Biomedical subjects

N P Kerezoudis

Publications and source records attributed to N P Kerezoudis.

15 recordsLinked to original sources

PubMed2006

Failure mechanism of ProTaper Ni-Ti rotary instruments during clinical use: fractographic analysis.

AIM: To evaluate the failure mechanism of ProTaper Ni-Ti rotary instruments fractured under clinical conditions. METHODOLOGY: A total of 46 ProTaper instruments that failed (fractured and/or plastically deformed) during the clinical use were collected from various dental clinics, whereas a new set of ProTaper instruments served as control. After inspection under stereomicroscopy the instruments were classified into three categories: (i) plastically deformed but not fractured, (ii) fractured with plastic deformation and (iii) fractured without plastic deformation. Three instruments from each group were analysed with computerized X-ray microtomography (micro-XCT) to detect surface and internal defects, whilst all the fracture surfaces were investigated under SEM. RESULTS: Stereomicroscopic inspection showed that 17.4% of the discarded instruments were only plastically deformed, 8.7% were fractured with plastic deformation and 73.9% were fractured without plastic deformation. Micro-XCT revealed instruments without any surface or bulk defects along with a few files with crack development below the fracture surface. No defects were identified in the unused instruments. SEM examination of fractured surfaces demonstrated the presence of dimples and cones, a typical pattern of dimple rupture developed because of ductile failure. CONCLUSIONS: The results suggest that a single overloading event causing ductile fracture of ProTaper instruments is the most common fracture mechanism encountered under the clinical conditions.

Equipment Failure↗

PubMed2003

Bilateral buccal radicular groove in maxillary incisors: case report.

AIM: To present the rare localization of a radicular groove on the buccal aspect of a tooth and to discuss the pathology and management of the concomitant endo-periodontal defect. SUMMARY: Bilateral buccal radicular grooves were found on the maxillary central incisors of a 60-year-old female Caucasian. One groove was associated with deep local pocketing resulting in pulp necrosis and the formation of a periodontal-endodontic lesion. After endodontic treatment of the affected tooth, periodontal surgery was performed during which an apicoectomy was carried out on the root-filled tooth. Both the buccal grooves were removed by grinding, the roots were planed with curettes and a guided-tissue regeneration technique applied using amelogenin (Emdogain, Biora, Sweden). Following a period of 2 years, re-examination showed excellent healing with the complete elimination of the periodontal pocket on both incisors and significant radiographic evidence of bone regeneration. KEY LEARNING POINTS: Deep radicular grooves can predispose to pulp necrosis and the establishment of combined periodontal-endodontic lesions. Evaluation of clinical signs and appropriate diagnostic tests are of paramount importance in order to prevent incorrect diagnosis and treatment. Endodontists must be capable of performing advanced periodontal regeneration techniques during endodontic surgery.

Alveolar Bone Loss↗

PubMed2000

The lateral periodontal cyst: aetiology, clinical significance and diagnosis.

The lateral periodontal cyst (LPC) is a relatively uncommon but widely recognized odontogenic cyst of developmental origin. It is found mostly in adults and has no sex predilection. LPC is usually discovered during routine radiographic examination, is located mainly between the roots of vital mandibular canines and premolars, and seldom causes pain or other clinical symptoms. The defect appears on radiographs as a round or teardrop-shaped, well circumscribed radiolucency. Due to its location it can easily be misdiagnosed as a lesion of endodontic origin. In this paper, two cases of lateral periodontal cysts are presented. In the first case, the patient (woman, 62 years old) complained of an asymptomatic gingival swelling in the region between the right maxillary canine and premolar. The radiographic examination revealed a well circumscribed radiolucency with a radiopaque margin between the roots of the canine and premolar. The adjacent teeth had vital pulp. Surgical enucleation of the lesion was performed and the histological examination revealed that the lesion was a "lateral periodontal cyst of developmental origin". In the second case, the patient (women, 44 years old) complained of a swelling in the area of tooth 32. During radiographic examination a well circumscribed radiolucency between the roots of the lateral incisor and the canine was discovered. Surgical enucleation of the lesion was performed and the histological examination revealed that the lesion was a "lateral periodontal cyst of developmental origin".

Adult↗

PubMed1999

A method of adapting gutta-percha master cones for obturation of open apex cases using heat.

