acid-phosphatase and Maxillary-Diseases

Statins are inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A reductase and have anti-inflammatory effects independent of cholesterol lowering. Recent clinical studies have indicated that statin intake has a beneficial effect on periodontal disease. However, the underlying mechanisms have not been well understood. In the current study, we employed a rat model with lipopolysaccharide (LPS)-induced periodontal disease and determined the effect of simvastatin, a commonly prescribed statin, on osteoclastogenesis, gingival inflammation and alveolar bone loss.. Sprague-Dawley rats were injected with Aggregatibacter actinomycetemcomitans LPS in periodontal tissue three times per week for 8 wk and part of the rats with LPS injection were also given simvastatin via gavage. After the treatments, the rat maxillae were scanned by microcomputed tomography and the images were analyzed to determine alveolar bone loss. To explore the underlying mechanisms, the effect of simvastatin on osteoclastogenesis and gingival expression of proinflammatory cytokines were also determined by tartrate-resistant acid phosphatase staining and real-time polymerase chain reaction assays, respectively.. Results showed that LPS treatment markedly increased bone loss, but administration of simvastatin significantly alleviated the bone loss. Results also showed that LPS treatment stimulated osteoclastogenesis and the expression of inflammatory cytokines, but simvastatin significantly modulates the stimulatory effect of LPS on osteoclastogenesis and cytokine expression.. This study demonstrated that simvastatin treatment inhibits LPS-induced osteoclastogenesis and gingival inflammation and reduces alveolar bone loss, indicating that the intake of simvastatin may hinder the progression of periodontal disease.

Topics: Acid Phosphatase; Aggregatibacter actinomycetemcomitans; Alveolar Bone Loss; Animals; Anti-Inflammatory Agents; Cytokines; Disease Models, Animal; Gingiva; Gingivitis; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Inflammation Mediators; Isoenzymes; Lipopolysaccharides; Matrix Metalloproteinase 9; Maxillary Diseases; Osteoclasts; Periodontal Diseases; Rats; Rats, Sprague-Dawley; Simvastatin; Tartrate-Resistant Acid Phosphatase; Toll-Like Receptors; X-Ray Microtomography

This study aimed to evaluate the adjunctive effect of LED light in platelet-derived growth factor (PDGF)-aided dentoalveolar osteogenesis.. Full-thickness osseous wounds were created on rat maxillae and were either unfilled or filled with poly-(D,L-lactide) and poly-(D,L-lactide-co-glycolide) microspheres encapsulating PDGF. Animals received daily 660 ± 25 nm LED light irradiation at 0, 10 (LD), or 20 (HD) J/cm(2) , were killed at days 4-28 (n = 6/group/time) and evaluated by microcomputed tomography (micro-CT), histology, and the expressions of osteopontin and tartrate-resistant acid phosphatase (TRAP).. Greater osteogenesis was noted in the PDGF-treated defects at day 14. Under the LED light irradiation, osteogenesis was significantly greater in both LD and HD groups of the non-PDGF-treated defects, but only in the LD group of the PDGF-treated defects. No significant differences in osteogenesis among groups were noted at day 28. Greater bone marrow space was noted in the LED light-irradiated specimens, especially in the PDGF-treated defects at both time points. Osteopontin was significantly promoted in the LD group at both time points, and TRAP was significantly promoted in all LED light-irradiated groups at day 28.. LED light could an adjunct to promote early PDGF-aided dentoalveolar osteogenesis by facilitating the osteoblast-osteoclast coupling.

