acid-phosphatase and Mandibular-Diseases

The W9 peptide has been shown to act as a receptor activator for nuclear factor-κB ligand (RANKL) antagonist and tumor necrosis factor (TNF)-α antagonist, which can promote bone formation and inhibit bone resorption. Studies on the W9 peptide at the cellular level have mainly focused on osteoblasts, and little research on the mechanism by which the W9 peptide regulates osteoclasts has been reported, which was the aim of this work. In this study, a rat mandibular defect model was established in vivo and implanted with hydrogel containing the W9 peptide for 2 weeks and 4 weeks, and histochemical staining was used to evaluate the formation of new bone and the changes in osteoclasts. RAW264.7 cells were cultured in vitro for osteoclast induction, and different concentrations of W9 peptide were added. Tartrate resistant acid phosphatase staining, monodansylcadaverine staining, TdT-mediated dUTP Nick-End Labeling assay, real-time PCR and Western blot were used to detect osteoclast differentiation, autophagy and apoptosis. Our results showed that the W9 peptide could reduce osteoclastogenesis and osteoclast activity induced by RANKL, and these effects were partly due to the inhibition of osteoclast autophagy. On the other hand, the W9 peptide could promote mature osteoclast apoptosis, in which autophagy might play an antagonistic role. Taken together, these results suggest that the W9 peptide inhibits osteoclastogenesis and osteoclast activity by downregulating osteoclast autophagy and promoting osteoclast apoptosis. Our results will benefit the development and application of new small molecule peptides for the treatment of bone resorption diseases.

Topics: Acid Phosphatase; Animals; Apoptosis; Autophagy; Blotting, Western; Cells, Cultured; Disease Models, Animal; Down-Regulation; Immunohistochemistry; In Situ Nick-End Labeling; Male; Mandibular Diseases; Osteoclasts; Osteogenesis; Peptides, Cyclic; Rats; Rats, Wistar; Real-Time Polymerase Chain Reaction

The aim of the present study was to compare between three possible osteoporotic treatments in prevention of glucocorticoid-induced alveolar bone loss.. Fifty adult female Wistar rats with an average weight 150-200 g were randomized into five groups: group I (control) was intraperitoneally injected with saline. The other experimental groups (II & III, IV & V) were intraperitoneally injected with 200 µg/100 g body weight dexamethasone. The experimental groups III, IV and V received intraperitoneal injection of 10 mg/kg/day pheniramine maleate (H1 receptor antagonist), ranitidine hydrochloride (H2 receptor antagonist) and concomitant doses of both H1 & H2 receptor antagonists respectively. After 30 days, the rats have been sacrificed. The mandibles were examined histologically, histochemically and histomorphometrically. The bone mineral density was measured using dual-energy X-ray absorptiometry (DEXA).. Histopathologically the glucocorticoid group showed wide medullary cavities with wide osteocytic lacunae. These marrow cavities were reduced in the prophylactic groups (III, IV) but increased in group V. Bone histomorphometric analysis revealed improvement in static bone parameters in groups III and IV and deterioration in group V in comparison to group II. The DEXA revealed significant reduction in the bone mineral density in all experimental groups compared to the control group.. In a rat model, the administration of H1 or H2 receptor antagonists separately could minimize the alveolar bone loss caused by the administration of glucocorticoids while concomitant administration of both H1 and H2 receptor antagonists deteriorated the bone condition.

Topics: Absorptiometry, Photon; Acid Phosphatase; Alveolar Bone Loss; Animals; Bone Density; Bone Marrow; Dexamethasone; Female; Glucocorticoids; Histamine H1 Antagonists; Histamine H2 Antagonists; Image Processing, Computer-Assisted; Isoenzymes; Mandible; Mandibular Diseases; Organ Size; Osteoblasts; Osteoclasts; Osteocytes; Pheniramine; Random Allocation; Ranitidine; Rats; Rats, Wistar; Tartrate-Resistant Acid Phosphatase