CLINICAL TECHNIQUE: It is generally accepted that the success of root-canal treatment is mainly dependent on the proper cleaning, shaping and hermetic obturation of root canals. Obturation of the root canal is of importance as 60% of endodontic failures are attributable to incomplete obliteration of the root-canal system. The clinical application of many obturation techniques used today demands the preservation of the natural apical construction or the preparation of an artificial equivalent during chemo-mechanical preparation. However, in clinical practice there are cases where the apical foramen is wide because of over-instrumentation, root-end resection during periradicular surgery, root resorption or because the apex of the root is incompletely formed. Thus the preparation of an artificial apical stop is very difficult to achieve. It is a common experience that performing usual gutta-percha condensation techniques in such canals often results in overfilling and therefore special obturation techniques are needed. Some clinical cases of teeth with wide apical foramen treated by a special obturation method are presented in this paper. In this method the end point of the primary gutta-percha cone is elasticized with a heated instrument and inserted into the root canal to record the internal morphology of the apical portion.

Gutta-Percha↗

PubMed1995

Serotonin in rat oral tissues: role of 5-HT1 receptors in sympathetic vascular control.

In this study we examined whether the indoleamine, serotonin (5-hydroxytryptamine, 5-HT), is contained in the rat incisor pulp and gingiva as well as its possible role in regulation of blood flow in these tissues. Tissue biochemical analysis, by means of high performance liquid chromatography coupled to electrochemical detection, revealed the presence of 5-HT and its metabolite, 5-hydroxyindoleacetic acid (5-HIAA), as well as the catecholamine, dopamine, in both pulp and gingiva. Unilateral surgical sympathectomy or resection of the inferior alveolar nerve failed to affect 5-HT levels in either tissue while dopamine contents in the pulp and gingiva were diminished following sympathectomy. Electrical stimulation of the sympathetic trunk induced a frequency-dependent vasoconstriction in the pulp and gingiva as measured by laser Doppler flowmetry. This vasoconstriction was unaffected by infusion of 5-HT2 or 5-HT3 receptor antagonists or dopamine receptor antagonists but it was significantly reduced in both tissues after alpha 1-adrenoceptor blockade. During this blockade the remaining vasoconstriction induced by high frequency stimulation (16 Hz) was reduced in gingiva by the 5-HT1 receptor blocker, methiothepin. The results indicate an involvement of 5-HT1 receptors and alpha 1-adrenoceptors in the sympathetic vascular control in the gingiva.

Adrenergic alpha-Antagonists↗

PubMed1995

Haemodynamic and immunohistochemical studies of rat incisor pulp after denervation and subsequent re-innervation.

The effects of injury to the inferior alveolar nerve on the distribution of neuropeptides and neurogenic blood-flow reactions were studied in rat mandibular dental pulp. In normal incisor pulps, calcitonin gene-related peptide (CGRP)-like immunoreactivity was common, while substance P- and neurokinin (NKA)-positive nerve fibres were much less abundant. There were no signs of vasoactive intestinal peptide-like, neuropeptide Y-like or 5-hydroxytryptamine-like immunoreactivity. In normal pulps, electrical stimulation (100 microA, 5 ms, 15 Hz for 30 s) of the tooth crown resulted in transient vasoconstriction followed by vasodilation, which was enhanced after alpha-adrenoceptor blockade. At 3 days-4 weeks after unilateral nerve section there were no signs of CGRP-, substance P- and NKA-immunoreactivity, and there was no vasodilation in response to tooth stimulation. The vasoconstrictor response was also absent during this period but at 4 weeks postoperatively a weak response was obtained and after 7 weeks the vasoconstrictor response had regained normal amplitude. At 7 weeks postoperatively, a large number of CGRP-positive fibres had reappeared and at 11 weeks the pattern of CGRP-immunoreactivity was normal. However, substance P- and NKA-immunoreactivity were not found at 7 or 11 weeks after surgery. Vasodilator responses appeared at 7 weeks, and showed normal amplitude at 11 weeks after the creation of the nerve lesion. The results show that during nerve regeneration, sympathetic vasoconstriction was regained earlier than neurogenic vasodilation in rat incisor teeth. The reappearance of neurogenic vasodilation after nerve injury was temporarily associated with the presence of CGRP-immunoreactivity in regenerating trigeminal afferent nerves.

Adrenergic alpha-Antagonists↗

PubMed1994

Involvement of substance P but not nitric oxide or calcitonin gene-related peptide in neurogenic plasma extravasation in rat incisor pulp and lip.

