Kim, Eun-Cheol;Park, Joon Bong;Hong, Ji-Youn;Kang, Kyung Lhi
Journal of Periodontal and Implant Science
/
v.45
no.2
/
pp.76-80
/
2015
Purpose: Methimazole is an anti-thyroid drug that can cause life-threatening neutropenia in rare situations. The aim of this case report is to describe a set of oral complications associated with methimazole-induced neutropenia and the healing of the gingiva after proper treatment. Methods: A 31-year-old female patient hospitalized for systemic symptoms of sore throat and fever and showing extensive gingival necrosis with pain was referred to the Department of Periodontics from the Department of Endocrinology. Methimazole-induced neutropenia was diagnosed based on blood test results and her medical history. Methimazole was discontinued and a range of treatments was administered, including the injection of granulocyte colony stimulating factor. Results: After systemic treatment, the gingiva began to heal as the neutrophil count increased. Approximately one year later, the gingiva had returned to a normal appearance. Twenty-one months after treatment, sequestra of the alveolar bone that had broken through the gingiva were removed. Periodic supportive periodontal treatment has been continued uneventfully. Conclusions: The oral manifestations of gingival necrosis and ulcerations, in combination with systemic symptoms such as fever and sore throat, are the critical signs presented in the early stages of drug-induced neutropenia. Therefore, dentists need to be aware of these oral complications in order to make an accurate diagnosis and to ensure that prompt medical intervention is provided.
Bone resorption involves sequential stages of osteoclast precursor migration and differentiation of osteoclast precursors into multinucleated osteoclasts. Stromal cell derived factor (SDF)-1 is a chemotactic factor for osteoclast precursor migration. Matrix metalloproteinase (MMP)-9 is involved in migration of osteoclast precursors and activation of $interleukin(IL)-1{\beta}$. Alveolar bone destruction is a characteristic feature of periodontal disease. Treponema lecithinolyticum is a oral spirochete isolated from the periodontal lesions. The effect of lipopolysaccharide(LPS) from T. lecithinolyticum on expression of SDF-1 and MMP-9 was examined in cocultures of bone marrow cells and osteblasts derived from mouse calvariae. T. lecithinolyticum LPS increased expression of MMP-9 in the coculture. Polymyxin B, an inhibitor of LPS, abolished the increase of MMP-9 mRNA expression by LPS. LPS did not increase the expression of SDF-1, $IL-1{\beta}$ and tumor necrosis $factor(TNF)-{\alpha}$ mRNA in cocultures. Prostaglandin $E_2(PGE_2)$ up-regulated the expression of MMP-9 and NS398, an inhibitor of $PGE_2$ synthesis, down-regulated the induction of MMP-9 expression by T. lecitbinolyticm LPS. These results suggest that T. lecitbinolyticm LPS increases MMP-9 expression in bone cells via $PGE_2$ and that the induction of MMP-9 expression by T. lecitbinolyticm LPS is involved in alveolar bone destruction of periodontitis patients by the increase of osteoclast precursor migration and the activation of bone resorption-inducing cytokine.
Purpose: In the anterior maxilla, hard and soft tissue augmentations are sometimes required to meet esthetic and functional demands. In such cases, primary soft tissue closure after bone grafting procedures is indispensable for a successful outcome. This report describes a simple method for soft tissue coverage of a guided bone regeneration (GBR) site using the double-rotated palatal subepithelial connective tissue graft (RPSCTG) technique for a maxillary anterior defect. Methods: We present a 60-year-old man with a defect in the anterior maxilla requiring hard and soft tissue augmentations. The bone graft materials were filled above the alveolar defect and a titanium-reinforced nonresorbable membrane was placed to cover the graft materials. We used the RPSCTG technique to achieve primary soft tissue closure over the graft materials and the barrier membrane. Additional soft tissue augmentation using a contralateral RPSCTG and membrane removal were simultaneously performed 7 weeks after the stage 1 surgery to establish more abundant soft tissue architecture. Results: Flap necrosis occurred after the stage 1 surgery. Signs of infection or suppuration were not observed in the donor or recipient sites after the stage 2 surgery. These procedures enhanced the alveolar ridge volume, increased the amount of keratinized tissue, and improved the esthetic profile for restorative treatment. Conclusions: The use of RPSCTG could assist the soft tissue closure of the GBR sites because it provides sufficient soft tissue thickness, an ample vascular supply, protection of anatomical structures, and patient comfort. The treatment outcome was acceptable, despite membrane exposure, and the RPSCTG allowed for vitalization and harmonization with the recipient tissue.