Intermittent administration of parathyroid hormone (PTH) promotes new bone formation in patients with osteoporosis and bone fractures. It was shown previously that PTH also reduces periodontitis-related bone loss. The aim of this study is to evaluate the effect of treatment with PTH on periodontal healing in rats.. Fenestration defects were created at the buccal surface of the distal root of the mandibular first molars, and both periodontal ligament (PDL) and cementum were removed. Animals were then assigned to two groups (eight animals per group): group 1: control, placebo administration; and group 2: test, human PTH (hPTH) 1-34 administration at a concentration of 40 μg/kg. For both groups, the animals were injected every 2 days, and the animals were sacrificed at 14 and 21 days after surgery. Specimens were harvested and processed for routine decalcified histologic sections. The following parameters were assessed: 1) remaining bone defect extension (RBDE); 2) newly formed bone density (NFBD); 3) total callus area (TCA); 4) osteoclast number (ON) in the callus region; and 5) newly formed dental cementum-like tissue (NFC). Birefringence of root PDL reattachment was also evaluated.. Birefringence analysis showed root PDL reattachment for both groups 21 days after treatment. Intermittent hPTH 1-34 administration decreased RBDE (P <0.01) and increased NFBD (P <0.01), TCA (P <0.01), area of NFC (P <0.01), and ON in the callus region (P <0.01).. Within the limits of the present study, intermittent administration of hPTH 1-34 led to an enhanced periodontal healing process compared with non-treated animals.

Topics: Acid Phosphatase; Administration, Metronomic; Alveolar Bone Loss; Animals; Bone Density; Bony Callus; Cell Count; Cementogenesis; Dental Cementum; Injections, Subcutaneous; Isoenzymes; Male; Mandibular Diseases; Osteoclasts; Osteogenesis; Parathyroid Hormone; Periodontal Ligament; Placebos; Rats; Rats, Wistar; Tartrate-Resistant Acid Phosphatase; Time Factors; Tooth Root; Wound Healing

The aim of this study was to determine the effects of glutathione-S-transferase-fused recombinant biglycan (GST-BGN) on craniofacial bone regeneration. We recently demonstrated a positive effect of tissue-derived BGN on bone morphogenetic protein 2 (BMP-2) function, which is exerted likely via the BGN core protein. Here, we investigated the effects of GST-BGN lacking any posttranslational modifications on BMP-2 function in vitro and in vivo. In the C2C12 cell culture system, BMP-2-induced Smad 1/5/8 phosphorylation and alkaline phosphatase activity were both enhanced by the addition of GST-BGN. For the in vivo effect, we employed a Sprague-Dawley rat mandible defect model utilizing 1 µg (optimal) or 0.1 µg (suboptimal) of BMP-2 combined with 0, 2, 4, or 8 µg of GST-BGN. At 2 weeks post-surgery, newly formed bone was evaluated by microcomputed tomography and histologic analyses. The results revealed that the greatest amounts of bone within the defect were formed in the groups of suboptimal BMP-2 combined with 4 or 8 µg of GST-BGN. Also, bone was well organized versus that formed by the optimal dose of BMP. These results indicate that recombinant BGN is an efficient substrate to promote low-dose BMP-induced osteogenesis.

Topics: Acid Phosphatase; Alkaline Phosphatase; Animals; Biglycan; Biomarkers; Bone Density; Bone Morphogenetic Protein 2; Bone Regeneration; Cell Culture Techniques; Cell Line; Collagen; Glutathione Transferase; Isoenzymes; Mandibular Diseases; MAP Kinase Signaling System; Osteogenesis; Rats; Rats, Sprague-Dawley; Recombinant Proteins; Signal Transduction; Smad1 Protein; Smad5 Protein; Smad8 Protein; Tartrate-Resistant Acid Phosphatase; Tissue Engineering; Tissue Scaffolds; X-Ray Microtomography