The possible involvement of the neuropeptides substance P and calcitonin gene-related peptide (CGRP) in the development of neurogenic plasma extravasation in the lower lip, gingiva and incisor pulp was examined in anaesthetized rats by means of the Evans blue method and by using newly developed blockers of substance P (CP-96,345) and CGRP (CGRP8-37). Electrical stimulation of the inferior alveolar nerve (15 V, 2 ms, 10 Hz) for 5 min significantly increased the Evans blue content of the ipsilateral lip, gingiva and pulp by 60 (p < 0.01), 62 (p < 0.01) and 92% (p < 0.05), respectively (n = 8). Pretreatment with CP-96,345 (total dose: 1.5 mg/kg, intravenously) counteracted the dye leakage in the lip and pulp but not in the gingiva (n = 6). The inactive enantiomer (CP-96,344, 1.5 mg/kg, n = 8) or the nitric oxide synthesis inhibitor (N omega-nitro-L-arginine methyl ester hydrochloride, 10 mg/kg, n = 7) did not reduce the stimulation-induced dye extravasation in any of the tissues. Pretreatment with CGRP8-37 (0.3 mg/kg, n = 7) did not significantly influence the development of neurogenic extravasation in the lip and incisor pulp, but it slightly attenuated extravasation in the gingiva. The results indicate that the afferent nerve-induced dye extravasation in the lip and pulp, but not in the gingiva, is to a large extent mediated by substance P acting via neurokinin-1 receptors. There was no evidence for an involvement of nitric oxide or CGRP in neurogenic extravasation in rat incisor and lip.

Animals↗

PubMed1994

Nerve-pulp interactions.

Pulpal haemodynamics are naturally intermeshed with inflammatory responses. Cellular and humoral factors may be the vehicles that aid in physiological regulation, but when these systems are overly activated, they may lead to pathological changes. Sensory nerves may initiate inflammatory reactions when activated, and interestingly, recent findings show that vasoconstrictor nerves in the pulp can inhibit the release of neurally stored vasoactive and inflammatory mediators. Thus, there are options for endogenous control of inflammation. Perhaps a variation in the effectiveness of such control can explain why symptoms of hypersensitivity and pain are so unpredictable and individual. What naturally occurring agents are involved in early tissue changes and how do they act? Some agents exert their effects both on vessels and nerves. Thus, there is an intriguing mutual interplay between nerves and tissue reactions. A prolonged, painful stimulation may generate increased blood flow and inflammation, and vice versa, inflammation may lead to pain. This complexity of mechanisms generates many questions that need answers.

Animals↗

PubMed1994

CGRP (8-37) reduces the duration but not the maximal increase of antidromic vasodilation in dental pulp and lip of the rat.

In this study the newly developed blockers of substance P (CP-96,345) and calcitonin gene-related peptide (CGRP8-37) were used to examine whether substance P and CGRP are involved in the afferent nerve induced vasodilation in the rat lower incisor pulp and lip. Electrical stimulation of the inferior alveolar nerve (10 V, 2 ms, 10 Hz, 30 s) in the presence of phenoxybenzamine (3 mg kg-1) induced an immediate vasodilation in the pulp and lip (52 and 186% increase in blood flow respectively, n = 12) with a long duration. Infusion of 2 mg kg-1 CP-96,345, a dose that inhibited the vasodilator effects of substance P (5-25 ng kg-1) in oral tissues, did not have any effect on antidromic vasodilation in either tissue. After infusion of CGRP8-37 (0.3 mg kg-1) the duration of the antidromic vasodilation in the pulp and lip was significantly reduced by 72 and 67% respectively (P < 0.05, n = 4), whereas the maximal increase of the response was unaffected. The blocking effect of the drug was short-lasting. When combined infusions of CP-96,345 and CGRP8-37 were given, a similar reduction in the duration of antidromic vasodilation in the pulp and lip occurred but in this case the amplitude of vasodilation in the pulp was reduced (from 35 +/- 9 to 12 +/- 3%, P < 0.05, n = 4). However, in the lip, the amplitude of vasodilation was not significantly reduced. The present findings indicate an involvement of CGRP in the mediation of the late phase of antidromic vasodilation in rat oral tissues and a role of substance P in the initiation of antidromic vasodilation in the incisor pulp.

Afferent Pathways↗

PubMed1993

Differential effects of nitric oxide synthesis inhibition on basal blood flow and antidromic vasodilation in rat oral tissues.

The role of nitric oxide in the mediation of (a) antidromic and (b) substance P-induced vasodilation in the pulp, lip, oral mucosa and submandibular gland was investigated in anaesthetized rats by means of laser Doppler flowmetry. Bolus or continuous infusion of N omega-nitro-L-arginine methyl ester (L-NAME) increased mean arterial blood pressure and reduced basal blood flow in the pulp but not in the lip. Electrical stimulation of the inferior alveolar nerve, in the presence of phenoxybenzamine, resulted in a long lasting vasodilation in lower lip and incisor pulp. Infusion of L-NAME enhanced the antidromic vasodilation in both lip and pulp. Pretreatment with L-arginine prevented these effects. Administration of the enantiomer (D-NAME) did not exert any effect on basal blood flow and on antidromic vasodilation. Infusion of substance P resulted in a transient vasodilation in all of the oral tissues studied. L-NAME reduced this vasodilation in the submandibular gland (only the lower doses) but it potentiated the responses in the pulp and oral mucosa. Pretreatment with L-arginine prevented the potentiated responses in the pulp and those induced by the lower doses of substance P in the oral mucosa. Thus, nitric oxide appears to differentially regulate the basal blood flow and the antidromic or substance P-induced vasodilation in the microvasculature of the lip and dental pulp.

