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Cassiano Kuchenbecker Rosing - One of the best experts on this subject based on the ideXlab platform.
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Effects of Chronic Ethanol Consumption and Ovariectomy on the Spontaneous Alveolar Bone Loss in Rats.
International journal of dentistry, 2020Co-Authors: Priscila Cunha Nascimento, Cassiano Kuchenbecker Rosing, Leonardo Oliveira Bittencourt, Soraya O Pinto, Luana N. S. Santana, Renata Duarte De Souza-rodrigues, Armando L Pereira-neto, Cristiane Socorro Ferraz Maia, Rafael Rodrigues LimaAbstract:Postmenopausal estrogen deficiency and ethanol (EtOH) abuse are known risk factors for different diseases including Bone tissues. However, little is known about the synergic effects of EtOH abuse and estrogen deficiency on Alveolar Bone Loss in women. The present study evaluated the effects of EtOH chronic exposure and ovariectomy on the Alveolar Bone Loss in female rats. For this, 40 female Wistar rats were randomly divided into 4 groups: control, EtOH exposure, ovariectomy (OVX), and OVX plus EtOH exposure. Initially, half of the animals were ovariectomized at 75 days of age. After that, the groups received distilled water or EtOH 6.5 g/kg/day (20% w/v) for 55 days via gavage. Thereafter, animals were sacrificed and the mandibles were collected, dissected, and separated into hemimandibles. Alveolar Bone Loss was evaluated by measuring the distance between the cementoenamel junction and the Alveolar Bone crest through a stereomicroscope in 3 different anatomical regions of the tissue. One-way ANOVA and post hoc Tukey were used to compare groups ( ). The results showed that the ovariectomy and EtOH exposure per se were able to induce Alveolar Bone Loss, and their association did intensify significantly the effect. Therefore, OVX associated with heavy EtOH exposure increase the spontaneous Alveolar Bone Loss in rats.
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Effect of obesity on Alveolar Bone Loss in experimental periodontitis in Wistar rats.
Journal of applied oral science : revista FOB, 2012Co-Authors: Giliano Nicolini Verzeletti, Eduardo Jose Gaio, Daniele Sigal Linhares, Cassiano Kuchenbecker RosingAbstract:Obesity has been linked to higher inflammatory status and periodontal breakdown. OBJECTIVE: The purpose of this study was to investigate the effect of obesity on Alveolar Bone Loss in experimental periodontitis in rats. MATERIAL AND METHODS: Twenty-four female Wistar rats were randomly divided into two groups: obese (n=13), which were fed with "cafeteria diet" (CAF diet - high amounts of sucrose and fat) for 90 days in order to gain weight, and non-obese (n=11) regularly fed rats. Ligature-induced experimental periodontitis was created in all animals. Body weight differed statistically between obese and non-obese groups (277.59 and 223.35 g, respectively) at the moment of the ligature placement. Morphometric registration of Alveolar Bone Loss was carried out after 30 days of ligature placement to determine the effect of obesity on the progression of experimental periodontitis. RESULTS: Intra-group comparisons showed significantly higher Alveolar Bone Loss mean values in maxillary teeth with ligature (P
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Correlation analysis of Alveolar Bone Loss in buccal/palatal and proximal surfaces in rats
Brazilian oral research, 2012Co-Authors: Carolina Barrera De Azambuja, Eduardo Jose Gaio, Juliano Cavagni, Marcius Comparsi Wagner, Cassiano Kuchenbecker RosingAbstract:The aim was to correlate Alveolar Bone Loss in the buccal/pala- tal and the mesial/distal surfaces of upper molars in rats. Thirty-three, 60-day-old, male Wistar rats were divided in two groups, one treated with alcohol and the other not treated with alcohol. All rats received silk ligatures on the right upper second molars for 4 weeks. The rats were then euthanized and their maxillae were split and defleshed with sodium hypochlorite (9%). The cemento-enamel junction (CEJ) was stained with 1% methylene blue and the Alveolar Bone Loss in the buccal/palatal sur- faces was measured linearly in 5 points on standardized digital photo- graphs. Measurement of the proximal sites was performed by sectioning the hemimaxillae, restaining the CEJ and measuring the Alveolar Bone Loss linearly in 3 points. A calibrated and blinded examiner performed all the measurements. Intraclass Correlation Coefficient revealed values of 0.96 and 0.89 for buccal/lingual and proximal surfaces, respectively. The Pearson Correlation Coefficient (r) between measurements in buccal/ palatal and proximal surfaces was 0.35 and 0.05 for the group treated with alcohol, with and without ligatures, respectively. The best corre- lations between buccal/palatal and proximal surfaces were observed in animals not treated with alcohol, in sites both with and without liga- tures (r = 0.59 and 0.65, respectively). A positive correlation was found between Alveolar Bone Loss in buccal/palatal and proximal surfaces. The correlation is stronger in animals that were not treated with alcohol, in sites without ligatures. Areas with and without ligature-induced peri- odontal destruction allow detection of Alveolar Bone Loss in buccal/pala- tal and proximal surfaces.
