Experimental Periapical Lesions Research Articles

Protective Effects of Follicle-stimulating Hormone Inhibitor on Alveolar Bone Loss Resulting from Experimental Periapical Lesions in Ovariectomized Rats

IntroductionThe direct effect of follicle-stimulating hormone (FSH) on bone resorption has been demonstrated recently. The aim of this study was to evaluate the effect of FSH inhibitor leuprorelin (LE) on alveolar bone loss resulting from experimental periapical lesions in ovariectomized (OVX) rats. MethodsTwenty-seven female rats were randomly assigned into 4 groups and subjected to ovariectomy or sham surgery (1.6 mg/kg body weight LE or vehicle was injected immediately). One week after surgery, the pulp of each rat's bilateral lower first molars was exposed to the oral environment. Three weeks after pulpal exposure, all the animals were killed, and bilateral mandibles were extracted for histologic processing. Radiographic and histologic examination for periapical bone loss area, enzyme histochemical examination for tartrate-resistant acid phosphatase (TRAP), and immunohistochemical examination for FSH receptor (FSHR) were performed. ResultsLE significantly decreased the alveolar bone loss area and osteoclast occurrence compared with non–LE treatment ovariectomized rats (P < .05), and the number of FSHR-positive cells was significantly correlated with alveolar bone loss area (r = 0.796, P < .01). ConclusionsLE has protective effects on alveolar bone loss resulting from experimental periapical lesions in OVX rats.

Critical role of NFATc1 in periapical lesions

To observe NFATc1 expression in experimental periapical lesions in rats. Apical periodontitis was induced in Wistar rats by occlusal pulp exposure in mandibular first molar teeth. After exposure, 30 rats were killed on days 0, 7, 14, 21 and 28. The jaws that contained the first molar were removed and prepared for histological examination, immunohistochemistry and enzyme histochemistry. From day 0 to day 28, the areas of periapical bone loss and the number of NFATc1-positive cells increased, peaking on day 28. The number of TRAP-positive cells increased substantially from day 0 to day 14 and then gradually decreased from day 14 to day 28. NFATc1 was detected and possibly involved in the inflammatory response and bone resorption of periapical tissues, as well as being associated with periapical lesion pathogenesis.

CCR2 Deficiency Results in Increased Osteolysis in Experimental Periapical Lesions in Mice

Introduction Periapical lesions are chronic inflammatory disorders of periradicular tissues caused by etiologic agents of endodontic origin. The inflammatory chemokines are thought to be involved in the latter observed osteolysis. With a murine model of experimental periapical lesion, the objective of this study was to evaluate the role of the chemokine receptor CCR2 in the lesion progression, osteoclast differentiation and activation, and expression of inflammatory osteolysis-related mediators. Methods For lesion induction, right mandibular first molars were opened surgically with a ¼ carbine bur, and 4 bacterial strains were inoculated in the exposed dental pulp; left mandibular first molars were used as controls. Animals were killed at 3, 7, 14, and 21 days after surgeries to evaluate the kinetics of lesion development. Results CCR2 KO mice showed wider lesions than WT mice. CCR2 KO mice also expressed higher levels of the osteoclastogenic and osteolytic factors, receptor activator of nuclear factor kappa B ligand (RANKL) and cathepsin K, of the proinflammatory cytokine tumor necrosis factor–alpha, and of the neutrophil migration related chemokine, KC. Conclusions These results suggest that CCR2 is important in host protection to periapical osteolysis.

Expression of a Novel PDGF Isoform, PDGF-C, in Experimental Periapical Lesions

The purpose of this study was to examine the expression of platelet-derived growth factor C (PDGF-C), which is a new member of the PDGF family, in experimental periapical lesions. Periapical lesions were induced in Sprague-Dawley rats by occlusal pulp exposure in the mandibular first molars. Animals were sacrificed randomly at 0, 7, 14, 21, and 28 days after pulp exposure. Frontal sections were prepared for histological analysis and enzyme histochemistry. Reverse-transcription polymerase chain reaction and immunohistochemistry were performed to detect PDGF-C expression. From day 0 to day 28, PDGF-C messenger RNA were expressed and increased until day 28. A few PDGF-C–positive cells and osteoclasts could be observed on day 7. Both ascended in number on day 14. In the 21- and 28-day samples, the PDGF-C–positive cells increased, whereas fewer osteoclasts were observed. Many of the PDGF-C–positive cells were inflammatory cells with different morphologies. These findings showed that PDGF-C could be observed and might also be involved in the pathogenesis of periapical lesions.