Topics: Acid Phosphatase; Animals; Becaplermin; Biocompatible Materials; Bone Density; Bone Marrow; Combined Modality Therapy; Drug Carriers; Isoenzymes; Lactic Acid; Low-Level Light Therapy; Male; Maxillary Diseases; Microspheres; Osteoblasts; Osteoclasts; Osteogenesis; Osteopontin; Polyesters; Polyglycolic Acid; Polylactic Acid-Polyglycolic Acid Copolymer; Proto-Oncogene Proteins c-sis; Random Allocation; Rats; Rats, Sprague-Dawley; Tartrate-Resistant Acid Phosphatase; Time Factors; Tooth Socket; X-Ray Microtomography

Micro-CT provides three-dimensional details and has been widely used for biomedical assessments. This study aimed to determine the most appropriate threshold method for quantitatively assessing the dynamics of periodontal destruction.. Inflammation was induced by submerging a silk ligature in the sulcus of the maxillary second molars of rats, and the animals were killed prior to ligature placement and after 7 and 21 days. The maxillae were examined for the bone resorptive activities by micro-CT, histology and tartrate-resistant acid phosphatase staining. The imaging threshold was determined by CT phantom, global and local algorithms. A bone fraction measurement from each threshold-determining technique was compared with histomorphometry. The reliability and reproducibility were examined by the intraclass correlation coefficient (ICC) and the coefficient of variation.. Significant reduction of inflammatory infiltration (p < 0.01) and active osteoclastic resorption (p < 0.05) from Day 7 to Day 21 were noted. High inter- and intraexaminer agreement were demonstrated in both histomorphometric and micro-CT assessments (ICC > 0.98). The algorithm-based technique demonstrated stronger correlation to histomorphometry than phantom-based thresholds, and the highest agreement was presented by the local algorithm (ICC > 0.96). This, however, was considerably computationally expensive.. The local threshold-determining algorithm is suggested for examining inflammation-induced bone loss. Further investigation will be aimed at enhancing computational efficiency.

Topics: Acid Phosphatase; Algorithms; Alveolar Bone Loss; Animals; Biomarkers; Collagen; Coloring Agents; Connective Tissue; Disease Models, Animal; Gingiva; Image Processing, Computer-Assisted; Imaging, Three-Dimensional; Isoenzymes; Male; Maxillary Diseases; Molar; Osteoclasts; Periodontitis; Phantoms, Imaging; Pilot Projects; Rats; Rats, Sprague-Dawley; Reproducibility of Results; Tartrate-Resistant Acid Phosphatase; Time Factors; Tooth Cervix; X-Ray Microtomography

The mitogen-activated protein (MAP) kinase phosphatase (MKP) family plays an important function in regulating the pro-inflammatory cytokines by deactivating MAP kinases. MKP-1 is essential for the dephosphorylation of p38 MAP kinase that regulates expression of IL-6, TNF-alpha, and IL-1 beta. We hypothesized that MKP-1 regulates inflammatory bone loss in experimental periodontitis. Wild-type and Mkp-1(-/-) mice received A. actinomycetemcomitans LPS injection in the palatal region or PBS control 3 times/wk for 30 days. Mice were killed, and maxillae were assessed by microcomputed tomography, histological analysis, and TRAP staining for measurement of bone loss, extent of inflammation, and degree of osteoclastogenesis. Results indicated that, in LPS-injected Mkp-1(-/-) mice, significantly greater bone loss occurred with more inflammatory infiltrate and a significant increase in osteoclastogenesis compared with Mkp-1(-/-) control sites or either wild-type group. Analysis of these data indicates that MKP-1 plays a key role in the regulation of inflammatory bone loss.

Topics: Acid Phosphatase; Aggregatibacter actinomycetemcomitans; Alveolar Bone Loss; Animals; Biomarkers; Cell Count; Cell Line; Cone-Beam Computed Tomography; Dual Specificity Phosphatase 1; Imaging, Three-Dimensional; Immunity, Innate; Interleukin-6; Isoenzymes; Leukocytes; Lipopolysaccharides; Maxillary Diseases; Mice; Mice, Knockout; Osteoclasts; p38 Mitogen-Activated Protein Kinases; Palate; Periodontitis; Phosphorylation; Tartrate-Resistant Acid Phosphatase; Time Factors; X-Ray Microtomography