Osteocytes are increasingly recognized as significant sources of osteoclast differentiation factor, receptor activator of nuclear factor-κB ligand (RANKL), and osteoblast differentiation inhibitory factor, sclerostin. In this study, RANKL and sclerostin expression of osteocytes is investigated in rats with ligature-induced periodontitis.. Rats were divided into control and periodontitis groups, and periodontitis was induced by ligature on the mandibular first molars. At 1, 3, 10, and 20 days after ligature, histologic analyses of alveolar bone (AB) and osteoid areas in the molar furcation were performed. The numbers of osteoclasts and RANKL- and sclerostin-positive osteocytes were estimated by tartrate-resistant acid phosphatase staining and immunohistochemistry, respectively.. The AB area gradually decreased at day 10 after ligature and increased at day 20. The number of osteoclasts markedly increased at day 3 and then decreased. Conversely, osteoid formation was suppressed up to day 3 and then showed a remarkable increase above control level at day 20. The number of RANKL-positive osteocytes increased at days 1 and 3 and then decreased. Sclerostin-positive osteocytes markedly increased at days 3 and 10 but decreased below control level at day 20.. These results show that AB loss is accompanied by enhanced osteoclast formation and suppressed osteoid formation. Osteocytes express RANKL when osteoclast formation increases, and they express sclerostin when osteoid formation is suppressed. Conversely, osteocytic sclerostin expression decreases when osteoid formation increases. These findings suggest that osteocytes may be important in AB loss via RANKL and sclerostin expression in periodontitis.

Topics: Acid Phosphatase; Alveolar Bone Loss; Alveolar Process; Animals; Apoptosis; Bone Matrix; Bone Morphogenetic Proteins; Genetic Markers; Isoenzymes; Leukocytes, Mononuclear; Male; Mandibular Diseases; Neutrophils; Osteoclasts; Osteocytes; Periodontitis; Random Allocation; RANK Ligand; Rats; Rats, Inbred F344; Tartrate-Resistant Acid Phosphatase; Time Factors

This study evaluates the influence of platelet-rich plasma derived from bone marrow aspirate (PRP-BMA) on the healing of periodontal fenestration defects in rats.. Periodontal fenestration defects were surgically created in the mandibles of 40 rats. The animals were randomly divided into two groups, control and PRP-BMA, in which defects were filled with blood clot or PRP-bma, respectively. Animals were euthanized at either 10 or 30 days post-surgery. Histologic, histometric, and immunohistochemical analyses were performed. Percentage of new bone area (NBA), area of bone trabeculae (ABT), new cementum (NC), and extension of remaining defect were histometrically evaluated. Proliferating cell nuclear antigen (PCNA), bone sialoprotein (BSP), osteocalcin (OCN), and tartrate-resistant acid phosphatase (TRAP) immunohistochemical staining were performed. Immunolabeled cells were quantified. Data were statistically analyzed (analysis of variance; Tukey, P <0.05).. At 10 days, control and PRP-BMA groups presented similar amounts of NBA and ABT; NC formation was not observed. At 30 days, control and PRP-BMA groups presented similar amounts of NBA and ABT; the PRP-BMA group showed NC formation with collagen fibers inserted obliquely or perpendicularly to the root surface. NC formation was not observed in any control group specimen. PRP- BMA presented higher numbers of PCNA-positive and BSP-positive cells than control at 10 and 30 days post-surgery. No significant differences in the number of either OCN-positive or TRAP-positive cells were observed between groups at 10 or 30 days.. PRP-BMA promoted NC formation with a functional periodontal ligament when applied at experimental periodontal fenestration defects.

Topics: Acid Phosphatase; Alveolar Bone Loss; Animals; Blood Coagulation; Bone Marrow Cells; Bone Regeneration; Cementogenesis; Collagen; Connective Tissue; Dental Cementum; Inflammation; Integrin-Binding Sialoprotein; Isoenzymes; Male; Mandibular Diseases; Necrosis; Osteocalcin; Osteogenesis; Periodontal Ligament; Platelet Count; Platelet-Rich Plasma; Proliferating Cell Nuclear Antigen; Random Allocation; Rats; Rats, Wistar; Tartrate-Resistant Acid Phosphatase; Time Factors

