acid-phosphatase has been researched along with Furcation-Defects* in 4 studies
4 other study(ies) available for acid-phosphatase and Furcation-Defects
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Introduction of a mixture of β-tricalcium phosphate into a complex of bone marrow mesenchymal stem cells and type I collagen can augment the volume of alveolar bone without impairing cementum regeneration.
The purpose of this study is to evaluate whether β-tricalcium phosphate (β-TCP) could be a promising modality to help augment alveolar bone in periodontal tissue regeneration by bone marrow mesenchymal stem cells (BMMSCs).. Expanded BMMSCs and atelocollagen (Col) were mixed together (MSC/Col). A combination of β-TCP with MSC/Col was also prepared (MSC/Col/TCP). MSC/Col/TCP or MSC/Col was transplanted into experimental periodontal Class III furcation defects that had been exposed to inflammation in beagle dogs. Periodontal tissue regeneration was evaluated by histologic and morphometric analyses at 4 and 8 weeks after transplantation.. MSC/Col and MSC/Col/TCP enhanced periodontal tissue regeneration compared to Col and TCP/Col according to hematoxylin and eosin staining. The percentage of new cementum length in the MSC/Col/TCP group was not significantly different from that in the MSC/Col group at 4 and 8 weeks. On the other hand, the percentage of new bone area in the MSC/Col/TCP group was much higher than that in the MSC/TCP group at 4 weeks. However, at 8 weeks, no significant difference in new bone area was found between the two groups. In the MSC/Col/TCP group, β-TCP was surrounded by newly formed bone. Multinucleated cells, which were positive for osteopontin and tartrate-resistant acid phosphatase, were present in the interconnected macropores of β-TCP.. These findings suggest that β-TCP is applicable as a scaffold for BMMSCs transplantation and helps augment alveolar bone without impairing regeneration of cementum. Topics: Acid Phosphatase; Alveolar Process; Animals; Bone Regeneration; Calcium Phosphates; Cell Culture Techniques; Cementogenesis; Collagen; Collagen Type I; Dental Cementum; Disease Models, Animal; Dogs; Female; Furcation Defects; Giant Cells; Guided Tissue Regeneration, Periodontal; Isoenzymes; Mesenchymal Stem Cell Transplantation; Organ Size; Osteogenesis; Osteopontin; Tartrate-Resistant Acid Phosphatase; Tissue Scaffolds; Tooth Ankylosis; Tooth Root | 2015 |
Cigarette smoke inhalation increases the alveolar bone loss caused by primary occlusal trauma in a rat model.
Occlusal trauma (OT) and smoking are both factors that alter alveolar bone metabolism and therefore could synergistically act on alveolar bone loss. The aim of this experimental study was to evaluate the influence of short-term cigarette smoke inhalation (CSI) on inter-radicular alveolar bone loss promoted by primary OT in a rat model.. Forty-eight animals were randomly assigned to one of three groups based on treatment type: OT + CSI (n = 16), animals were exposed to CSI three times per day, for 8 min per exposure, and they concomitantly received unilateral vertical augmentation creating an occlusal interference inducing experimental OT; OT (n = 16), animals received only unilateral vertical augmentation; negative control (NC; n = 16), animals maintained for equal periods to achieve periodontal baseline values of periodontal ligament dimension. Each group was divided into two subgroups (n = 8) based on treatment length: 7 or 14 d.. After 7 d, the OT + CSI group exhibited significantly higher bone loss compared to the NC group (p = 0.0022). After 14 d, the OT (p < 0.0001) and OT + CSI (p < 0.0001) groups presented significantly higher bone loss compared to the NC group, and OT + CSI resulted in significantly higher bone loss than OT alone (p = 0.0241). The number of tartrate-resistant acid phosphatase-positive cells on the linear surface of the bone crest after 7 d was significantly higher in the OT + CSI group as compared to the NC and OT groups (p < 0.0001 and p = 0.0045, respectively) and remained significantly higher in the OT + CSI group after 14 d, compared to the OT group (p < 0.0001).. Short-term CSI increases early bone loss in association with OT after 7 d, and this worsens in severity after 14 d of exposure. Topics: Acid Phosphatase; Alveolar Bone Loss; Alveolar Process; Animals; Biomarkers; Dental Occlusion, Traumatic; Disease Models, Animal; Disease Progression; Furcation Defects; Isoenzymes; Male; Random Allocation; Rats; Rats, Wistar; Smoking; Tartrate-Resistant Acid Phosphatase; Time Factors | 2014 |
Periodontal regeneration following application of basic fibroblast growth factor-2 in combination with beta tricalcium phosphate in class III furcation defects in dogs.
