Spontaneous Periodontal Disease Research Articles

Effects of Autologous Platelet-Rich Fibrin in Post-Extraction Alveolar Sockets: A Randomized, Controlled Split-Mouth Trial in Dogs with Spontaneous Periodontal Disease.

Simple SummaryThe effects of autologous platelet-rich fibrin were evaluated in dogs with spontaneous periodontal disease after tooth extraction. Both radiographic and histological findings attributed to the platelet-rich fibrin a potential ability to stimulate the natural process of tissue healing and regeneration of bone and soft tissues. Platelet-rich fibrin could, therefore, be considered as a simple and effective therapeutic aid in the management of post-extraction socket healing in dogs. Periodontal disease (PD) is a common inflammatory condition in dogs; in severe stages, dental extraction is frequently required. Platelet-rich fibrin (PRF) has been used in human oral surgical procedures and has been experimentally tested on post-extraction sockets in healthy dogs. This is the first split-mouth, randomized, controlled trial designed to compare post-extractive alveolar socket healing with and without topical application of PRF in canine spontaneous PD. Clinical evaluation, radiographic density, and histological scores for inflammation and regeneration were assessed at recruitment (T0) and after a three-week follow up (T1) on 12 dogs, for a total of 31 pairs of sockets. No complications or clinically evident differences between the treated sites and the control sites were observed. Comparing the radiographic densities of the extraction sites measured at T0 and T1, a significant enhancement was observed within the PRF group, but not within control group. The histological score decreased significantly from T0 to T1 within group PRF, but not within the control group; at T1, the PRF group showed a significantly lower histological score than the control group. These findings suggest that PRF could be able to stimulate the natural process of tissue healing and regeneration of post-extraction sites in dogs with spontaneous periodontal disease (PD).

High-fat diet-induced obesity triggers alveolar bone loss and spontaneous periodontal disease in growing mice.

BackgroundThe relationship between high-fat food consumption and obesity is well-established. However, it is as yet unclear whether high-fat diet (HFD)-induced obesity in childhood and adolescence determines age-related changes in jaw bone health. The aim of this study is to examine the age-related influence of HFD-induced obesity on mandibular bone architecture and the structure of the periodontium in growing mice.MethodsMale C57BL/6 J mice (6-weeks-old) were divided into two groups (n = 6 each): the control group received a control diet and the experimental group a HFD. After treatment for 4, 8, or 12 weeks, trabecular and cortical bone architecture was assessed using micro-computed tomography. The periodontium and alveolar bone structure were evaluated by histopathology.ResultsIn HFD mice, body weight, serum total cholesterol, and serum leptin levels were significantly higher than those in age-matched control mice (p < 0.05, all comparisons). Reductions in trabecular bone volume and in cortical bone growth (measured as the thickness and cross sectional area) in HFD mice were significant compared with the control mice after 4 weeks of treatment (p < 0.05, both comparisons). Significant decreases in cortical bone density in HFD-fed vs. age-matched control mice were determined after 12 weeks (p < 0.05). In the HFD mice, the periodontal ligament fibres were disrupted, having lost their orientation with respect to the bone surface, and constriction of the periodontal ligament space was inhibited.ConclusionsThese results suggest that HFD-induced obesity during growth not only triggers mandibular osteoporosis but also increases the risk of spontaneous periodontal disease.

Occurrence of spontaneous periodontal disease in the SAMP1/YitFc murine model of Crohn disease.

Oral involvement is often associated with inflammatory bowel disease (IBD). Recent evidence suggests a high incidence of periodontal disease in patients with Crohn disease (CD). To the best of the authors' knowledge, no animal model of IBD that displays associated periodontal disease was reported previously. The aim of this study is to investigate the occurrence and progression of periodontal disease in SAMP1/YitFc (SAMP) mice that spontaneously develop a CD-like ileitis. In addition, the temporal correlation between the onset and progression of periodontal disease and the onset of ileitis in SAMP mice was studied. At different time points, SAMP and parental AKR/J (AKR) control mice were sacrificed, and mandibles were prepared for stereomicroscopy and histology. Terminal ilea were collected for histologic assessment of inflammation score. Periodontal status, i.e., alveolar bone loss (ABL) and alveolar bone crest, was examined by stereomicroscopy and histomorphometry, respectively. ABL increased in both strains with age. SAMP mice showed greater ABL compared with AKR mice by 12 weeks of age, with maximal differences observed at 27 weeks of age. AKR control mice did not show the same severity of periodontal disease. Interestingly, a strong positive correlation was found between ileitis severity and ABL in SAMP mice, independent of age. The present results demonstrate the occurrence of periodontal disease in a mouse model of progressive CD-like ileitis. In addition, the severity of periodontitis strongly correlated with the severity of ileitis, independent of age, suggesting that common pathogenic mechanisms, such as abnormal immune response and dysbiosis, may be shared between these two phenotypes.