Pathological alterations in the balance of bone metabolism are central to the progression of inflammatory bone diseases such as periodontal disease. We have developed and characterized a novel ex vivo murine mandible model of inflammatory bone destruction. Slices of mandible were cultured for 14 days in the presence or absence of P. gingivalis lipopolysaccharide (LPS) or pro-inflammatory cytokines. Following culture, cell viability and tissue histomorphometry were assessed with quantification of matrix proteins, resident osteoclasts, ligament cells, monocytes, macrophages, and neutrophils. In the absence of inflammatory factors, culture viability, osteoclasts, and matrix components were maintained. LPS or TNFα stimulation demonstrated an increase in cellular proliferation, monocyte cells, osteoclast differentiation, and matrix degradation. Pathophysiological bone metabolism can be induced via exposure to LPS and direct influence of TNFα within the model despite the absence of systemic circulation, providing a model for inflammatory bone destruction and investigation of the effects of novel therapeutics.

Topics: Acid Phosphatase; Alveolar Bone Loss; Animals; Cell Differentiation; Cell Proliferation; Cell Survival; Collagen Type I; Disease Models, Animal; Extracellular Matrix Proteins; Inflammation Mediators; Integrin-Binding Sialoprotein; Interleukin-23; Interleukin-6; Isoenzymes; Lipopolysaccharides; Macrophages; Male; Mandibular Diseases; Mice; Monocytes; Neutrophils; Organ Culture Techniques; Osteocalcin; Osteoclasts; Osteopontin; Periodontal Ligament; Periodontitis; Porphyromonas gingivalis; Tartrate-Resistant Acid Phosphatase; Tumor Necrosis Factor-alpha

The management of bisphosphonate-related osteonecrosis of the jaw (BRONJ) is still difficult in many cases that do not respond to conservative treatments. We report a case of BRONJ treated by adjunctive teriparatide therapy for 6 months with monitoring of bone turnover markers (at baseline, at 1, 3, and 6 months of treatment, and after 9 months off therapy) and bone scintigraphy (at baseline, 3 and 6 months, and after 9 months off therapy). The patient was a 78-year-old woman with osteoporosis and BRONJ. She had not responded to previous conventional treatment. Teriparatide was added for resolution of BRONJ. The pain disappeared after 1 month, and remarkable bone regeneration was obtained after 6 months, with significantly increasing bone formation and resorption markers. Bone scintigraphy showed regression of the uptake area. This case suggests the usefulness of monitoring bone turnover markers and using bone scintigraphy to increase the effectiveness of teriparatide therapy.

Topics: Acid Phosphatase; Aged; Alendronate; Alkaline Phosphatase; Amino Acids; Biomarkers; Bisphosphonate-Associated Osteonecrosis of the Jaw; Bone Density Conservation Agents; Bone Regeneration; Bone Resorption; Collagen Type I; Female; Follow-Up Studies; Humans; Isoenzymes; Mandible; Mandibular Diseases; Osteocalcin; Osteogenesis; Peptide Fragments; Peptides; Procollagen; Radionuclide Imaging; Radiopharmaceuticals; Tartrate-Resistant Acid Phosphatase; Technetium Tc 99m Medronate; Teriparatide

The purpose of this study was to examine histological alterations on osteoblasts from the alveolar bone of transgenic mice with targeted ablation of osteoctyes. Eighteen weeks-old transgenic mice based on the diphtheria toxin (DT) receptor-mediated cell knockout (TRECK) system were used in these experiments. Mice were injected intraperitoneally with 50 µg/kg of DT in PBS, or only PBS as control. Two weeks after injections, mice were subjected to transcardiac perfusion with 4% paraformaldehyde in 0.1M phosphate buffer (pH 7.4), and the available alveolar bone was removed for histochemical analyses. Approximately 75% of osteocytes from alveolar bones became apoptotic after DT administration, and most osteocytic lacunae became empty. Osteoblastic numbers and alkaline phosphatase (ALP) activity were markedly reduced at the endosteum of alveolar bone after DT administration compared with the control. Osteoblastic ALP activity in the periodontal ligament region, on the other hand, hardly showed any differences between the two groups even though numbers were reduced in the experiment group. Silver impregnation showed a difference in the distribution of bone canaliculi between the portions near the endosteum and the periodontal ligament: the former appeared regularly arranged in contrast to the latter's irregular distribution. Under transmission electron microscopy (TEM), the osteoblasts in the periodontal ligament showed direct contact with the Sharpey's fibers. Thus, osteoblastic activity was affected by osteocyte ablation in general, but osteoblasts in contact with the periodontal ligament were less affected than endosteal osteoblasts.

