Sickle cell anemia: An etiological factor in pulpal necrosis

Andrews, Clyde H.; England, Marshall C.; Kemp, W. B.

doi:10.1016/s0099-2399(86)80023-1

Cited by 53 publications

(42 citation statements)

References 5 publications

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“…These studies also illustrated the necessity of administration of this high dose to induce this disseminated thrombotic crisis, the type that is also seen in sickle cell patients. The patterns of thrombosis seen in this study affirm previous studies claiming this to be an appropriate chemically induced animal model for researching human thrombotic disorders (Andrews et al, 1983;Cox and Soni, 1984;Smith, 1996;Nyska et al, 1999b;Eldor and Rachmilewitz, 2002;Ezov et al, 2002;Koshkaryev et al, 2003;Redlich et al, 2004;Shabat et al, 2004).…”

Section: X-ray Image Analysis and Histopathological Findings For Animsupporting

confidence: 88%

2-Butoxyethanol Female-Rat Model of Hemolysis and Disseminated Thrombosis: X-Ray Characterization of Osteonecrosis and Growth-Plate Suppression

Lewis

Nyska²,

Johnson³

et al. 2005

Toxicol Pathol

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We recently proposed a chemically induced rat model for human hemolytic disorders associated with thrombosis. The objective of the present investigation was to apply a noninvasive, high-magnification X-ray analysis, the Faxitron radiography system, to characterize the protracted bone damage associated with this 2-butoxyethanol model and to validate it by histopathology. Groups of female Fischer 344 rats were given 0, 250, or 300 mg of 2-butoxyethanol/kg body weight daily for 4 consecutive days. Groups were then sacrificed 2 hours or 26 days after the final treatment. The treated animals displayed a darkened purple-red discoloration on the distal tail. Histopathological evaluation, including phosphotungstic acid-hematoxylin staining of animals sacrificed 2 hours after the final treatment, revealed disseminated thrombosis and infarction in multiple organs, including bones. The Faxitron MX-20 specimen radiography system was used to image selected bones of rats sacrificed 26 days posttreatment. Premature thinning of the growth plate occurred in the calcaneus, lumbar and coccygeal vertebrae, femur, and ilium of the treated animals. Areas of decreased radiographic densities were seen in the diaphysis of the femur of all treated animals. The bones were then examined histologically and showed a range of changes, including loss or damage to growth plates and necrosis of cortical bone. No thrombi were seen in the animals sacrificed at 30 days, but bone and growth plate changes consistent with prior ischemia were noted. The Faxitron proved to be an excellent noninvasive tool that can be used in future studies with this animal model to examine treatment modalities for the chronic effects of human thrombotic disorders.

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Section: X-ray Image Analysis and Histopathological Findings For Animsupporting

confidence: 88%

2-Butoxyethanol Female-Rat Model of Hemolysis and Disseminated Thrombosis: X-Ray Characterization of Osteonecrosis and Growth-Plate Suppression

Lewis

Nyska²,

Johnson³

et al. 2005

Toxicol Pathol

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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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“…As such, the most prevalent complications include diseases of nervous, cardiopulmonary, musculoskeletal, hepatobiliary, endocrine and genitourinary systems [10]. The most frequent oral manifestations of SCD greatly affect the oral mucosa, gingival tissue, mandible, osteonecrosis, facial swelling, increased risks for caries nerve supply, and tooth enamel and pulp [11][12][13][14][15][16][17][18][19] (Table 1). In addition, paleness of the oral mucosa, delayed tooth eruption, depapillation leading to atrophic alteration of the tongue, high degree of abnormality in the hypophosphatemic teeth, odontogenic infection, orofacial pain, craniofacial disorders such as protrusion of the midface area, maxillary expansion, mandibular retrusion, and maxillary protrusion.…”

Section: Clinical Presentation Of Scdmentioning

confidence: 99%