Amino Acid Oxidoreductases↗

PubMed1993

Localization of NADPH-diaphorase activity in the dental pulp, periodontium and alveolar bone of the rat.

In this study we examined the presence and localization of nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) activity in the dental pulp, periodontal tissues and alveolar bone of the rat. The presence of NADPH-d activity was also examined in cat pulp. The rat histochemical analysis revealed the presence of prominent NADPH-d activity both in cells of the sub-odontoblastic cell layer and in the odontoblasts, in the root as well as in the coronal pulp regions. In the pulpal horns, odontoblasts often had long processes with a high level of labelling indicating NADPH-d activity extending through the predentin and dentin. Moreover, endothelial cells of pulpal blood vessels were positive for NADPH-d in both species. However, no clearcut examples were found of pulpal nerve fibres positive for NADPH-d in the rat or cat and denervation performed in rats did not alter the enzyme staining patterns. In the periodontal tissue, NADPH-d activity was localized to cells on the alveolar bone surface of the periodontal ligament and, in addition, alveolar bone marrow crypts were filled with intensely labelled cells. In the gingival papillae, NADPH-d activity was observed in the basal cell layer of the epithelium. Endothelial cells of periodontal and gingival blood vessels showing positive staining for NADPH-d were occasionally noted.

Alveolar Process↗

PubMed1993

Evans blue extravasation in rat dental pulp and oral tissues induced by electrical stimulation of the inferior alveolar nerve.

Whether increased extravasation of plasma protein may occur in the rat incisor pulp as a result of antidromic stimulation of afferent nerves was investigated, and this preinflammatory reaction compared with that in adjacent soft tissues. In anaesthetized rats, the inferior alveolar nerve was exposed and stimulated electrically (10-15 V, 2 ms, 10 Hz for 30 s or 5 min). Blood flow changes in the lower lip and incisor pulp were recorded by laser Doppler flowmetry. Increased vascular permeability in the lip, gingiva and pulp was indirectly determined by means of the Evans blue dye method and spectrophotometric analysis. Stimulation of the inferior alveolar nerve for 30 s, in the presence of the alpha-adrenergic blocker phenoxybenzamine (3 mg/kg), increased blood flow in the lip by 172 +/- 16% and in the pulp by 38 +/- 5% as compared to basal blood flow. Intravenous (i.v.) administration of atropine (1 mg/kg), chlorisondamine (3 mg/kg), timolol (150 micrograms/kg), cimetidine plus mepyramine (3 mg/kg of each), methysergide (1 mg/kg) and diclofenac sodium (3 mg/kg) was without effect on this response. Acute pretreatment with capsaicin (1-3 mg/kg, i.v.), however, abolished the vasodilation in the pulp and reduced that in the lip by 58% (p < 0.05). In untreated animals, stimulation of the inferior alveolar nerve for 5 min increased the Evans blue content in the ipsilateral lip by 164% (p < 0.001), gingiva by 55% (p < 0.01) and pulp by 67% (p < 0.01). Pretreatment (i.v.) with a combination of cimetidine and mepyramine counteracted the dye extravasation only in the gingiva.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Inhibitory influence of sympathetic nerves on afferent nerve-induced extravasation in the rat incisor pulp upon direct electrical stimulation of the tooth.