Effects of alcohol and/or tobacco exposure on spontaneous alveolar bone loss in rat.

The aim of the present study was to evaluate the effect of alcohol and/or tobacco exposure on spontaneous alveolar bone loss in Wistar rats. Twenty-four, male, 60 day-old, Wistar rats were assigned to 4 groups: Group 1 received 10 mL/kg of glucose solution (5%). Group 2 received 2 g/kg alcohol (20%). Group 3 was exposed to tobacco smoke (6 cigarettes/60 min). Group 4 received both interventions of groups 2 and 3. Alcohol was given by gastric gavage and cigarette exposure was performed using a forced ventilation chamber. After 30 days, animals were sacrificed and the upper maxillae removed and defleshed. Morphometric analysis of alveolar bone loss (ABL) around the second molar was performed in standardized digital photographs. Statistical analysis was conducted using paired t-test, one-way ANOVA and occurrence of spontaneous periodontal disease (ABL ≥ 0.39 mm) was analyzed by Fisher's exact test. Significant differences in body weight were observed between all groups. Group 2 presented higher body weight as compared to the 3 other groups at 4 weeks (p≤0.05). Mean ABL values were 0.31 mm (±0.08), 0.29 mm (±0.07), 0.33 mm (±0.10), and 0.33 mm (±0.08) for groups 1, 2, 3, and 4, respectively. No significant differences were found among groups. In the analysis of occurrence of periodontal breakdown, alcohol exposure decreased the occurrence of ABL and cigarette exposure increased ABL. The combination of alcohol and cigarette exposure did not differ from the control group. Alcohol consumption decreased the occurrence of periodontal breakdown, while tobacco increased this rate.

Obesity may increase the occurrence of spontaneous periodontal disease in Wistar rats

ObjectiveTo evaluate the effect of body weight on the occurrence of spontaneous alveolar bone loss in Wistar rats. MethodsTwenty-eight rats were randomly divided in two groups. Control group received standardized rat chow diet and water. Test group received cafeteria (CAF) diet during 17 weeks. Diet was available for both groups ad libitum. Body weight and Lee Index were evaluated. At the end of the experimental period, rats were killed by decapitation and maxillae were defleshed with 9% sodium hypochlorite. Morphometric analysis was performed in digital standard photographs. Presence of spontaneous periodontitis was considered when mean alveolar bone loss was ≥0.51mm (75th percentile). Statistical analysis was performed with chi-square test, Mann–Whitney test and independent samples t-test (significance level P≤0.05). ResultsAfter 17 weeks of exposure to standard CAF diet, a statistically significant mean difference in body weight (g±SD) (478±43 vs. 580±60) and Lee Index (3.07±0.05 vs. 3.24±0.07) was observed between control and obesity groups, respectively. Median (interquartile range) of alveolar bone loss in control group was 0.344 (0.313–0.367) and 0.491 (0.427–0.506) for buccal and palatal site, respectively. For obese group was 0.308 (0.289–0.354) and 0.549 (0.482–0.616) for buccal and palatal site, respectively. In animals submitted to CAF diet, 20 sites were classified as spontaneous periodontal disease, whereas in control animals, only 8 sites exhibited periodontal breakdown according cut-off point. A significant difference between groups was detected (P=0.009). ConclusionsIt may be concluded that obesity increases the occurrence of spontaneous periodontal disease in Wistar rats.

Measurements of eicosanoid and inflammatory cytokines in rats with spontaneous periodontal disease

Measurements of eicosanoid and inflammatory cytokines in rats with spontaneous periodontal disease

自然発症歯周病ラットのエイコサノイドおよび炎症性サイトカインの測定(大阪歯科大学大学院歯学研究科博士(歯学)学位論文内容要旨および論文審査結果要旨の公表)

自然発症歯周病ラットのエイコサノイドおよび炎症性サイトカインの測定(大阪歯科大学大学院歯学研究科博士(歯学)学位論文内容要旨および論文審査結果要旨の公表)

Dynamics of inflammatory cytokines in rats with spontaneous periodontal disease

Dynamics of inflammatory cytokines in rats with spontaneous periodontal disease

Dynamics of inflammatory cytokines in rats with spontaneous periodontal disease

Dynamics of inflammatory cytokines in rats with spontaneous periodontal disease

Naturally occurring periodontal bone loss in the wild deer mouse, genus Peromyscus.