In Vitro Evaluation of Antimicrobial Efficacy of Iontophoresis against Enterococcus faecalis, Candida albicans, Pseudomonas aeruginosa and Bacillus subtilis

This in vitro study examined the antimicrobial efficacy of iontophoresis against Enterococcus faecalis, Candida albicans, Pseudomonas aeruginosa and Bacillus subtilis, all of which are often found in the root canals of teeth with refractory apical periodontitis. An experimental periapical lesion model was made from a transparent plastic root canal model. Iontophoresis was performed with Kantop Junior®; with (1) diammine silver fluoride solution (2) ammoniacal silver hydroxide solution and (3) iodine zinc iodide solution as the iontophoretic solutions. Iontophoresis using diammine silver fluoride solution eradicated all four microorganisms whereas iontophoresis using ammonium silver solution and iodine zinc iodide solution could not. The results of this study suggested that iontophoresis with diammine silver fluoride is an effective treatment for E. faecalis, C. albicans, P. aeruginosa and B. subtilis, all of which often found in the root canals of teeth with refractory apical periodontitis.

Correlation between the Expression of c-Fos and Osteoclasts in Induced Periapical Lesions in Rats

The experiment was undertaken to observe the correlation between the expression of c-Fos and osteoclasts in experimental periapical lesions in rats. Apical periodontitis was induced in Wistar rats by occlusal exposure of the pulp of their mandibular first molars. After the exposure, 25 Wistar rats were killed on days 0, 7, 14, 21, and 28. The jaws that contained the first molar were obtained and routinely prepared for immunohistochemistry and enzyme histochemistry. A few c-Fos-positive cells and osteoclasts could be observed on day 7, and both climaxed on day 14. In the 21-day and 28-day samples, the expression of c-Fos decreased, and fewer osteoclasts could be observed. From day 7 to day 28, a significant positive correlation was found between the expression of c-Fos and osteoclasts. These findings demonstrated that c-Fos might be associated with the differentiation of osteoclasts in the periapical lesions.

Effect of an Estrogen-deficient State and Alendronate Therapy on Bone Loss Resulting from Experimental Periapical Lesions in Rats

The aim of the research was to evaluate the impact of an estrogen-deficient state and alendronate (ALD) therapy on bone loss resulting from experimental periapical lesions in rats. Periapical lesions were induced on ovariectomized (OVX) and sham-ovariectomized (Sham) rats. After sample preparation, histologic and radiographic examination for periapical bone loss area and an enzyme histochemical test for tartrate-resistant acid phosphatase (TRAP) were performed. The results showed that OVX significantly increased bone loss resulting from periradicular lesions. After daily subcutaneous injection of ALD, the bone loss area and the number of TRAP-positive cells (osteoclasts) were reduced. These findings suggested that alendronate may protect against increased bone loss from experimental periapical lesions in estrogen-deficient rats. Given recent recognition of adverse effects of bisphosphonates, including an increased risk for osteonecrosis, the findings from this study should not be interpreted as a new indication for ALD treatment. However, they may offer insight into understanding and predicting outcomes in female postmenopausal patients already on ALD therapy for medical indications.

In vivo estimation of periapical bone reconstruction by chondroitin sulfate in calcium phosphate cement

Abstract Biphasic calcium phosphate cements using an equimolar mixture of tetracalcium phosphate and dicalcium phosphate dihydrate (TeDCPD) for the powder phase were experimentally developed for endodontic clinical use. The liquid for standard cement (CP-1) in this study was 2.1% citric acid solution. In the liquid for the modified cements, 2% (CP-2) or 6% (CP-3) chondroitin sulfate (CS) was added. The microstructure of the cements was observed by scanning electron microscope (SEM). X-ray diffraction analyses (XRD) were also performed. The cements were respectively placed in prepared mandibular first molar canals of rats. Results of SEM and XRD examinations of the cements indicated that the addition of CS accelerated the setting reaction of calcium phosphate cement. In experimental periapical lesion, alveolar bone could be significantly reconstructed with polarized cells along the margin using CP-3, but CP-1. It seems that CS in TeDCPD compound induce osteoblasts or osteoblast-like cells.