Journal of the korean academy of Pediatric Dentistry
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v.21
no.2
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pp.518-524
/
1994
A traumatically intruded tooth is one that is forcefully and abruptly dispaced from its position into the surrounding alveolar bone. Although intrusion of permanent teeth is infrequent, the sequelae compromise the longevity of the tooth and often include pulp necrosis, internal and external root resorption, rupture of periodontal ligament and loss of marginal bone. The purpose of this study was to examine three common management techniques for traumatic intrusion, observation for re-eruption, surgical repositioning & fixation and orthodontic extrusion. In the recent, the accepted treatment was to allow the permanent teeth to reerupt spontaneously for 6-8 weeks. If this did not occur, orthodontic traction was applied. The pulpal status of the teeth was monitored and either calcium hydroxide therapy or conventional endodontics was instituted following pulpal necrosis depending on the maturity of the root end. Pulpectomy and a calcium hydroxide filling were also the treatment of choice if there was evidence of internal or external root resorption. This will reduce the chance of root resorption and provide a period of monitoring prior to a definitive root canal filling.
Purpose: Sclerostin, an inhibitor of Wnt/${\beta}$-catenin signaling, exerts negative effects on bone formation and contributes to periodontitis-induced alveolar bone loss. Recent studies have demonstrated that serum sclerostin levels are increased in diabetic patients and that sclerostin expression in alveolar bone is enhanced in a diabetic periodontitis model. However, the molecular mechanism of how sclerostin expression is enhanced in diabetic patients remains elusive. Therefore, in this study, the effect of hyperglycemia on the expression of sclerostin in osteoblast lineage cells was examined. Methods: C2C12 and MLO-Y4 cells were used in this study. In order to examine the effect of hyperglycemia, the glucose concentration in the culture medium was adjusted to a range of levels between 40 and 100 mM. Gene expression levels were examined by quantitative reverse transcription-polymerase chain reaction and Western blot assays. Top-Flash reporter was used to examine the transcriptional activity of the ${\beta}$-catenin/lymphoid enhanced factor/T-cell factor complex. Tumor necrosis factor-alpha ($TNF{\alpha}$) protein levels were examined with the enzyme-linked immunosorbent assay. The effect of reactive oxygen species on sclerostin expression was examined by treating cells with 1 mM $H_2O_2$ or 20 mM N-acetylcysteine. Results: The high glucose treatment increased the mRNA and protein levels of sclerostin. High glucose suppressed Wnt3a-induced Top-Flash reporter activity and the expression levels of osteoblast marker genes. High glucose increased reactive oxygen species production and $TNF{\alpha}$ expression levels. Treatment of cells with $H_2O_2$ also enhanced the expression levels of $TNF{\alpha}$ and sclerostin. In addition, N-acetylcysteine treatment or knockdown of $TNF{\alpha}$ attenuated high glucose-induced sclerostin expression. Conclusions: These results suggest that hyperglycemia increases sclerostin expression via the enhanced production of reactive oxygen species and $TNF{\alpha}$.
In order to clarify the histopathological changes resulting from nitrate poisoning, rabbits were experimentally poisoned by the oral administration of $KNO_3$ or $NaNO_2$ and examined clinically and histopathologically. In addition, the quantitative changes of glycogen level in hepatic cells were histochemically observed. The results obtained were summarized as follows: 1. Clinical symptoms observed from the acute cases which died within 2 hours after the administration were severe cyanosis of visible mucosa, frequent urination, and dyspnea. However, in chronic cases administrated daily with $KNO_3$ for 43, 50 and 74 days respectively, no marked symptoms were observed. 2. Macroscopic changes observed in acute cases were severe methemoglobinemia, cloudy swelling of hepatic cells, hemorrhage and hyperemia of gastric mucosa, and hyperemia of other organs. In chronic cases there were marked hyperemia, dark-red coloring and increasing of consistency in liver and kidney, and swelling of spleen. 3. Microscopic changes observed in acute cases were hemorrhage and hyperemia of various organs, cloudy swelling and centrilobular necrosis of hepatic cells and necrosis of convoluted tubular epithelium in kidney. In chronic cases there were round cell infiltration of the interlobular connective tissue and epithelial proliferation of interlobular bile ducts in the liver, and necrosis of the convoluted tubular epithelium and proliferation of interstitial connective tissue in kidney, thickening of alveolar septa of lungs, activated hemopoiesis of bone marrow, and myeloid metaplasia of sqlenic pulp. 4. Glycogen storage in liver cells was decreased in acute cases, on the contrary, increased in chronic cases.