Historically, animal models for the study of periodontal diseases have incorporated surgically created defects, plaque retentive ligatures, as well as soft and high-sucrose diets which may not accurately reflect progression of the natural disease. Spontaneous periodontal disease is seen in a few animal species, but these are often expensive to maintain and are unsuitable for manipulation using advanced molecular biology techniques. Mice are inexpensive, easy to maintain, and are routinely used for transgenic experiments and are therefore an optimal animal for research purposes. However, it is commonly accepted that mice do not spontaneously develop periodontal disease. The purpose of this study was to determine if a mouse population that exhibits periodontal breakdown in the wild could be found, allowing for genetic manipulation of naturally occurring periodontal disease. We examined over 2,500 dry skulls of several Peromyscus species from various locations and habitats on the west coast of North America for periodontal bone loss in the molars, using furcation involvement as an indicator of disease severity. Alveolar bone loss was classified as Grade I) horizontal component of bone loss in the furcations; II) through-and-through furcations; and III) through-and-through furcations with alveolar bone loss into the apical third of the root. The proportions of individual mice experiencing bone loss were 3.8% for Class I-III involvement, 1.3% for Class II-III involvement, and 0.5% for Class III alone. Three subspecies of P. keeni and one subspecies of P. maniculatus had periodontal disease prevalences in 7% to 13.5% of their samples. Mice from isolated islands had 1.8- to 4.7-fold higher disease prevalence than those located on the mainland, with even greater prevalence on small islands. No statistically significant differences between genders were found. It appears that periodontal disease is far more common in this mouse genus than previously believed. Some of the subspecies demonstrated severe periodontal disease at a prevalence comparable to that found in humans.

Quantification of bacterial penetration in spontaneous periodontal disease in beagle dogs.

The role of bacteria in the pathogenesis of periodontal disease is controversial. Although bacterial penetration has been demonstrated in human periodontitis, relationships of bacteria to varying levels of periodontal health in other animals has not been well documented. In this study of beagle dog periodontium, bacteria were counted within the various tissue regions of sites which exhibited periodontal health, gingivitis, or periodontitis. Affected sites within whole block sections from two aged beagle dogs were prepared for investigation by light (LM) and scanning electron microscopy (SEM), and bacterial counts were subjected to statistical analysis for differences. Periodontitis sites viewed with LM had more bacteria than healthy sites. Neither LM nor SEM observations yielded any other differences in bacterial counts between the levels of periodontal health. When viewed using SEM, the sulcular epithelium had more bacteria than the other tissue regions in diseased sites. Relative to the number of bacteria in plaque, however, counts from all microscopic observations were very low. These findings indicate that the presence of bacteria within the periodontium is of questionable significance in the pathogenesis of spontaneous periodontal disease in beagle dogs.

Histopathogenesis of spontaneous periodontal disease in conventional rats. III. The mononuclear cell infiltrate and cytoplasmic changes in associated fibroblasts.

Spontaneously developing periodontitis lesions in rats fed a regular pelleted chow and a powdered high sucrose diet were examined by electron microscopy. Inflamed connective tissue contained numerous monocytes and large and small lymphocytes. Most large lymphocytes possessed the cytoplasmic features of blast‐type cells. Fibroblasts located within the inflamed connective tissue were found to be closely juxtaposed to mononuclear cells, many clearly belonging to the lymphocyte line. A narrow intercellular space separated adjacent cells in these fibroblast‐lymphocyte aggregates. Although the fibroblasts did not demonstrate the characteristic features usually attributed to cytotoxic damage, they did contain an increased number of dense and pleomorphic granules which contained poorly polymerized collagenous material. These features resemble, in part, those seen in colchicinetreated fibroblast suggesting that collagen secretion may be impaired in fibroblasts closely juxtaposed to lymphocytes in inflamed periodontal connective tissue.

