Endoplasmic reticulum stress and mineralization inhibition mechanism by the resinous monomer HEMA.

AIM: To investigate the expression of two endoplasmic reticulum (ER)-resident key chaperone proteins, ERdj5 and BiP, under the influence of resinous monomers and its relationship with the inhibition of mineralization caused by the monomer 2-hydroxyethyl methacrylate (HEMA). METHODOLOGY: The ERdj5 and BiP expression was studied in vitro, in primary human pulp cell cultures after treatment with three different HEMA concentrations at different time periods. Subsequently, the expression of both the odontoblast markers dentine sialoprotein (DSP) and osteonectin (OSN) was studied in human pulp cells under the same conditions. RESULTS: The ERdj5 and BiP expression was upregulated in the pulp cells. DSP and OSN were largely dispersed in the cytoplasm in control cell cultures but accumulated in a perinuclear area after exposure to HEMA. Their expression levels were not affected. CONCLUSIONS: The increased expression of ERdj5 and BiP may reflect activation of ER stress. DSP and OSN accumulation into the cells may lead to their secretion arrest and inhibition of dentine matrix formation. These events may elucidate the mechanism by which HEMA inhibits the mineralization process.

Generalized pulp stones: report of a case with 6-year follow-up.

AIM: To present a mildly mentally retarded patient with generalized pulp stone formation and the six-year follow-up and to discuss the differential diagnosis of the case. SUMMARY: Pulp stones were radiographically detected in the pulp chamber of all permanent teeth in a 25-year-old woman with mild mental retardation who presented for endodontic treatment on tooth no 11 (FDI). The patient's medical, dental and family history was noncontributory. The pulp stone in the pulp chamber of tooth no 11 was removed during canal filing, and root canal treatment completed uneventfully. Six years later, the patient was re-evaluated and the pulp stones were unchanged radiographically. The patient's family history, facial phenotype and karyotype as well as the radiographic, laboratory and physical examination were not consistent with any of the known genetic syndromes associated with generalized pulp stones. Molecular analysis for the DSPP gene proved negative. The aetiology of this case remains unknown. KEY POINTS: Generalized pulp stones occur rarely; Such patients should be referred for genetic evaluation because pulp stones are mostly associated with genetic dentine defects; Pulp stones may hinder root canal treatment; Pulp stones may remain unchanged overtime.

Evidence that substance P is a mediator of antidromic vasodilatation using somatostatin as a release inhibitor.

The effect of somatostatin on nerve-induced vasodilatation and the release of substance P (SP) was studied in the dental pulp of anesthetized cats. Changes in pulpal blood flow were determined by measuring the rate of disappearance of a local depot of radioactive tracer. The release of SP was studied indirectly by determining the residual amounts of substance P-like immunoreactivity (SPLI) in the pulps by radioimmunoassay. Electrical stimulation (3 min at 10 V, 15 Hz and 5 ms) of the distal end of the cut inferior alveolar nerve (IAN) increased pulpal blood flow. After pretreatment (10 min) with somatostatin (30 pmol/min) similar nerve stimulation was without effect on pulpal blood flow. Intra-arterial infusion of somatostatin (30 pmol/min) had no effect on pulpal blood flow and did not influence the vasodilator response to SP. Following IAN stimulation (3--45 min) and subsequent incubation (30 min, 37 degrees C) of the lower canine teeth, the SPLI levels in ipsilateral pulps were significantly lower (47.5% reduction) than those in contralateral, unstimulated controls. In cats pretreated with somatostatin (30 pmol/min for 10 min, i.a.) similar nerve stimulation (3 min) did not reduce the pulpal SPLI levels as compared to controls. The results show that nerve-induced vasodilatation and release of SPLI are inhibited by somatostatin. They are consistent with the hypothesis that vasodilatation in the cat dental pulp produced by stimulation of the IAN is mediated by substance P.