Pulp canal obliteration after replantation of avulsed immature teeth: a systematic review.

BACKGROUND: Avulsion of permanent teeth is one of the most serious dento-alveolar traumatic injuries. Pulp canal obliteration (PCO) is one of the consequences after replantation of avulsed immature teeth. The aim of this systematic review was to determine when calcification following replantation of an avulsed immature tooth begins and to evaluate the prevalence of PCO in these cases. MATERIALS AND METHODS: Electronic database MEDLINE via Ovid, PubMed, Cochrane, and Web of science databases were searched. Hand searching was performed through reference lists of endodontic and trauma textbooks, endodontic and trauma-related journals, and relevant articles from electronic searching. Pooled data from the selected articles were analyzed for prevalence of healing and PCO as well as mean first evidence of PCO. RESULTS: Pulp healing after replantation of immature teeth occurred in 32.9%, while pulpal necrosis occurred in 67.1% of teeth. PCO was the most frequent outcome of pulpal healing as it occurred in 96% of healed pulps. First evidence of obliteration was observed from 3 to 14 months with mean time of 9.5 months (95% CI = 4.5-14.5 months). CONCLUSIONS: PCO is considered the mechanism by which the pulp heals after replantation of avulsed immature permanent teeth. PCO is very fast and can be recognized radiographically during the first year from the onset of the trauma.

Osteocalcin expression in pulp inflammation.

INTRODUCTION: Dental pulp inflammation and repair are closely related. Osteocalcin (OCN), a glycoprotein present in dentin matrix, is expressed by odontoblasts. Although OCN is considered a reparative molecule inside the dental pulp, it is not clear if it is involved in pulpal inflammation. The objective of this study was to localize OCN in reversible and irreversible pulpitis and to describe its possible function in inflammation. METHODS: Pulp tissues in the form of reversible and irreversible pulpitis were collected from the endodontic clinic. Those from impacted teeth were used as controls. Immunohistochemistry was used to localize OCN. Samples were analyzed for OCN and inflammatory mediator expression using multiplex assay. RESULTS: OCN in inflamed tissues was localized in cells and matrix around calcification areas and in cells around blood vessels but not in normal tissues. The plex assay (Bio-Plex 200, Bio-Rad Laboratories Ltd, Mississauga, ON, Canada) showed OCN expression in reversible pulpitis significantly higher than in irreversible pulpitis, and both were significantly higher than in the controls. A panel of inflammatory mediators showed an increase in reversible and irreversible pulpitis. Another panel was decreased in both stages compared with the controls. OCN expression in reversible pulpitis was positively correlated to the expression of vascular endothelial growth factor, fibroblast growth factor, macrophage inflammatory protein-1ß, monocyte-derived chemokine, monocyte chemoattractant protein-1, interleukin (IL)-17, and soluble IL-2 receptor α and negatively correlated to that of IL-1α, IL-1ß, IL-8, granulocyte macrophage colony-stimulating factor, and macrophage inflammatory protein-1α. CONCLUSIONS: Profound understanding of the pulp inflammatory process would lead to new molecular treatment strategies. Our data indicate that OCN expression in reversible pulpitis is associated with angiogenic markers, suggesting its potential use in regenerative treatment.

Dentin matrix protein-1 activates dental pulp fibroblasts.

INTRODUCTION: Dentin matrix protein-1 (DMP-1) is involved in the mineralization of hard dental tissues. DMP-1 is localized in several soft tissues, but its role is unclear. METHODS: Human inflamed dental pulps were collected from the endodontic clinic and human normal pulps from impacted teeth. Dental pulp cells from 8 subjects were explanted to test the effect of DMP-1 on interleukin-6 (IL-6) and IL-8 production by using enzyme-linked immunosorbent assay. RESULTS: DMP-1 was localized in pulp inflammation by using immunohistochemistry but was not present in impacted root pulps. Wherever found, areas of calcification were positively stained against DMP-1, suggesting its possible involvement in pulp inflammation and in pathologic calcification. To test this hypothesis, primary human pulp fibroblasts were cultured. The fibroblasts were identified on the basis of their morphology, immunoreactivity against vimentin and collagen 1a1 by immunofluorescence and negative staining to CD45, CD34, and cytokeratin by flow cytometry. DMP-1 (10 ng/mL) stimulated the production of IL-6 and IL-8 from pulp fibroblasts. DMP-1 showed an additive effect with lipopolysaccharide in IL-6 and IL-8 production. Inhibition of the p38 mitogen-activated protein kinase pathway blocked the proinflammatory effect of DMP-1 on pulp fibroblasts. CONCLUSIONS: Our data indicate that DMP-1 might participate in the development of inflammatory changes in the dental pulp. DMP-1 inhibition might be a new therapeutic strategy to target pulp inflammation and pathologic calcification.

Dental pulp neurophysiology: part 2. Current diagnostic tests to assess pulp vitality.

In this second part of our 2-part review, we discuss recent research about pulp tests that determine the vitality of the tooth and clinically accepted pulp testers. A pain response to hot, cold or an electric pulp tester indicates the vitality of only a tooth's pulpal sensory supply; the response does not give any idea about the state of the pulp. Although the sensitivity of these tests is high, when false-positive and false-negative results occur, they may affect the treatment of the tooth. A tooth falsely diagnosed as nonvital with an electric pulp tester may undergo an unnecessary root canal, whereas one falsely diagnosed as vital may be left untreated, causing the necrotic tissue to destroy the supporting tissues (resorption). The vascular supply is more important to the determination of the health of the pulp than the sensory supply. Pulp death is caused by cessation of blood flow and may result in a necrotic pulp, even though the pulpal sensory supply may still be viable. The pulp can be healed only if the circulating blood flow is healthy. Although still under investigation, diagnostic devices that examine pulpal blood flow, such as the pulse oximeter and laser Doppler flowmetry, show promising results for the assessment of pulp vitality.

Dental pulp neurophysiology: part 1. Clinical and diagnostic implications.

Diagnosis in endodontics requires an understanding of pulpal histology, neurology and physiology, and their relationship to the various diagnostic tests commonly used in dental practice. Thermal changes in the oral environment cause rapid displacement of dentinal tubular contents, resulting in pain. This effect, known as the hydrodynamic effect, is the regulator of pain sensation in thermal-pulp testing. Hundreds of axons enter the tooth from the apical foramen to provide it with its sensory supply. The nerve supply of the dentin-pulp complex is mainly made up of A fibres (both delta and beta) and C fibres. They are classified according to their diameter and their conduction velocity. The A fibres are mainly stimulated by an application of cold, producing sharp pain, whereas stimulation of the C fibres produces a dull aching pain. Because of their location and arrangement, the C fibres are responsible for referred pain. This first part of a 2-part review examines the relation between clinical sensations during the diagnostic visit and the neurophysiology of the dental pulp to explore the connection between the art (clinical diagnosis) and the science (neurophysiology) of endodontics.