Topics: Ablation Techniques; Acid Phosphatase; Alkaline Phosphatase; Alveolar Bone Loss; Alveolar Process; Animals; Biomarkers; Bone Density; Diphtheria Toxin; Disease Models, Animal; Isoenzymes; Mandibular Diseases; Mice; Mice, Transgenic; Osteoclasts; Osteocytes; Periodontal Ligament; RANK Ligand; Silver Staining; Tartrate-Resistant Acid Phosphatase

Bone loss associated with cyclosporin A (CsA) therapy can result in serious morbidity to patients. Intermittent administration of 1,25 Vitamin D and calcitonin reduces osteopenia in a murine model of postmenopausal osteoporosis. The purpose of this study was to evaluate the effects of this therapeutic approach on CsA-induced alveolar bone loss in rats. Forty male Wistar rats were allocated to four experimental groups according to the treatment received during 8 weeks: (1) CsA (10 mg/kg/day, s.c.); (2) 1,25 Vitamin D (2 microg/kg, p.o.; in weeks 1, 3, 5, and 7) plus calcitonin (2 microg/kg, i.p.; in weeks 2, 4, 6, and 8); (3) CsA concurrently with intermittent 1,25 Vitamin D and calcitonin administration; and (4) the control treatment group (vehicle). At the end of the 8-week treatment period, serum concentrations of bone-specific alkaline phosphatase, tartrate-resistant acid phosphatase (TRAP-5b), osteocalcin, interleukin (IL)-1 beta, IL-6, and tumor necrosis factor alpha (TNF-alpha) were measured and an analysis of bone volume, bone surface, number of osteoblasts, and osteoclasts was performed. CsA administration resulted in significant alveolar bone resorption, as assessed by a lower bone volume and an increased number of osteoclasts, and increased serum bone-specific alkaline phosphatase, TRAP-5b, IL-1 beta, IL-6, and TNF-alpha concentrations. The intermittent administration of calcitriol and calcitonin prevented the CsA-induced osteopenic changes and the increased serum concentrations of TRAP-5b and inflammatory cytokines. Intermittent calcitriol/calcitonin therapy prevents CsA-induced alveolar bone loss in rats and normalizes the production of associated inflammatory mediators.

Topics: Acid Phosphatase; Administration, Oral; Alveolar Bone Loss; Animals; Bone Density Conservation Agents; Calcitonin; Calcitriol; Cell Count; Cyclosporine; Drug Administration Schedule; Interleukins; Isoenzymes; Male; Mandibular Diseases; Osteoclasts; Rats; Rats, Wistar; Tartrate-Resistant Acid Phosphatase; Tumor Necrosis Factor-alpha