The aim of this study was to investigate the effect of tunnel structured β-tricalcium phosphate (β-TCP) on the regenerative potential of basic fibroblast growth factor-2 (bFGF-2) in class III furcation defects in dogs. The furcations of 30 mandibular premolar teeth received: 1) 0.3% bFGF-2 solution in conjunction with β-TCP; 2) 0.3% bFGF-2 solution; and 3) no implant material (Control group). The dogs were sacrificed 8 weeks post-surgery, and healing was evaluated histologically. New bone formation was significantly greater in the bFGF-2/β-TCP group compared to the bFGF-2 solution and Control groups (p<0.01). New cementum formation in the bFGF-2/β-TCP and bFGF-2 solution groups was significantly greater than that in the Control group (p<0.01). These findings suggested that bFGF-2 alone enhances connective tissue attachment in a manner similar to the combination of bFGF-2 and β-TCP. Furthermore, this combination enhances bone formation up to the fornix in class III furcation defects. Topics: Acid Phosphatase; Animals; Bicuspid; Biocompatible Materials; Biomarkers; Bone Substitutes; Calcium Phosphates; Cementogenesis; Collagen; Connective Tissue; Dogs; Epithelium; Female; Fibroblast Growth Factor 2; Furcation Defects; Guided Tissue Regeneration, Periodontal; Isoenzymes; Osteogenesis; Periodontal Ligament; Random Allocation; Regeneration; Root Planing; Root Resorption; Tartrate-Resistant Acid Phosphatase; Tooth Ankylosis | 2013 |
The influence of thyroid hormones on periodontitis-related bone loss and tooth-supporting alveolar bone: a histological study in rats.
Recent studies have pointed to potentially periodontal risk indicators, however no information is available on the impact of changes in thyroid hormone levels on the progression of periodontitis and on the quality of alveolar bone. Thus, the aim of the present study was to evaluate histologically, in rats, the influence of thyroid hormones on the rate of periodontal bone loss resulting from ligature placement and on the quality of tooth-supporting alveolar bone.. Thirty-six male Wistar rats were randomly assigned to the following groups: healthy (control, n = 12), hypothyroidism (n = 12) and hyperthyroidism (n = 12). Once alterations were confirmed by total serum levels of triiodothyronine and thyroxine, ligatures were randomly placed around one of the first mandibular molars. Thirty days later, the animals were killed and specimens routinely processed for serial decalcified sections. The parameters assessed were periodontitis-related bone loss, quality of tooth-supporting alveolar bone and the number of cells positive for tartrate-resistant acid phosphatase (TRAP), a marker of bone resorption.. At the ligated sites, intergroup analysis revealed that hypothyroidism significantly increased the bone loss resulting from ligature-induced periodontitis (p = 0.02) and the number of TRAP-positive cells on the linear surface of bone crest (p = 0.01). In addition, no significant differences were detected regarding the quality of the bone (p = 0.24) or the number of TRAP-positive cells in the area of the interradicular bone for ligated teeth among the groups (p = 0.17).. It may be concluded that decreased serum levels of thyroid hormones may enhance periodontitis-related bone loss, as a function of an increased number of resorbing cells, whereas the tooth-supporting alveolar bone seems to be less sensitive to alterations in hormone levels. Topics: Acid Phosphatase; Alveolar Bone Loss; Alveolar Process; Animals; Biomarkers; Bone Density; Disease Progression; Furcation Defects; Gingivitis; Hyperthyroidism; Hypothyroidism; Isoenzymes; Male; Periodontitis; Random Allocation; Rats; Rats, Wistar; Tartrate-Resistant Acid Phosphatase; Thyroid Hormones; Thyroxine; Triiodothyronine | 2009 |