We examined whether topical administration of a bisphosphonate clodronate could prevent alveolar bone loss in rats with experimental periodontitis.. On day 0, elastic rings were placed around the cervix of the right and left maxillary first molars (M1) to induce inflammatory periodontitis. Fifty microl of clodronate solution at a concentration of either 0 (0.9% NaCl), 20, 40, or 60 mM was injected into the subperiosteal palatal area adjacent to the interdental area between M1 and M2 on either the left or right (experimental) side on days 0, 2, 4, and 6. The contralateral side served as a control and received 0.9% NaCl solution without clodronate. The animals were sacrificed on day 7.. Histological examination and determination of bone mineral density in the interdental alveolar bone area between M1 and M2 revealed that placement of an elastic ring caused severe vertical and horizontal bone resorption on the control side, while the topical administration of clodronate significantly prevented such alveolar bone loss. The number of osteoclasts on the experimental side was decreased compared with the control side. Furthermore, many of the osteoclasts on the experimental side were detached from the surface of the alveolar bone and had degenerated appearances, such as rounded shapes and a loss of polarity.. These results suggest that topical administration of clodronate may be effective in preventing osteoclastic bone resorption in periodontitis.

Topics: Acid Phosphatase; Administration, Topical; Alveolar Bone Loss; Analysis of Variance; Animals; Antimetabolites; Azo Compounds; Biomarkers; Bone Density; Bone Resorption; Cell Count; Clodronic Acid; Coloring Agents; Disease Models, Animal; Eosine Yellowish-(YS); Fluorescent Dyes; Injections; Isoenzymes; Male; Maxillary Diseases; Methyl Green; Molar; Osteoclasts; Periodontitis; Radiography; Rats; Rats, Wistar; Statistics as Topic; Tartrate-Resistant Acid Phosphatase

The effects of recombinant human interleukin-1 beta (rhIL-1 beta) on alveolar bone resorptive activity in rats were examined. Continuous administration of rhIL-1 beta or phosphate-buffered saline (PBS) was given via osmotic pumps for 3, 7 and 14 days to rats with silk ligatures around second maxillary molars. Other animals without ligatures received insertion of pumps containing rhIL-1 beta or remained untreated. Sections were subject to three different stains:--hematoxylin and eosin (H-E) for histology, acid phosphatase (ACPase) activity for osteoclast detection, and immunohistochemistry using anti-rat monocyte/macrophage monoclonal antibody (ED 1). In addition, body weight, plasma calcium and phosphorus levels were monitored. The mean body weight of rats receiving rhIL-1 beta was significantly lower (P < 0.05 to P < 0.01) compared with untreated rats throughout the experimental period. On Day 7, plasma calcium and phosphorus levels were significantly lower in rats receiving rhIL-1 beta than in rats receiving PBS only (P < 0.05). Sections revealed a moderate inflammatory cell infiltrate reaching near the alveolar crest in both groups with ligatures on Day 3. Only rats receiving rhIL-1 beta exhibited enhancement of inflammatory cell invasion on Days 7 and 14. In rats receiving rhIL-1 beta with ligatures, numerous resorption lacunae containing ACPase-positive multinucleated giant cells (MNGCs), coinciding with ED1-positive cells, were located on the mesial side of the septum where extensive bone resorption had occurred throughout the experimental period. In animals receiving rhIL-1 beta without ligatures, compared with untreated rats, increased ACPase-positive cells were observed on the mesial side of the septum on Day 3. In animals receiving PBS only, a few ACPase-positive cells were observed confined to the mesial regions where slight bone resorption occurred on Days 7 and 14. These results indicate that the administration of rhIL-1 beta accelerated alveolar bone destruction in ligature-induced periodontal tissue inflammation over a two-week period.

Topics: Acid Phosphatase; Alveolar Bone Loss; Animals; Antibodies, Monoclonal; Body Weight; Bone Resorption; Calcium; Coloring Agents; Giant Cells; Humans; Immunohistochemistry; Infusion Pumps; Insect Proteins; Interleukin-1; Ligation; Macrophages; Male; Maxillary Diseases; Molar; Monocytes; Osteoclasts; Periodontitis; Phosphorus; Proteins; Rats; Rats, Wistar; Recombinant Proteins; Silk; Sutures