scholarly journals Histopathologic investigations of nifedipine-induced gingival hyperplasia in Wistar rats

2005 ◽  
Vol 62 (3) ◽  
pp. 207-211 ◽  
Author(s):  
Zlata Brkic

Background. Nifedipine, a calcium channel blocker, used in the therapy of cardiovascular diseases, can induce gingival overgrowth. The aim of the study was to assess the influence of nifedipine on the deeper periodontal tissues of the experimental animals concerning connective tissue and blood vessels proliferation. Methods. The research was performed on Wistar rats, and they received the precise doses of nifedipine water suspension while the changes were followed up in pre-determined time intervals. The analyses of samples of tissues were done on the cross-sections of papilla from the top to the bottom on five levels. Results. Considerable level of changes was observed in the area of dental alveolar edge and in the gingivo-dental interspace. Epithelial hyperplasia and inflammatory subepithelial infiltration of lymphoplasmocyte type were also present. Alveolar bone destruction, the increased number of osteoclasts and periodontal destruction were found, as well. Conclusion. The results of this study showed a significant gingival hyperplasia in the experimental animals which received high doses of drug during extended period of time.

2007 ◽  
Vol 64 (1) ◽  
pp. 19-23
Author(s):  
Zlata Brkic

Background/Aim. The use of calcium channel blockers, especially nifedipine, causes gingival hyperplasia which leads to the destruction of the deeper periodontal tissues. During this process, inflammatory changes and the changes of colagen fibers occur. The aim of this study was to metrically compare the extent of proliferation of connective tissue in the deeper periodontal tissue in experimental animals regarding the dose and duration of nifedipine administration. Methods. The study involved 50 Wistar rats to which water solution of nifedipine was given in certain time intervals and doses. Before starting the experiment, i.e. before nifedipine administration, and in the defined time intervals, measuring of the morphology of gingival size was performed including the buccolingual and mesiodistal wideness and vertical altitude of the central interdental papilla. The measurement was performed by the use of a special graduated probe. Histometric analyses of the tissue samples were done on the sagital cross-sections in the direction from the top to the bottom of papilla on five levels. For the statistical analysis of the data, the established values to the extent of the most present changes were used. The mesiodistal and buccolingual diameters for the levels L2 and L3 were quantitively determined and compared. These values were compared to the vertical diameter of gingival growth determined before the onset of patohistologic analyses of the tissue samples. Results. At the beginning of the experiment, the volume of the lower incisive central papilla in the rats was 12 mm3. The central interdental papilla vertical altitude was 6.6 mm in rats which had received a lower dose of nifedipine, 8 mm in rats which had received a higher dose in the defined time intervals while the value for the control group was 3.8 mm. Conclusion. The obtained results showed that the administration of nifedipine led to the extensive gingival hyperplasia in the experimental animals. Gingival hyperplasia correlates with both the dose of nifedipine and the duration of its administration.


2018 ◽  
Vol 7 (2) ◽  
pp. 33-37
Author(s):  
Md Huzzatul Islam Khan ◽  
Sultana Akter Eka ◽  
Md Ashif Iqbal

Periodontitis is a chronic inflammatory disease of the periodontal tissues (periodontium) which surround and support the teeth, that results in attachment loss and alveolar bone destruction leads to ultimate tooth loss. It is caused by the bacteria present in dental plaque, which is a tenacious substance that forms on teeth and gingiva just after teeth are brushed. Periodontal treatment is aimed at controlling the infection in order to stop the progression of the disease and to be able to maintain a healthy periodontium. Mechanical debridement of supragingival and subgingival biofilms, together with adequate oral hygiene measures is the standard periodontal therapy. This mechanical subgingi- val biofilm debridement consists of an initial (nonsurgical /phase I) phase involving scaling and root planing (SRP) and the elimination of plaque retentive factors, followed by a surgical phase (if needed) including the elevation of a tissue flap and bone remodeling in further stages. The adjunct use of antibiotics has proven to additionally improve the outcome of periodontal treatment. A clinical case of a 40-years-old male patient with generalized severe chronic periodontitis with localized gingival swell- ing was treated with nonsurgical (phase I) periodontal therapy that was confined to oral hygiene instruction (OHI), SRP with an adjunct antimicrobial regimen.Update Dent. Coll. j: 2017; 7 (2): 33-37


2020 ◽  
pp. 29-34
Author(s):  
G.M. Silenko ◽  
O.B. Belikov ◽  
N.I. Belikova ◽  
M.V. Khrebor ◽  
Y.I. Silenko