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Effect of inhaled corticosteroid on TNF-α production and Alveolar Bone Loss in Wistar rats
Archives of oral biology, 2011Co-Authors: Luciana Dondonis Daudt, Eduardo Jose Gaio, Juliano Cavagni, Andressa De Souza, Iraci Lucena Da Silva Torres, Maria Beatriz Cardoso Ferreira, Cassiano Kuchenbecker RosingAbstract:Abstract Objective To evaluate the effect of different concentrations of inhaled budesonide on secretion of tumoral necrosis factor-alpha (TNF-α) and on ligature-induced Alveolar Bone Loss in Wistar rats. Materials and methods Forty-two animals were randomly divided in four groups. Control group (G1) did not receive any procedure. For the other 3 groups, Alveolar Bone Loss was induced by placement of ligatures around the upper second molar. The contralateral molar was considered intra-group control. Group 2 (G2) was nebulized with saline solution (NaCl 0.9%). Groups 3 and 4 (G3 and G4) were nebulized with 30 μg and 100 μg budesonide, respectively. Administration of drugs was performed daily for 14 days. Blood samples were collected from all animals for analysis of TNF-α. The maxillae from G2, G3 and G4 were removed and defleshed with 9% sodium hypochlorite. Morphometric analysis of Bone Loss was performed in digital standard photographs. Statistical analysis was performed with one-way ANOVA, followed by Tukey HSD or Scheffe multiple comparison's test (significance level P ≤ 0.05). Results Mean Alveolar Bone Loss values for teeth with ligature were 0.72, 0.70 and 0.77 mm for Groups 2, 3 and 4, respectively. No statistically significant differences were found amongst groups with or without ligature. The production of TNF-α was 60% higher in the presence of ligature (G1 vs. G2/G3/G4). No effect was observed in TNF-α secretion after inhalation of budesonide. Conclusion Inhaled budesonide in different concentrations did not alter Alveolar Bone Loss and TNF-α secretion in male Wistar rats.
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low concentration alcohol intake may inhibit spontaneous Alveolar Bone Loss in wistar rats
Archives of Oral Biology, 2011Co-Authors: Diego Nique Liberman, Roberta Manjabosco Pilau, Eduardo Jose Gaio, Lorena Floriani Orlandini, Cassiano Kuchenbecker RosingAbstract:Objective The aim of the present study was to evaluate the influence of ethanol in low concentration (5%) in ligature-induced Alveolar Bone Loss in Wistar rats. Material and methods Thirty rats were randomly assigned to test and control groups (n=15). Test group received a liquid diet containing ethanol 5% (vol./vol.) and standard rat chow. Control group received only tap water as the liquid diet and the same rat chow. In both groups, diet was delivered ad libitum. Alveolar Bone Loss was induced prior to the beginning of the study by means of ligatures placed around the upper second molars. The contra-lateral tooth remained as intra-group control. At the end of the nine weeks, the animals were killed and morphometric analysis of Alveolar Bone Loss was performed by a blinded and calibrated examiner. Intra-group comparisons were performed by paired sample T-test and inter-group differences were compared by independent sample T-test (α=.05). Results Animals that drank ethanol in low concentration systematically presented less Alveolar Bone Loss than the control group, regardless of the presence of ligature. Test group showed less Alveolar Bone Loss (p=0.04) in unligated teeth when compared to control group (0.32 ± 0.07 and 0.37 ± 0.07 mm, respectively). However, no significant difference (p=0.14) was observed between Test and Control groups (0.78 ± 0.14 and 0.84 ± 0.18 mm, respectively) in ligated teeth. Conclusion The results of this study lead to the conclusion that low concentration alcohol intake did not affect the Alveolar Bone Loss in ligature induced periodontal breakdown.