Previous studies have shown that sympathetic nerve stimulation reduces afferent nerve-induced vasodilation by mechanisms unrelated to vasoconstriction in the rat incisor pulp. The present investigation concerned whether similar modulatory mechanisms might also influence neurogenic plasma extravasation in dental pulp. Rat mandibular incisors were electrically stimulated and blood flow reactions in the pulp were recorded by laser Doppler flowmetry. Plasma extravasation in the incisor pulp, gingiva and lip were indirectly assessed by the Evans-blue method. Stimulation of teeth with 50 microA (5 min) did not cause increased dye accumulation in the stimulated pulps whereas stimulation with 100 microA significantly increased the dye content in ipsilateral pulps by 32% as compared to controls; 100 microA stimulation was without effect in unilaterally denervated animals. Tooth stimulation with 50 microA (5 min), in the presence of either the alpha-adrenergic blocker phenoxybenzamine (3 mg/kg), or the alpha 1-adrenergic antagonist prazosin (50 micrograms/kg), as well as in chronically sympathectomized animals, significantly increased the Evans-blue content in the stimulated pulps by 47, 83 and 86%, respectively. Application of short trains of impulses (same number of impulses as for the continuous stimulation but producing minimal vasoconstriction) resulted in some dye accumulation, which was enhanced in the ipsilateral pulps in the presence of prazosin (100 micrograms/kg) or after acute resection of the superior cervical sympathetic ganglion by 70 and 64%, respectively. The Evans-blue content in the lip and gingiva was uninfluenced by the tooth stimulation. The results indicate that activation of sympathetic nerves inhibits the afferent nerve-induced plasma extravasation in rat incisor pulp and this effect is mediated by alpha-adrenoceptors not associated with vasoconstriction.

Animals↗

PubMed1993

Activation of sympathetic nerves exerts an inhibitory influence on afferent nerve-induced vasodilation unrelated to vasoconstriction in rat dental pulp.

In order to elucidate a possible influence of the sympathetic nervous system on afferent nerve function, rat mandibular incisors were electrically stimulated and blood flow changes monitored in the incisor pulp of untreated and sympathectomized animals by a laser Doppler flowmeter. Monopolar electrical stimulation of the tooth (200 microA, 5 ms, 40 Hz, 1 s) in normal animals resulted in a transient reduction in pulpal blood flow (PBF) (16% reduction, n = 10) followed by a small but long-lasting increase (11% increase). After administration of phenoxybenzamine or phentolamine (3 mg kg-1, i.v.) the initial dip in PBF was reduced by 59% (P < 0.001) while the subsequent increase was enhanced by 185% (P < 0.001). Similarly, infusion of prazosin (50 micrograms kg-1, i.v.) and idazoxan (0.5 mg kg-1, i.v.) significantly enhanced the increase in PBF by 118 and by 79%, respectively. In chronically sympathectomized animals the increase in PBF was 250% larger than that seen in untreated animals (P < 0.001). This increase in PBF was not further enhanced after alpha-adrenergic blockade. Acute resection of the superior cervical sympathetic ganglion, also resulted in some enhancement (by 56%) of the stimulation-induced increase in PBF (P < 0.01, n = 6). The increase in PBF was unaffected by infusion of timolol (150 micrograms kg-1) and atropine (1 mg kg-1) but was totally abolished by intravenous pre-treatment with capsaicin (1-3 mg kg-1). The present results suggest that activation of sympathetic nerves exerts inhibitory effects on the afferent nerve-induced vasodilation in the rat incisor pulp unrelated to sympathetic vasoconstriction.

Adrenergic alpha-Antagonists↗

PubMed1992

Activation of sympathetic fibres in the pulp by electrical stimulation of rat incisor teeth.

Previous studies of the sympathetic nerve supply of the rat mandibular incisor pulp have shown conflicting results. Here, the neurovascular control of the rat lower incisor pulp was investigated by stimulating the tooth crown and the cervical sympathetic trunk electrically and monitoring blood-flow changes in the pulp by laser Doppler flowmetry. In addition the presence of noradrenaline (NA) in the pulp and gingiva was examined biochemically in untreated and sympathectomized animals by high-performance liquid chromatography. The tissue concentrations of NA in the pulp were 11-fold greater than those of gingiva. Surgical sympathectomy significantly reduced the NA content in the pulp by 76%. Monopolar electrical stimulation of teeth (25-50 microA) for 1 min resulted in a frequency-dependent reduction followed by an increase in pulpal blood flow. At 16 Hz the reduction in blood flow was 65% and the subsequent increase was 9%. After intravenous administration of the alpha-adrenoceptor antagonist phentolamine, the stimulation-induced reduction in pulpal blood flow was diminished by 94% while the increase was significantly enhanced (from 9 to 40%). Infusion of the beta-adrenoceptor antagonists propranolol and timolol significantly reduced this increase in blood flow by 53 and 55%, respectively. Preganglionic sympathetic nerve stimulation also induced a frequency-dependent reduction followed by a slight increase in pulpal blood flow. This reduction in blood flow was almost abolished after alpha-adrenergic blockade and there was no subsequent increase. These findings suggest that there are sympathetic nerve fibres in rat incisor pulp and that they are activated upon monopolar electrical stimulation of teeth resulting in alpha- and beta-adrenoceptor mediated blood-flow responses.

Adrenergic Fibers↗