The aim of this article is to study the indices of cellular, humoral immunity and nonspecific resistance, indices of free radical lipid oxidation and thrombocytoactive properties of periodontal tissues in animals with adjuvant periodontitis. In our study, adjuvant periodontitis was reproduced by the method of A.M. Kaminsky, immunizing rats with a homologous periodontal tissue in admixture with a Freund's adjuvant in a 1: 1 ratio. The course consisted of four single injections of 0.2 ml per animal intramuscularly at weekly intervals. Immunization did not lead to changes in the development and behavior of rats. One month after immunization, experimental animals experienced symptoms characteristic of generalized periodontitis in humans. They were manifested in the form of gums, resorption of alveolar bone, mobility and tooth loss. The induction of adjuvant periodontitis in experimental animals led to a significant increase in lipid peroxidation processes in periodontal tissues and a decrease in SOD and catalase activity. In animals with adjuvant periodontitis, which have been injected with periodontal polypeptides, there is a decrease in the reactions of GF compared with patients. In particular, there was a 40.9% decrease in the level of TBK-active products, although the level of MDA accumulation in the incubation process had not decreased significantly. It is noteworthy that in this group of animals increased activity of AO enzymes, which in patients was sharply reduced. Significant changes in the BPO lipid state were also observed in the blood of animals. The peroxidation reactions were significantly reduced, but not as significantly as in periodontal tissues. In particular, spontaneous erythrocyte hemolysis was lower by 14.2%, the level of TBK-active products by 39.4%, and MDA by 34.9%. An increase in the activity of SOD and catalase was observed, as well as a 40.4% decrease in the concentration of ceruloplasmin, which testifies to the elimination of the inflammatory response upon introduction of polypeptides. The treatment of animals with periodontylline was accompanied by an increase in the anti-aggregation properties of periodontal tissues. This is confirmed by the following indicators of the aggregate: the angle of aggregation is reduced by 31.8%, the optical density by 29%, the aggregation time is increased by 42.9% compared with the group of animals with adjuvant periodontitis. The introduction of parodontilin had a pronounced effect on the condition of blood clotting and fibrinolysis. We observed a significant increase in recalcification time, thrombin, prothrombin time. If the disease has a significant increase in the time of euglobulin fibrinolysis, then in the treatment of this indicator becomes less by 69.4%, the products of para-coagulation disappear from the bloodstream and the concentration of fibrin degradation products decreases. The treatment of animals was accompanied by an increase in immunity, which was manifested by an increase in T and B lymphocytes and Ig G. titer. Studies have shown that the treatment of diseased animals with a polypeptide drug leads to an improvement in the cellular, humoral immunity and nonspecific resistance of the organism, as well as the presence of a pronounced immunomodulatory effect of periodontin. The previously established relationship between blood clotting systems, sex, immunity, nonspecific resistance of the organism is confirmed in these experimental studies. If the induction of periodontitis is primarily associated with autoimmune processes, leading to impaired homeostasis, then the introduction of periodontin has a modulating effect on both immunity and indicators of lipid peroxidation and microcirculatory and coagulative hemostasis . In animals, regression of dental symptoms was noted, signs of periodontal inflammation, bleeding, swelling disappeared, and tooth mobility decreased. These data indicate the high therapeutic efficacy of thymic drugs in the treatment of generalized periodontitis. Research in this area remains relevant.


2005 ◽  
Vol 73 (6) ◽  
pp. 3453-3461 ◽  
Author(s):  
Yen-Tung A. Teng ◽  
Deeqa Mahamed ◽  
Bhagirath Singh

ABSTRACT Recent studies have shown the biological and clinical significance of signaling pathways of osteogenic cytokines RANKL-RANK/OPG in controlling osteoclastogenesis associated with bone pathologies, including rheumatoid arthritis, osteoporosis, and other osteolytic disorders. In contrast to the inhibitory effect of gamma interferon (IFN-γ) on RANKL-mediated osteoclastogenesis reported recently, alternative new evidence is demonstrated via studies of experimental periodontitis using humanized NOD/SCID and diabetic NOD mice and clinical human T-cell isolates from diseased periodontal tissues, where the presence of increasing IFN-γ is clearly associated with (i) enhanced Actinobacillus actinomycetemcomitans-specific RANKL-expressing CD4+ Th cell-mediated alveolar bone loss during the progression of periodontal disease and (ii) a concomitant and significantly increased coexpression of IFN-γ in RANKL(+) CD4+ Th cells. Therefore, there are more complex networks in regulating RANKL-RANK/OPG signaling pathways for osteoclastogenesis in vivo than have been suggested to date.


Author(s):  
Bianca Caroline Custodio dos Santos ◽  
Jossinelma Camargo Gomes ◽  
Angela Esmeralda Zaparolli Miola ◽  
Simone Karine Rothen ◽  
Célia Patricia Muller Rodrigues ◽  
...  