Young Joon Lee - One of the best experts on this subject based on the ideXlab platform.
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Inhibitory effects of Persicariae Rhizoma aqueous extracts on experimental periodontitis and Alveolar Bone Loss in Sprague-Dawley rats
Experimental and therapeutic medicine, 2016Co-Authors: Su Jin Kang, C. H. Han, Eun Kyung Lee, Bong Hyo Lee, Young Joon LeeAbstract:Persicariae Rhizoma (PR) is the dried stem parts of Persicaria tinctoria H. Gross (Polygonaceae), and has been traditionally used as anti-inflammatory and detoxifying agent. In the present study, the effects of PR aqueous extracts on ligation-induced experimental periodontitis (EPD) and associated Alveolar Bone Loss in rats were examined. Following the induction of EPD in rats, PR extracts were orally administered once a day for 10 days, and the changes and gains in body weight, Alveolar Bone Loss and total aerobic bacterial counts of buccal gingiva were observed with histopathological analysis. In addition, anti-inflammatory effects were evaluated by monitoring myeloperoxidase (MPO) activities, and interleukin (IL)-1β and tumor necrosis factor (TNF)-α contents, and anti-oxidant effects were investigated by measuring inducible nitric oxide synthase (iNOS) activities and malondialdehyde (MDA) levels. Bacterial proliferation, periodontitis and associated Alveolar Bone Loss induced by ligature placement were significantly and dose-dependently inhibited by the treatment with PR extracts. The inhibitory effects of 200 mg/kg PR were similar to those of 5 mg/kg indomethacin on ligation-induced periodontitis and associated Alveolar Bone Losses in this study. The results suggest that PR effectively inhibits ligature placement-induced periodontitis and Alveolar Bone Loss in rats via antibacterial, antioxidative and anti-inflammatory activities.
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Effects of Polycan, a β-glucan, on experimental periodontitis and Alveolar Bone Loss in Sprague-Dawley rats.
Journal of periodontal research, 2012Co-Authors: Y. S. Kim, Su Jin Kang, J. W. Kim, H. R. Cho, S. B. Moon, K. Y. Kim, Hyeung-sik Lee, C. H. Han, Young Joon LeeAbstract:Kim YS, Kang SJ, Kim JW, Cho HR, Moon SB, Kim KY, Lee HS, Han CH, Ku SK, Lee YJ. Effects of Polycan, a β-glucan, on experimental periodontitis and Alveolar Bone Loss in Sprague-Dawley rats. J Periodont Res 2012; 47: 800–810. © 2012 John Wiley & Sons A/S Background and Objective: Polycan is a promising candidate for the treatment of periodontal disease. This study was undertaken to examine whether Polycan, a type of β-glucan, has a protective effect on ligature-induced experimental periodontitis and related Alveolar Bone Loss in Sprague-Dawley rats. Material and Methods: Polycan was orally administered, daily, for 10 d, at 21.25, 42.5 or 85 mg/kg, beginning 1 d after ligation. Changes in body weight and Alveolar Bone Loss were monitored, and the anti-inflammatory effects of Polycan were determined by measuring the levels of myeloperoxidase (MPO), interleukin-1beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) in gingival tissue. We also evaluated inducible nitric oxide synthase (iNOS) activity and malondialdehyde (MDA) concentrations as a measure of the antioxidant effect. Results: Ligature placement led to a marked decrease in body weight, increased Alveolar Bone Loss and increased concentrations of MPO, IL-1β, TNF-α and MDA, as well as increased iNOS activity and inflammatory cell infiltration and decreased collagen-fiber content. Histological examination revealed increases in the number and activity of osteoclast cells, decreases in Alveolar Bone volume and elevated percentages of osteclasts on the Alveolar Bone surface. Daily oral treatment with 42.5 or 85 mg/kg of Polycan for 10 d led to significant, dose-dependent inhibition of the effect of ligature placement. Conclusion: Taken together, these results suggest that 10 d of oral treatment with Polycan effectively inhibits ligature placement-induced periodontitis and related Alveolar Bone Loss via an antioxidant effect.
