Ischemic infarction of the pulp: Sequential degenerative changes of the pulp after traumatic injury

Stanley, Harold R.; Weisman, Manuel I.; Michanowicz, Andrew E.; Bellizzi, Ralph

doi:10.1016/s0099-2399(78)80229-5

Cited by 31 publications

(18 citation statements)

References 5 publications

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“…The reparative dentin deposition pattern was always random or irregular, and could be called, from a microscopical point of view, dysplastic dentin. When nutritional reserves are available, the pulp tends to respond to trauma by producing new mineralized tissue . In some areas of the teeth in Groups I and II, as well as almost all teeth in Group III, reparative dentin deposition around pulp cells was observed in an intense and irregular manner in the newly formed tissue, with the microscopic morphology of osteodentin‐like tissue .…”

Section: Discussionmentioning

confidence: 99%

Calcific metamorphosis of pulp after extrusive luxation

Queiroz

Hidalgo

Consolaro

et al. 2019

Dental Traumatology

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Background/Aim The literature on the pathogenesis of extrusive dental luxation has been focused on periodontal tissue responses, with little attention given to the pulp. The aim of this study was to evaluate the response of dental pulp of teeth following extrusive luxation in a rat model. Material and Methods The maxillary right central incisors of 30 rats were extrusively luxated and repositioned after 5 minutes. The animals were euthanized after 7, 15, and 30 days to provide three groups: I, II, and III, respectively (n = 10). Histological sections were stained with H and E for histomorphometric analysis of the odontoblast layer, reparative dentin deposition, Hertwig's epithelial root sheath, pulp necrosis, and periapical inflammatory infiltrate. Results In most cases, new vascular formation occured in association with reparative dentin deposition on the root walls and within the pulp. In some cases, dentin deposition occupied the entire pulp space over time, with no other types of non‐odontogenic hard tissues being observed. Pulp necrosis with the presence of periapical inflammatory infiltrate was also observed in a few cases. No statistical differences were observed among the studied groups. Conclusions Following extrusive luxation, calcific metamorphosis of the pulp is very likely to occur.

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Section: Discussionmentioning

confidence: 99%

Calcific metamorphosis of pulp after extrusive luxation

Queiroz

Hidalgo

Consolaro

et al. 2019

Dental Traumatology

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“…Pulp microcirculation may also be adversely affected by accidental injury or any event that causes long-term interruption of the blood supply to the pulp. 143 As time progresses, necrotic pulp tissue will become infected by oral micro-organisms penetrating into the root canal system via caries, cracks or marginal breakdown of restorations. The microbes will migrate apically through the tooth root and digest the pulp tissue which renders the tooth pulpless.…”

Section: Disease Progressionmentioning

confidence: 99%

An overview of the dental pulp: its functions and responses to injury

Yu¹,

Abbott²

2007

Australian Dental Journal

239

158

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The dental pulp is a unique tissue and its importance in the long-term prognosis of the tooth is often ignored by clinicians. It is unique in that it resides in a rigid chamber which provides strong mechanical support and protection from the microbial rich oral environment. If this rigid shell loses its structural integrity, the pulp is under the threat of the adverse stimuli from the mouth, such as caries, cracks, fractures and open restoration margins, all of which provide pathways for micro-organisms and their toxins to enter the pulp. The pulp initially responds to irritation by becoming inflamed and, if left untreated, this will progress to pulp necrosis and infection. The inflammation will also spread to the surrounding alveolar bone and cause periapical pathosis. The magnitude of pulp-related problems should not be underestimated since their most serious consequence is oral sepsis, which can be life threatening, and hence correct diagnosis and management are essential. Clinicians must have a thorough understanding of the physiological and pathological features of the dental pulp as well as the biological consequences of treatment interventions.

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“…Ischemic infarction of the dental pulp has been described in humans following traumatic injury (24 (1,28). In one of these cases, pulp vessels were dilated and filled with microthrombi composed of sickle cells (28).…”

Section: Resultsmentioning

confidence: 99%

Dental Pulp Infarction in Female Rats Following Inhalation Exposure to 2-Butoxyethanol

et al. 2000

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Female Fischer 344 (F344)/N rats (10 per exposure group) were exposed to 2-butoxyethanol (BE) vapors (0, 31, 62.5, 125, 250, or 500 ppm 6 h/d, 5 d/wk, for 13 weeks) to characterize its prechronic toxicity. Dental lesions consisting of bilateral multifocal dental pulp thrombosis, pulp infarction, and odontoblast infarction were noted in the maxillary incisors of 3 of 4 rats from the 500-ppm group that were sacrificed when moribund during the first week of exposure. In addition, 1 rat from the 500-ppm group that was sacrificed on day 32 had similar unilateral incisor lesions but with additional findings consistent with a unilateral maxillary incisor fracture. In contrast, rats sacrificed after 13 weeks of exposure lacked dental lesions. In conclusion, BE has the potential to cause pulp thrombosis and odontoblast infarction in female rats. The apparent variability in response to BE noted in moribund sacrificed vs terminally sacrificed rats was attributed to development of tolerance to BE-induced hemolysis and subsequent incisor regeneration.

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Ischemic infarction of the pulp: Sequential degenerative changes of the pulp after traumatic injury

Cited by 31 publications

References 5 publications

Calcific metamorphosis of pulp after extrusive luxation

Calcific metamorphosis of pulp after extrusive luxation

An overview of the dental pulp: its functions and responses to injury

Dental Pulp Infarction in Female Rats Following Inhalation Exposure to 2-Butoxyethanol

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