Objective: To analyze the effects of melatonin administration on the periodontal tissues of rats, linked or not with ligature-induced periodontal disease. Materials and Methods: 40 male Wistar rats aged eight weeks, divided into Control Group (GCON), Ligature Group (GLIG), Melatonin Group (GMEL) and Ligature and Melatonin Group (GLIGMEL). GLIG and GLIGMEL were induced to experimental periodontitis by placing a ligature on the lower molars for 30 days. During the experiment, after 16 days with the ligature, melatonin was administered orally for 10 mg/kg for 14 days in GMEL and GLIGMEL. In the end, euthanasia was performed and the hemi-mandibles were collected for the respective histological and radiographic analyzes; for the results, Shapiro-Wilk, ANOVA-One-Way and Tukey's multiple comparison tests were used. Results: A significantly lower alveolar bone loss (p<0.05) was demonstrated in the animals that received the administration of melatonin, in which it had a prophylactic function against the effects of the disease, evidenced in radiographic, histomorphometric and histological analyzes in the bone cell count. Conclusion: Results show that the therapy with administration of melatonin promotes a protective effect on the alveolar bone tissue of rats with induced experimental periodontitis.


Author(s):  
Ozkan Karatas ◽  
Fikret Gevrek

Background: 3,4,5-Trihydroxybenzoic acid, which is also known as gallic acid, is an anti-inflammatory agent who could provide beneficial effects in preventing periodontal inflammation. The present study aimed to evaluate the anti-inflammatory effects of gallic acid on experimental periodontitis in Wistar rats. Alveolar bone loss, osteoclastic activity, osteoblastic activity, and collagenase activity were also determined. Methods: 32 Wistar rats were used in the present study. Study groups were created as following: Healthy control (C,n=8) group; periodontitis (P,n=8) group; periodontitis and 30 mg/kg gallic acid administered group (G30,n=8); periodontitis and 60 mg/kg gallic acid administered group (G60,n=8). Experimental periodontitis was created by placing 4-0 silk sutures around the mandibular right first molar tooth. Morphological changes in alveolar bone were determined by stereomicroscopic evaluation. Mandibles were undergone histological evaluation. Matrix metalloproteinase (MMP)-8, tissue inhibitor of MMPs (TIMP)-1, bone morphogenetic protein (BMP)-2 expressions, tartrate-resistant acid phosphatase (TRAP) positive osteoclast cells, osteoblast, and inflammatory cell counts were determined. Results: Highest alveolar bone loss was observed in the periodontitis group. Both doses of gallic acid decreased alveolar bone loss compared to the P group. TRAP-positive osteoclast cell counts were higher in the P group, and gallic acid successfully lowered these counts. Osteoblast cells also increased in gallic acid administered groups. Inflammation in the P group was also higher than those of C, G30, and G60 groups supporting the role of gallic acid in preventing inflammation. 30 and 60 mg/kg doses of gallic acid decreased MMP-8 levels and increased TIMP-1 levels. BMP levels increased in gallic acid administered groups, similar to several osteoblasts. Conclusion: Present results revealed an anti-inflammatory effect of gallic acid, which was indicated by decreased alveolar bone loss and collagenase activity and increased osteoblastic activity.


2010 ◽  
Vol 04 (03) ◽  
pp. 338-340
Author(s):  
Kamile Erciyas ◽  
Serhat Inaloz ◽  
A. Fuat Erciyas

Haim-Munk syndrome is an extremely rare autosomal recessive disorder characterized clinically by palmoplantar hyperkeratosis, aggressive periodontitis with severe alveolar bone destruction, onychogryphosis, pes planus, arachnodactyly, and acro-osteolysis. Consanguinity seems a notable prerequisite. The aim of this study was therefore to report one case of this syndrome and to focus on the periodontal manifestations, in order to attract the attention of dental clinicians to this rare anomaly. (Eur J Dent 2010;4:338-340)


2021 ◽  
pp. 002203452110199
Author(s):  
Y. Xie ◽  
Q. Tang ◽  
S. Yu ◽  
W. Zheng ◽  
G. Chen ◽  
...  