Su Jin Kang - One of the best experts on this subject based on the ideXlab platform.
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Inhibitory effects of Persicariae Rhizoma aqueous extracts on experimental periodontitis and Alveolar Bone Loss in Sprague-Dawley rats
Experimental and therapeutic medicine, 2016Co-Authors: Su Jin Kang, C. H. Han, Eun Kyung Lee, Bong Hyo Lee, Young Joon LeeAbstract:Persicariae Rhizoma (PR) is the dried stem parts of Persicaria tinctoria H. Gross (Polygonaceae), and has been traditionally used as anti-inflammatory and detoxifying agent. In the present study, the effects of PR aqueous extracts on ligation-induced experimental periodontitis (EPD) and associated Alveolar Bone Loss in rats were examined. Following the induction of EPD in rats, PR extracts were orally administered once a day for 10 days, and the changes and gains in body weight, Alveolar Bone Loss and total aerobic bacterial counts of buccal gingiva were observed with histopathological analysis. In addition, anti-inflammatory effects were evaluated by monitoring myeloperoxidase (MPO) activities, and interleukin (IL)-1β and tumor necrosis factor (TNF)-α contents, and anti-oxidant effects were investigated by measuring inducible nitric oxide synthase (iNOS) activities and malondialdehyde (MDA) levels. Bacterial proliferation, periodontitis and associated Alveolar Bone Loss induced by ligature placement were significantly and dose-dependently inhibited by the treatment with PR extracts. The inhibitory effects of 200 mg/kg PR were similar to those of 5 mg/kg indomethacin on ligation-induced periodontitis and associated Alveolar Bone Losses in this study. The results suggest that PR effectively inhibits ligature placement-induced periodontitis and Alveolar Bone Loss in rats via antibacterial, antioxidative and anti-inflammatory activities.
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Effects of Polycan, a β-glucan, on experimental periodontitis and Alveolar Bone Loss in Sprague-Dawley rats.
Journal of periodontal research, 2012Co-Authors: Y. S. Kim, Su Jin Kang, J. W. Kim, H. R. Cho, S. B. Moon, K. Y. Kim, Hyeung-sik Lee, C. H. Han, Young Joon LeeAbstract:Kim YS, Kang SJ, Kim JW, Cho HR, Moon SB, Kim KY, Lee HS, Han CH, Ku SK, Lee YJ. Effects of Polycan, a β-glucan, on experimental periodontitis and Alveolar Bone Loss in Sprague-Dawley rats. J Periodont Res 2012; 47: 800–810. © 2012 John Wiley & Sons A/S Background and Objective: Polycan is a promising candidate for the treatment of periodontal disease. This study was undertaken to examine whether Polycan, a type of β-glucan, has a protective effect on ligature-induced experimental periodontitis and related Alveolar Bone Loss in Sprague-Dawley rats. Material and Methods: Polycan was orally administered, daily, for 10 d, at 21.25, 42.5 or 85 mg/kg, beginning 1 d after ligation. Changes in body weight and Alveolar Bone Loss were monitored, and the anti-inflammatory effects of Polycan were determined by measuring the levels of myeloperoxidase (MPO), interleukin-1beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) in gingival tissue. We also evaluated inducible nitric oxide synthase (iNOS) activity and malondialdehyde (MDA) concentrations as a measure of the antioxidant effect. Results: Ligature placement led to a marked decrease in body weight, increased Alveolar Bone Loss and increased concentrations of MPO, IL-1β, TNF-α and MDA, as well as increased iNOS activity and inflammatory cell infiltration and decreased collagen-fiber content. Histological examination revealed increases in the number and activity of osteoclast cells, decreases in Alveolar Bone volume and elevated percentages of osteclasts on the Alveolar Bone surface. Daily oral treatment with 42.5 or 85 mg/kg of Polycan for 10 d led to significant, dose-dependent inhibition of the effect of ligature placement. Conclusion: Taken together, these results suggest that 10 d of oral treatment with Polycan effectively inhibits ligature placement-induced periodontitis and related Alveolar Bone Loss via an antioxidant effect.