An immunoelectron-microscopic study of class II major histocompatibility complex molecule-expressing macrophages and dendritic cells in experimental rat periapical lesions

Previous studies have demonstrated that heterogeneous populations of class II major histocompatibility complex (MHC) molecule-expressing non-lymphoid cells, ultrastructurally classified as macrophages and dendritic cell (DC) cell-like cells, comprise the major immune cell population in experimental periapical lesions in rat molars. In this study, the temporal changes in relative proportions of the two types of cells were examined, on the hypothesis that they are involved in different aspects of the pathogenesis of the lesions. The lesions were induced by making surgical pulp exposures in mandibular first molars of 5-week-old Wistar rats. Observation periods were set at 0 (normal), 3, 14, 28, and 56 days. Non-lymphoid cells immunoreactive to OX6 (reactive to class II MHC molecules) were classified as macrophages and DC cell-like cells according to their ultrastructure, and the frequencies of the two types of cells were assessed at each time-point. ED1 (reactive to nearly all macrophages and DCs) was also used to identify macrophages and DC cell-like cells. At 3 days, most OX6+ cells and ED1+ cells in the periapical tissue had the ultrastructural appearance of newly recruited macrophages. At 14 days, when the lesion was actively expanding, there were significantly more OX6+ macrophages than OX6+ DC cell-like cells ( P<0.01). However, at 28 days, when lesion expansion had ceased, DC cell-like cells significantly outnumbered OX6+ macrophages ( P<0.01); this remained constant at 56 days. Cell-to-cell contact between OX6+ non-lymphoid cells and OX6− lymphocytes, suggesting a functional interaction, was most frequently seen at 28 days. These results support the notion that class II MHC molecule-expressing macrophages play some part in the initial lesion expansion, and suggest that DC cell-like cells may primarily be involved in immune defence against perpetuated antigenic challenges following lesion stabilization.

An immunohistochemical study of the behavior of cells expressing interleukin-1α and interleukin-1β within experimentally induced periapical lesions in rats

Cells expressing interleukin-1 (IL-1) were examined in rat periapical lesions using immunohistochemical methods. During the acute phase, both IL-1 alpha- and IL-1 beta-expressing cells were observed adjacent to many osteoclasts that contained large cytoplasms, and consequently the periapical lesions tended to expand. However, the number of IL-1 beta-expressing cells was about twice that of IL-1 alpha-expressing cells during the same period. On the other hand, there were significantly less IL-1 beta-expressing cells during the chronic phase and consequently a significant expansion of the periapical lesions was not seen. Furthermore, IL-1 alpha- and IL-1 beta-expressing cells were located far from the bone surfaces, whereas a fibroblastic cell layer lay between the IL-1-expressing cells and the bone surfaces. Both IL-1 alpha and IL-1 beta were mainly expressed by macrophages. In addition, after the percolated application of formocresol to experimentally induced periapical lesions, numerous macrophages expressing IL-1 beta became conspicuous within the vicinity of the extensive bone resorption sites. These results suggest that macrophages expressing IL-1 beta may play an important role in the activation and recrudescence of osteoclastic bone resorption, and this may be due to their localization close to the bone resorption sites noted within experimental periapical lesions.

Endotoxin and Gram-negative bacteria in the rat periapical lesions

The purpose of this study was to measure the amount of endotoxin as well as to identify Gram-negative bacteria in experimental periapical lesions in rats. Molar pulps were exposed and infected and the amount of endotoxin in the periapical tissue of the right mandibular first molar was measured by Endospecy, while the colony number of Gram-negative bacteria was determined in the same region of the left mandibular first molar. In the control animals, the amount of endotoxin in the periapical tissues did not change at all during the experimental period, and no Gram-negative bacteria were isolated. In the experimental animals, the amount of endotoxin in the periapical tissues increased gradually from 1 to 70 days, and its level was significantly greater than that of control animals after 7 days. Gram-negative bacteria were isolated from the periapical tissues and their number gradually increased from 1 to 14 days (26 to 82%), but decreased at 21 days. It was approximately 60% from 28 to 70 days. The results of this study showed that the amount of endotoxin in the periapical tissues gradually increased with increasing time and that Gram-negative bacteria were isolated from the same region but did not increase in number concurrently with the increase in the amount of endotoxin.