Orthodontic tooth movement (OTM) depends on periodontal ligament cells (PDLCs) sensing biomechanical stimuli and subsequently releasing signals to initiate alveolar bone remodeling. However, the mechanisms by which PDLCs sense biomechanical stimuli and affect osteoclastic activities are still unclear. This study demonstrates that the core circadian protein aryl hydrocarbon receptor nuclear translocator–like protein 1 (BMAL1) in PDLCs is highly involved in sensing and delivering biomechanical signals. Orthodontic force upregulates BMAL1 expression in periodontal tissues and cultured PDLCs in manners dependent on ERK (extracellular signal–regulated kinase) and AP1 (activator protein 1). Increased BMAL1 expression can enhance secretion of CCL2 (C-C motif chemokine 2) and RANKL (receptor activator of nuclear factor–κB ligand) in PDLCs, which subsequently promotes the recruitment of monocytes that differentiate into osteoclasts. The mechanistic delineation clarifies that AP1 induced by orthodontic force can directly interact with the BMAL1 promoter and activate gene transcription in PDLCs. Localized administration of the ERK phosphorylation inhibitor U0126 or the BMAL1 inhibitor GSK4112 suppressed ERK/AP1/BMAL1 signaling. These treatments dramatically reduced osteoclastic activity in the compression side of a rat orthodontic model, and the OTM rate was almost nonexistent. In summary, our results suggest that force-induced expression of BMAL1 in PDLCs is closely involved in controlling osteoclastic activities during OTM and plays a vital role in alveolar bone remodeling. It could be a useful therapeutic target for accelerating the OTM rate and controlling pathologic bone-remodeling activities.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Hui Yu ◽  
Tianyi Zhang ◽  
Haibin Lu ◽  
Qi Ma ◽  
Dong Zhao ◽  
...  

Abstract Background Granulocyte colony-stimulating factor (G-CSF) is an important immune factor that mediates bone metabolism by regulating the functions of osteoclasts and osteoblasts. Bone loss is a serious and progressive result of periodontitis. However, the mechanisms underlying the effects of G-CSF on periodontal inflammation have yet not been completely elucidated. Here, we examined whether an anti-G-CSF antibody could inhibit bone resorption in a model of experimental periodontitis and investigated the local expression of G-CSF in periodontal tissues. Methods Experimental periodontitis was induced in mice using ligatures. The levels of G-CSF in serum and bone marrow were measured; immunofluorescence was then performed to analyze the localization and expression of G-CSF in periodontal tissues. Mice with periodontitis were administered anti-G-CSF antibody by tail vein injection to assess the inhibition of bone resorption. Three-dimensional reconstruction was performed to measure bone destruction‐related parameters via micro-computed tomography analysis. Immunofluorescence staining was used to investigate the presence of osteocalcin-positive osteoblasts; tartrate-resistant acid phosphatase (TRAP) staining was used to observe osteoclast activity in alveolar bone. Results The level of G-CSF in serum was significantly elevated in mice with periodontitis. Immunofluorescence analyses showed that G-CSF was mostly expressed in the cell membrane of gingival epithelial cells; this expression was enhanced in the periodontitis group. Additionally, systemic administration of anti-G-CSF antibody significantly inhibited alveolar bone resorption, as evidenced by improvements in bone volume/total volume, bone surface area/bone volume, trabecular thickness, trabecular spacing, and trabecular pattern factor values. Immunofluorescence analysis revealed an enhanced number of osteocalcin-positive osteoblasts, while TRAP staining revealed reduction of osteoclast activity. Conclusions G-CSF expression levels were significantly up-regulated in the serum and gingival epithelial cells. Together, anti-G-CSF antibody administration could alleviates alveolar bone resorption, suggesting that G-CSF may be one of the essential immune factors that mediate the bone loss in periodontitis.


2021 ◽  
Vol 22 (2) ◽  
pp. 539
Author(s):  
Yüksel Korkmaz ◽  
Behrus Puladi ◽  
Kerstin Galler ◽  
Peer W. Kämmerer ◽  
Agnes Schröder ◽  
...  

Nitric oxide (NO) binds to soluble guanylyl cyclase (sGC), activates it in a reduced oxidized heme iron state, and generates cyclic Guanosine Monophosphate (cGMP), which results in vasodilatation and inhibition of osteoclast activity. In inflammation, sGC is oxidized and becomes insensitive to NO. NO- and heme-independent activation of sGC requires protein expression of the α1- and β1-subunits. Inflammation of the periodontium induces the resorption of cementum by cementoclasts and the resorption of the alveolar bone by osteoclasts, which can lead to tooth loss. As the presence of sGC in cementoclasts is unknown, we investigated the α1- and β1-subunits of sGC in cementoclasts of healthy and inflamed human periodontium using double immunostaining for CD68 and cathepsin K and compared the findings with those of osteoclasts from the same sections. In comparison to cementoclasts in the healthy periodontium, cementoclasts under inflammatory conditions showed a decreased staining intensity for both α1- and β1-subunits of sGC, indicating reduced protein expression of these subunits. Therefore, pharmacological activation of sGC in inflamed periodontal tissues in an NO- and heme-independent manner could be considered as a new treatment strategy to inhibit cementum resorption.


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