Tobacco use is the most significant risk factor of periodontal disease. Clinical evidence has demonstrated that tobacco may negatively influence the results after surgical and non-surgical periodontal therapy. Enamel matrix derivative (EMD) have been used in periodontal regenerative procedures resulting in improvement of clinical parameters. The effect of EMD in the presence of tobacco compounds is unclear. Thus, the aim of the present study is to evaluate the impact of cigarette smoke inhalation (CSI) on the results of EMD treatment.. Twenty-two Wistar rats were assigned to two groups: Group 1, CSI (n = 11); Group 2, non-exposed (n = 11). Thirty days after initiation of CSI, fenestration defects were created at the buccal aspect of the first mandibular molar. The study followed a split-mouth design. After the surgeries the defects were randomly assigned to two subgroups: non-treated control and treated with EMD. The animals were sacrificed 21 days later and the percentage of defect fill, density of newly formed bone, and new cementum formation were histometrically assessed. The number of osteoclasts was determined by tartrate-resistant acid phosphatase.. CSI was associated with less bone density compared to the non-exposed group. EMD provided an increased defect fill and new cementum formation in both groups. The number of tartrate-resistant acid phosphatase-positive osteoclasts was significantly higher in the CSI non-treated control group compared to the non-treated control of the non-exposed animals.. EMD may provide increased defect fill and cementum formation in the presence or absence of CSI. However, tobacco smoke produced a detrimental effect on bone healing when density of newly formed bone was considered.

Topics: Acid Phosphatase; Alveolar Bone Loss; Animals; Biomarkers; Bone Density; Calcification, Physiologic; Cementogenesis; Dental Enamel Proteins; Guided Tissue Regeneration, Periodontal; Image Processing, Computer-Assisted; Isoenzymes; Male; Mandible; Mandibular Diseases; Molar; Osteoclasts; Osteogenesis; Random Allocation; Rats; Rats, Wistar; Tartrate-Resistant Acid Phosphatase; Time Factors; Tobacco Smoke Pollution; Treatment Outcome

The purpose of this study was to investigate the activation of p38 mitogen-activated protein kinase (MAPK) during the development of periapical lesions in rats. Periapical lesions developed within 28 days after pulp exposure of mandibular first molars in Wistar rats. The animals were sacrificed randomly at 0, 7, 14, 21, and 28 days after pulpal exposure. The jaws that contained the first molar were obtained and routinely prepared for immunohistochemistry and enzyme histochemistry. A few phosphorylated p38 MAPK (P-p38)-positive cells and osteoclasts could be observed on day 7; both peaked in number on day 14. In the 21- and 28-day samples, the P-p38 MAPK expression decreased and fewer osteoclasts were observed. From day 7 to day 28, a significant positive correlation was found between P-p38 MAPK expression and osteoclasts. These findings showed that the activation of p38 MAPK might be associated with bone resorption in periapical lesions.

Topics: Acid Phosphatase; Alveolar Bone Loss; Animals; Biomarkers; Cell Count; Cell Nucleus; Coloring Agents; Dental Pulp Exposure; Enzyme Activation; Immunohistochemistry; Isoenzymes; Male; Mandibular Diseases; Osteoclasts; p38 Mitogen-Activated Protein Kinases; Periapical Diseases; Periapical Periodontitis; Random Allocation; Rats; Rats, Wistar; Tartrate-Resistant Acid Phosphatase

It has been shown that prostaglandin E2 (PGE2) locally released adjacent to the mandible over a 20-day period increases alveolar bone area, in part, due to a reduction in the percentage of eroded surface. To determine the effect of PGE2 on alveolar bone resorption, left mandibles from 24 Lewis rats were treated over a 20-day period with a local application of PGE2 (0.1, 0.05 or 0.025 mg/day) or placebo. The right side served as the non-treated matched control. Tissue sections were stained for tartrate resistant acid phosphatase (TRAP) calcitonin receptor (CTR) and metalloproteinase-2 (MMP-2). Matched samples were analysed by Wilcoxon matched pairs test and, a non-parametric one-way analysis of variance compared groups of treatment. Those tissues treated with PGE2 at doses of 0.1 and 0.05 mg/day showed significantly reduced numbers of TRAP and CTR-positive multinucleated cells compared with matched controls (p<0.005), as well as significantly reduced numbers of TRAP- and CTR-positive multinucleated cells when compared with the placebo-treated group (p<0.001). The number of periodontal ligament cells expressing MMP-2 was also significantly reduced in tissues treated with the two higher doses of PGE2 (p<0.001) comparing with both matched controls and the placebo-treated group. Following a 20-day period, locally released PGE2 at doses of 0.1 and 0.05 mg/day appears to affect alveolar bone resorption in the periodontium of rats, as the number of multinucleated cells expressing TRAP and CTR are significantly reduced. Furthermore, the same doses of PGE2 also significantly reduced the expression of MMP-2 by the periodontal cells.