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effects of calcium gluconate on experimental periodontitis and Alveolar Bone Loss in rats
Basic & Clinical Pharmacology & Toxicology, 2011Co-Authors: Saekwang Ku, Yun Sub Sung, Su Jin KangAbstract:We examined the effects of calcium gluconate, an anti-inflammatory calcium salt, on ligature-induced experimental periodontitis and related Alveolar Bone Loss. Calcium gluconate was orally administered daily for 10 days at 250, 125 or 62.5 mg/kg, beginning 1 day after ligation. We recorded changes in body-weight and Alveolar Bone Loss and quantified the anti-inflammatory effects of calcium gluconate by measuring levels of myeloperoxidase (MPO), IL-1β and TNF-α. We also evaluated inducible nitric oxide synthase (iNOS) activity and malondialdehyde (MDA) concentration as a measure of antioxidant effects. Ligature placement produced a marked decrease in body-weight, increased Alveolar Bone Loss, and led to increased MPO, IL-1β, TNF-α and MDA concentrations, as well as elevated iNOS activity, increased inflammatory cell infiltration and decreased collagen fibre content in gingival tissue. Histopathology revealed decreased Alveolar Bone volume, increased osteoclast cell numbers and activity, and an elevated percentage of osteclasts on the Alveolar Bone surface. The effects of ligature placement were significantly and dose-dependently inhibited by 10 days of daily oral treatment with 250 and 125 mg/kg of calcium gluconate. The results suggest that 10 days daily oral treatment with calcium gluconate effectively inhibits ligature placement-induced periodontitis and related Alveolar Bone Loss via antioxidant effects.
Sadao Sato - One of the best experts on this subject based on the ideXlab platform.
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Blockade of sympathetic β-receptors inhibits Porphyromonas gingivalis-induced Alveolar Bone Loss in an experimental rat periodontitis model
Archives of oral biology, 2010Co-Authors: Yuka Okada, Y. Kim, Nobushiro Hamada, Yusuke Takahashi, Kenichi Sasaguri, Satoru Ozono, Sadao SatoAbstract:Abstract Introduction Periodontal disease is characterised by Alveolar Bone Loss. Some studies have suggested the involvement of sympathetic nervous system in the deterioration of periodontal disease. Noradrenaline, released from sympathetic nerve terminals due to various stimuli, binds to specific adrenergic receptors on immune cells. Recently, we reported that restraint stress augmented the Alveolar Bone Loss induced by Porphyromonas gingivalis infection. In this study, we investigated the effects of the β-blocker (propranolol) on Alveolar Bone Loss induced by P. gingivalis infection to examine the involvement of sympathetic nerves in periodontal breakdown. Methods Sprague–Dawley rats were treated as follows: saline injection (Group A), propranolol injection (Group B), saline injection and oral challenge with P. gingivalis (Group C), and propranolol injection and oral challenge with P. gingivalis (Group D). Horizontal Alveolar Bone Loss was evaluated by measuring the distance between the cemento-enamel junction and the Alveolar Bone crest. Specimens from periodontal tissue were evaluated by staining with hematoxylin–eosin and tartrate-resistant acid phosphatase. Results Blockade of β-receptors in periodontal tissue by propranolol inhibited osteoclast differentiation and prevented Alveolar Bone Loss induced by P. gingivalis infection. Histological study revealed that the number of osteoclasts detected was proportional to the level of Bone Loss. Conclusions These results indicate that the sympathetic nervous system is involved in the development of periodontitis and suggest that sympathetic signal modulation with β-blockers enables the control of Alveolar Bone mass metabolism.
