The innervation of chronic inflammatory human periapical lesions

Martinelli, C; Rulli, Mauro A.

doi:10.1016/0003-9969(67)90078-7

Cited by 12 publications

(5 citation statements)

References 3 publications

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“…CGRP-containing sensory fibers are also closely associated with reparative dentin formation (Taylor and . Although neurogenic mechanisms have been most extensively studied in the pulp, pulpal necrosis as a result of infection or injury also leads to a local proliferation of sensory nerve fibers in the periapical region (Martinelli and Rulli, 1967;Lin andLangeland, 1981, Holland, 1988, 1992; Khayat etal, 1988; Kimberly and Byers, 1988;Byers et al, 1990).…”

Section: IImentioning

confidence: 99%

Periapical Inflammatory Responses and Their Modulation

Stashenko¹,

Teles²,

D’Souza

1998

Critical Reviews in Oral Biology & Medicine

338

288

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Periapical inflammatory responses occur as a consequence of bacterial infection of the dental pulp, as a result of caries, trauma, or iatrogenic insult. Periapical inflammation stimulates the formation of granulomas and cysts, with the destruction of bone. These inflammatory responses are complex and consist of diverse elements. Immediate-type responses--including vasodilatation, increased vascular permeability, and leukocyte extravasation--are mediated by endogenous mediators, including prostanoids, kinins, and neuropeptides. Non-specific immune responses--including polymorphonuclear leukocyte and monocyte migration and activation, and cytokine production--are elicited in response to bacteria and their products. Interleukin-1 and prostaglandins in particular have been implicated as central mediators of periapical bone resorption. Chronic periapical inflammation further involves specific T- and B-cell-mediated anti-bacterial responses, and activates a network of regulatory cytokines which are produced by Th1- and Th2-type T-lymphocytes. Various naturally occurring and genetically engineered models of immunodeficiency are beginning to help elucidate those components of the immune system which protect the pulpal/periapical complex. Both specific and non-specific responses interface with and are regulated by the neural system. The modulation of these responses by immune response modifies, cytokine antagonists, and other novel therapeutic agents is discussed. As an experimental model, periapical inflammation has many advantages which permit it to be used in studies of microbial ecology and pathogenesis, host response, neuroimmunology, and bone resorption and regeneration.

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Section: IImentioning

confidence: 99%

Periapical Inflammatory Responses and Their Modulation

Stashenko¹,

Teles²,

D’Souza

1998

Critical Reviews in Oral Biology & Medicine

338

288

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“…It is highly probable that all of the teeth listed in Table 1 were associated with varying degrees of chronic inflammation (Brynolf 1978, 1979, Pascon et al 1991, Holland 1992) Furthermore, it is well established that periradicular regions of chronic inflammation are associated with increased levels of innervation (Martinelli & Rulli 1967, Holland 1992 and sprouting of nerve fibers (Khayat et al 1988, Byers et al 1990. Therefore, there appears to be an interaction between inflammation and changes in neural tissues in the periradicular tissues .…”

Section: Discussionmentioning

confidence: 99%

“…Since varying degrees of chronic inflammation are highly probable in all the cases ( Brynolf 1978, 1979, Pascon et al . 1991 , Holland 1992), and increased levels of innervation are associated with regions of chronically inflamed tissues ( Martinelli & Rulli 1967, Kimberly & Byers 1988, Holland 1992), it is conceivable that this could account for the immediate response to thermal stimulation.…”

Section: Discussionmentioning

confidence: 99%

Thermal sensitivity of endodontically treated teeth

et al. 1999

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The problem of thermal sensitivity following non-surgical root-canal treatment is explored and case reports are presented. Possible causes for post-treatment discomfort from endodontic and restorative aetiologies are discussed, as are the mechanisms to explain the patients' painful experiences. Treatment of this problem may vary from the simple replacement of a defective restoration to a more extensive non-surgical retreatment of the case, despite radiographic evidence of an acceptable root filling and normal periradicular tissues.

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“…In this damaged area, there is a proliferation ofnerve fibers simultaneous with the inflammation (Holland, 1988;Khayat et al, 1988;Kim-berly and Byers, 1988). In long-standing lesions, an aberrant innervation remains (Bynum and Flieder, 1960;Martinelli and Rulli, 1967;Lin and Langeland, 1981). Currently, it is not known how extensively the damaged innervation remodels in lesions that have been treated and healed.…”

Section: Introductionmentioning

confidence: 94%

Periapical Innervation of the Ferret Canine One Year After Pulpectomy

Holland

1992

J Dent Res

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Previous studies have shown that, following removal of the dental pulp and its replacement with a filling material, the nerves in the periapical region proliferate within an area of chronic inflammation. This study examined these responses in the ferret in more detail, both quantitatively and in three dimensions, 12 months after pulpectomy which was followed by obturation with gutta percha and zinc oxide and eugenol sealer. The results were compared with the responses after three months. The basic patterns, in terms of both inflammation and neural proliferation, were similar at the two time periods. Both the sizes of the inflammatory lesions and the degree of neural proliferation were lower at 12 months than at three, although the differences were not significantly different in the small number of specimens examined. Bacterial stains failed to show bacteria either in the apical root canal delta or in the periapical area. It is possible that the persistent inflammation was due to the irritant nature of the obturating materials used but not due to the original tissue damage, since extraction sites, by comparison, healed very quickly. Apparently, following endodontic treatment, chronic periapical inflammation and concomitant neural proliferation can continue for long periods.

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The innervation of chronic inflammatory human periapical lesions

Cited by 12 publications

References 3 publications

Periapical Inflammatory Responses and Their Modulation

Periapical Inflammatory Responses and Their Modulation

Thermal sensitivity of endodontically treated teeth

Periapical Innervation of the Ferret Canine One Year After Pulpectomy

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