Topics: Acid Phosphatase; Alveolar Bone Loss; Animals; Bone Resorption; Cell Count; Dinoprostone; Female; Immunohistochemistry; Isoenzymes; Mandibular Diseases; Matrix Metalloproteinase 2; Periodontium; Rats; Rats, Inbred Lew; Receptors, Calcitonin; Tartrate-Resistant Acid Phosphatase

Giant cell granuloma (GCG) is an osteolytic tumour of the jaw which is characterised by the presence of both mononuclear and multinucleated (osteoclast-like) giant cell components. The nature of these component cells and the pathogenesis of the extensive osteolysis associated with this lesion is uncertain.. Using cell culture techniques and immunohistochemistry, we defined the phenotypic characteristics of the mononuclear and multinucleated cells present in four cases of GCG of the jaw. We also analysed the cellular and humoral factors associated with osteoclast formation and osteolysis in these tumours and determined whether GCG stromal cells are capable of supporting osteoclast formation.. GCG-derived giant cells expressed the phenotypic characteristics of osteoclasts (TRAP+, VNR+, and calcitonin responsive) and were capable of lacunar resorption. In addition to macrophages, the mononuclear cell population contained numerous spindle-shaped stromal cells which proliferated in culture and expressed RANKL; these GCG-stromal cells were capable of supporting human osteoclast formation from circulating monocyte precursors.. Our findings indicate that the giant cells in GCG of the jaw are osteoclast-like and formed from monocyte/macrophage precursors which differentiate into osteoclasts under the influence of RANKL-expressing mononuclear stromal cells found in this lesion.

Topics: Acid Phosphatase; Adult; Biomarkers; Bone Resorption; Calcitonin; Carrier Proteins; Cell Culture Techniques; Cell Differentiation; Cell Division; Child; Female; Giant Cells; Granuloma, Giant Cell; Humans; Isoenzymes; Macrophages; Male; Mandibular Diseases; Membrane Glycoproteins; Middle Aged; NF-kappa B; Osteoclasts; Osteolysis; Phenotype; RANK Ligand; Receptor Activator of Nuclear Factor-kappa B; Receptors, Vitronectin; Tartrate-Resistant Acid Phosphatase

The present study was undertaken to determine the frequency and extent of apical root resorption associated with induced periradicular lesions in mice.. Bone and root resorption was quantified by using two- and three-dimensional micro-computed tomography (mu-CT) in the lower first molars of mice subjected to pulp exposure and infection.. mu-CT measurements showed significant apical resorption in exposed and infected teeth, resulting in an average distal root shortening of 12.7% (P <.001 vs unexposed). These findings were confirmed with three-dimensional reconstituted images that showed thinning and shortening of the distal root. Tartrate-resistant acid phosphatase clastic cells were associated with resorption lacunae on the cementum of root apices, as well as on bone at the periphery of the periradicular lesions. Brown and Brenn staining showed the presence of bacteria in dentinal tubules adjacent to resorbed cementum.. Apical root resorption is a prominent and consistent finding associated with periradicular infection in the mouse. This species represents a convenient model for studying the pathogenesis of inflammatory root resorption in vivo.

Topics: Acid Phosphatase; Animals; Biomarkers; Bone Resorption; Coloring Agents; Dental Cementum; Dental Pulp Diseases; Dental Pulp Exposure; Dentin; Disease Models, Animal; Gram-Negative Bacteria; Image Processing, Computer-Assisted; Imaging, Three-Dimensional; Isoenzymes; Male; Mandibular Diseases; Mice; Mice, Inbred C57BL; Mice, Inbred Strains; Molar; Periapical Diseases; Regression Analysis; Root Resorption; Statistics as Topic; Tartrate-Resistant Acid Phosphatase; Tomography, X-Ray Computed; Tooth Apex; Tooth Root