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Cervical sympathectomy causes Alveolar Bone Loss in an experimental rat model
Journal of periodontal research, 2009Co-Authors: Y. Kim, Nobushiro Hamada, Yusuke Takahashi, Kenichi Sasaguri, Keiichi Tsukinoki, Minoru Onozuka, Sadao SatoAbstract:Background and Objective: Periodontal disease, a pathological destructive inflammatory condition, is characterized by Alveolar Bone Loss. Recent studies have suggested a correlation between the sympathetic nervous system and Bone remodeling. To confirm the importance of the sympathetic nervous system in Bone resorption, we investigated the effects of superior cervical ganglionectomy and oral challenge with Porphyromonas gingivalis on Alveolar Bone Loss in rats. Material and Methods: Rats were divided into three groups: group A underwent a sham operation as the control group; group B underwent superior cervical ganglionectomy; and group C underwent a sham operation and oral challenge with P. gingivalis. Horizontal Alveolar Bone Loss was evaluated by measuring the distance between the cemento-enamel junction and the Alveolar Bone crest. Cytokine gene expression in the gingival tissues was assessed using reverse transcription–polymerase chain reaction analyses. The furcation areas of the mandibular molars were examined histologically. Results: Both superior cervical ganglionectomy and oral challenge with P. gingivalis resulted in accelerated Alveolar Bone Loss. Gingival tissues in the superior cervical ganglionectomy group showed increased expression of the cytokines interleukin-1alfa, tumor necrosis factor-alfa and interleukin-6. The density of neuropeptide Y-immunoreactive fibers was decreased following superior cervical ganglionectomy. Osteoclasts were observed in the superior cervical ganglionectomy and P. gingivalis-challenged groups. Conclusion: Both superior cervical ganglionectomy and oral challenge with P. gingivalis induced Alveolar Bone Loss. These results provide new information on the occurrence of Alveolar Bone Loss, in that both oral challenge with P. gingivalis and superior cervical ganglionectomy are important accelerating factors for Alveolar Bone Loss. Thus, we suggest that the sympathetic nervous system is linked with the prevention of Alveolar Bone Loss.
Philip Stashenko - One of the best experts on this subject based on the ideXlab platform.
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the interleukin 10 knockout mouse is highly susceptible to porphyromonas gingivalis induced Alveolar Bone Loss
Journal of Periodontal Research, 2004Co-Authors: Hajime Sasaki, Yoshimasa Okamatsu, Toshihisa Kawai, Ralph Kent, Martin A Taubman, Philip StashenkoAbstract:OBJECTIVE Interleukin-10 is an anti-inflammatory cytokine that reduces periapical Bone Loss, but its role in periodontal Bone Loss is unclear. In the present study, we tested the hypothesis that endogenous interleukin-10 is a potent suppressor of Porphyromonas gingivalis-induced Alveolar Bone Loss in vivo. METHODS Interleukin-10 knockout (-/-) and wild-type mice were inoculated intraorally with P. gingivalis. Non-infected animals served as negative controls. Alveolar Bone Loss, gingival cytokine levels, and gingival gene expression were assessed using morphometric analysis, enzyme-linked immunosorbent assay (ELISA), and semiquantitative reverse transcription polymerase chain reaction (RT-PCR), respectively. RESULTS P. gingivalis-infected interleukin-10(-/-) mice exhibited severe Alveolar Bone Loss compared to non-infected interleukin-10(-/-) and wild-type mice by day 42. Surprisingly, Bone resorptive cytokines interleukin-1alpha and tumor necrosis factor alpha (TNF-alpha) were not up-regulated in gingival tissues by P. gingivalis-infection. Although interleukin-1beta was marginally increased, blockade of both interleukin-1 isoforms or interleukin-1 receptor type I with neutralizing antisera failed to reduce Alveolar Bone Loss in interleukin-10(-/-) mice, indicating the operation of an interleukin-1-independent mechanism. No strong correlations between Bone Loss and other cytokines was observed, although interferon gamma (IFNgamma), interleukin-6, interleukin-4, and prostaglandin E2 were modestly up-regulated in infected interleukin-10(-/-) mice. P. gingivalis infection reduced the expression of cell markers in gingival tissue on days 7 and 14 in both interleukin-10(-/-) and wild-type animals, suggestive of bacteria-induced cytotoxicity or apoptosis. This was followed by up-regulated expression of receptor activator of nuclear factor kappa B ligand (RANKL) and CD40 ligand (CD40L on days 28 and 70 in infected interleukin-10(-/-) mice only. CONCLUSION The interleukin-10(-/-) mouse is highly susceptible to Bone Loss induced by the periodontal pathogen P. gingivalis, which is mediated via an interleukin-1-independent pathway.