Histopathogenesis of spontaneous periodontal disease in conventional rats

Spontaneously developing gingiitis lesions in the interdental tissue of rats fed a regular pelleted chow and apowdered high sucrose diet were examined in the electron microscope. The subepithelial inlamed connective tissues demonstrated a loss of collagen fibers concomittant with the infiltration of neutrophils, macrophages and lymphocytes. Fibroblasts adjacent to the inflamed gingival epithelium demonstrated cytopathic changes such as dilation of the granular endoplasmic reticulum and diminution of the Golgi complex. Endothelial cells and pericytes were characterized by prominent Gogi apparatuses, numberous mitochondria and well developed granular endoplasmic reticulum. Cytoplasmic processes of both cell types penetrated the vascular basa lamina. Apical migration of the juntional epthelium was preceeded by denudation of the cemental surface by breakdown of the connective tissue attachment.These changes reflect subepithelial tissue breakdwon and a vascular and epithelial micgratory response, probably involving increased synthetic activities.

Histopathogenesis of spontaneous periodontal disease in conventional rats

The development of gingivitis and periodontitis lesions in rats fed a normal laboratory chow diet was compared to that which occurred in rats fed a high sucrose diet (Keyes'diet 2000). Histometric analysis of mesio‐distal sections through the 1st maxillary interdetal area revealed that the area of inflamed connectve tissue(ICT) increased more rapidly in the diet 2000 group. A greater incidence of periodontitis lesions with active bone resorption was noted in the diet 2000 group. Analysis of cell types in the ICT revealed no statistically significant differences between the two diet groups. However when the percent age of various cell types present in the periodontitis lesions of both dietary groups were compared to the percentage of the cell typed present in the periodontitis lesions of both dietary groups were compared to the percentage of the cell typed persent in gingivitis lesions a statistically significant increase in both large mononuclear cells was found to exist in the ICT of the Periodontitis lisions. A statistically significant decrease in the number of endothelial cells was also observed in periodontitis lesions. At the ultrastructural level cytopathologic alterations of fibroblasts and decreased collagen fibers were noted beneath the gingival epithelium. Denudation of the cemental surface beneath the epithelial attachment became progressively more severe and preceded the migration of the epithelium along the cemental surface.

The retardation of spontaneous periodontal disease and the prevention of caries in hamsters with dextranase.

showed that dex­ tranase produced by a culture of Penicillium funiculosum was able to remove plaques grown in vitro. These plaques were products of cariogenic streptococci in su­ crose containing broths. Later the same investigators working with Keyes2 showed that dextranase reduced plaque formation and retarded caries development in albino hamsters previously infected with cariogenic organisms. Smooth surface lesions in the third molars did not form when administration of dextranase was begun prior to the eruption of this tooth. The present communication is concerned with the capacity of dextranase to prevent smooth surface caries completely in all molar teeth of golden hamsters fed a test diet containing 56% sucrose. The formation of plaque in the gingival sulcus and the development of periodontal pathosis was greatly reduced during the test period. Also a curative experiment is described in which dextranase removed preformed plaque in hamsters after 2 days of treatment.

Spontaneous periodontal disease in the mongolian gerbil.

The pathogenesis of periodontal lesions in the Mongolian gerbil (meriones ungiculatus) was studied in sixty‐one animals varying in age from two months to five years. Both gross morphologic and histological techniques were employed. The results of this investigation indicate a slowly progressing, insidious form of inflammatory periodontal breakdown in this animal apparently related to the accumulation of plaque and calculus‐like accretions. Because of the many morphologic similarities of the periodontal lesion in the gerbil to those of the human periodontal problem, it is felt that this animal is ideally suited for periodontal research.

Odontomyces viscosus, gen. nov., spec. nov., a filamentous microorganism isolated from periodontal plaque in hamsters.

It is proposed that a new genus, Odontomyces, with Odontomyces viscosus as the type species, be created for the organism previously described from plaques from spontaneous periodontal disease in hamsters. Odontomyces viscosus should be placed in the Actinomycetaceae.

Aerobic, gram-positive, filamentous bacteria as etiologic agents of experimental periodontal disease in hamsters

The bacteriology of a spontaneous periodontal disease of hamsters was investigated. This disease is characterized by a heavy, adherent, subgingival plaque and accompanies the feeding of a high carbohydrate diet. Pure cultures of aerobic branching filaments isolated from the plaque induced the disease when inoculated orally into uninfected albino hamsters. Other plaque organisms including streptococci and various unidentified gram-negative rods did not induce the disease. A filamentous strain “labelled” by making it resistant to terramycin was used to induce the disease and to trace implantation, persistence and transfer of the organism. The “labelled” strain was recovered in high numbers from all hamsters infected with this strain and its transfer from infected mothers to offspring was observed. Simultaneous inoculations with the aerobic filament and a specific streptococcus induced both periodontal disease and caries in the same animal.