Three‐dimensional wall structure and the innervation of dental pulp blood vessels

Iijima

Zhang

2002

Microscopy Res & Technique

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“…The authors suggest that the negative associations between periodontal attachment loss and bone loss were related to the use of antihistamines, which may offer protection against periodontal tissue destruction. It is unclear as to whether this association is related to antihistamine therapy as a suppressant of mast cell degranulation or an alternative mechanism of histamine activation, such as that elicited by substance P, which is involved in neurogenic inflammation (209) or via the kininlkallikrein system. Alternatively, allergies tend to occur in atopic individuals, who represent a subset of the normal population in terms of immune responsiveness.…”

Section: Allergymentioning

confidence: 99%

Influence of risk factors on the pathogenesis of periodontitis

Salvi¹,

Lawrence²,

Offenbacher³

et al. 1997

Periodontology 2000

229

157

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“…Neuropeptides, released from activated peripheral nerve terminals into surrounding tissue, can evoke an inflammatory response (Green et al, 1992;Gyorfi et al, 1992;Ohkubo et al, 1993;Pincelli et al, 1993;Smith et al, 1993). Substance P (SP) and calcitonin gene-related peptide (cGRP) are examples of neuropeptides that can evoke such a response (i.e., activation of pro-inflammatory cytokines, arachidonic acid catabolism) when injected into tissue (Yaksh, 1988;Lotz et al, 1988;Laurenzi et al, 1990;Said, 1990;Basbaum and Levine, 1991;Pincelli et al, 1993).…”

Section: (C) Neurogenic Inflammationmentioning

confidence: 99%

Pathogenesis of Degenerative Joint Disease in the Human Temporomandibular Joint

Haskin

Milam²,

Cameron

1995

Critical Reviews in Oral Biology & Medicine

136

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ABSTRACT:The wide range of disease prevalences reported in epidemiological studies of temporomandibular degenerative joint disease reflects the fact that diagnoses are frequently guided by the presence or absence of non-specific signs and symptoms. Treatment is aimed at alleviating the disease symptoms rather than being guided by an understanding of the underlying disease processes. Much of our current understanding of disease processes in the temporomandibular joint is based on the study of other articular joints. Although it is likely that the molecular basis of pathogenesis is similar to that of other joints, additional study of the temporomandibular joint is required due to its unique structure and function. This review summarizes the unique structural and molecular features of the temporomandibular joint and the epidemiology of degenerative temporomandibular joint disease. As is discussed in this review, recent research has provided a better understanding of the molecular basis of degenerative joint disease processes, including insights into: the regulation of cytokine expression and activation, arachidonic acid metabolism, neural contributions to inflammation, mechanisms of extracellular matrix degradation, modulation of cell adhesion in inflammatory states, and the roles of free radicals and heat shock proteins in degenerative joint disease. Finally, the multiple cellular and molecular mechanisms involved in disease initiation and progression, along with factors that may modify the adaptive capacity of the joint, are presented as the basis for the rational design of new and more effective therapy.

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Role of substance P in neurogenic inflammation in the rat incisor pulp and the lower lip

Cited by 34 publications

References 41 publications

Three‐dimensional wall structure and the innervation of dental pulp blood vessels

Three‐dimensional wall structure and the innervation of dental pulp blood vessels

Influence of risk factors on the pathogenesis of periodontitis

Pathogenesis of Degenerative Joint Disease in the Human Temporomandibular Joint

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