Objective: When an alveolar cleft is too large to close with adjacent mucobuccal flaps or large secondary fistula following a primary bilateral palatoplasty exists, a one-stage procedure for bone grafting becomes challenging. In such a case, we used the tongue flap to repair the fistula and cleft alveolus in the first stage, and bone grafting to the cleft defect was performed in the second stage several months later. The purpose of this paper is to report our experiences with the use of an anteriorly-based Y-shaped tongue flap to fit the palatal and labial alveolar defects and the ultimate result of the bone graft. Patients: A series of 14 patients underwent surgery of this type from January 1994 to December 1998.The average age of the patients was 15.8 years old (range: 5 to 28 years old). The mean period of follow-up following the 2nd stage bone raft operation was 45.9 months (range: 9 to 68 months). In nine of the 14 cases, the long-fork type of a Yshaped tongue flap was used for extended coverage of the labial side alveolar defects with the palatal fistula in the remaining cases the short-forked design was used. Results: All cases demonstrated a good clinical result after the initial repair of cleft alveolus and palatal fistula. There was no fistula recurrence, although Partial necrosis of distal margin in long-forked tongue flap was occurred in one case. Furthermore, the bone graft, which was performed an average of 8 months after the tongue flap repair, was always successful. Occasionally, the transferred tongue tissue was bulging and interfering with the hygienic care of nearby teeth; however, these problems were able to be solved with proper contour-pasty performed afterwards. No donor site complications such as sensory disturbance, change in taste, limitations in tongue movement, normal speech impairments or tongue disfigurement were encountered. Conclusion: This two-stage reconstruction of a bilateral cleft alveolus using a Y-shaped tongue flap and iliac bone graft was very successful. It may be indicated for a bilateral cleft alveolus patient where the direct closure of the cleft defect with adjacent tissue or the buccal flap is not easy due to scarred fibrotic mucosa and/or accompanied residual palatal fistula.
This study was carried out to investigate the pathogenesis of canine herpesvirus(CHV) infection in dogs. The 17 puppies, one day old, delivered from CHV seronegative 3 dams were divided into two groups. The 13 puppies were inoculated intranasally with 1ml of CHV-KK inoculum($5{\times}10^{5.6}TCID_{50}/ml$) and 4 puppies were served as control. And then the puppies were sacrificed at 2, 4, 6 and 7 days after the treatment, and collected blood, nasal mucosa, trigeminal nerve, trigeminal ganglion, bone marrow, eye, brain and other major organs. These organs were examined histopathologically and electron microscopically. The platelets of puppies infected with CHV were dramatically decreased because of the damages of vascular endothelial cells. Histopathologically, necrotizing vasculitis and neuritis were proceeded the generalized focal necrosis of all organs. Necrotic changes in trigeminal ganglion, trigeminal nerve and ventroposteriomedial nucleus of thalamus were observed in 4 puppies infected with CHV. Herpesviral particles, various forms of maturation, were observed in endothelial cells of the alveolar capillary and hepatic sinusoid with electron microscopy. These results suggest that the generalized focal necrcsis of all organs including brain and eyes in canine herpesvirus infection were resulted from generalized vasculitis, and also the hemonecrotizing meningoencephalitis was related to the necrosis of trigeminal nerve pathway.
Objective: The aim of this study was to measure tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) levels around miniscrews used for anchorage during a 3-month period of canine distalization. Methods: Sixteen patients (8 boys, 8 girls; mean age, $16.6{\pm}2.4$ years) whose upper first premolars were extracted for orthodontic treatment were included in this study. Miniscrews were used as an anchorage unit in canine distalization. Thirty-two (32) miniscrew implants were placed bilaterally in the alveolar bone between the maxillary second premolars and first molars. The treatment, miniscrew, and control groups comprised upper canines, miniscrew implants, and upper first premolars, respectively. Peri-miniscrew implant crevicular fluid and gingival crevicular fluid were obtained before applying force and at 1, 24, and 48 hours, and at 7 and 21 days, and 3 months after applying force. Results: During the 3-month period, the (TNF-${\alpha}$) levels increased significantly at 24 hours only in the treatment group (p < 0.01). In the miniscrew and control groups, there were no statistically Significant changes. No significant differences were observed between groups. Conclusions: Miniscrews can be conveniently used for anchorage in orthodontics.
Purpose: Various complications occur when a maxillofacial fracture is malunionized or improperly resolved. Malocclusion is the most common complication, followed by facial deformity, temporomandibular joint disorder (TMD), and neurological symptoms. The purpose of this study was to evaluate the dental treatment of postoperative complications after maxillofacial fracture. Materials and methods: In this study, nine patients with a postoperative complication after maxillofacial fracture who had been performed the initial operation from other units and were referred to the authors' department had been included. Of the nine patients, six had mandibular fractures, one had maxillary fractures, one had maxillary and mandibular complex fractures, and one had multiple facial fractures. All the patients had tooth fractures, dislocations, displacements, and alveolar bone fractures at the time of trauma, but complications occurred because none of the patients underwent preoperative and postoperative dental treatment. Malocclusion and TMD are the most common complications, followed by dental problems (pulp necrosis, tooth extrusion, osteomyelitis, etc.) due to improper treatment of teeth and alveolar bone injuries. The patients were referred to the department of dentistry to undergo treatment for the complications. One of the nine patients underwent orthognathic surgery for a severe open bite. Another patient underwent bone reconstruction using an iliac bone graft and vestibuloplasty with extensive bone loss. The other patients, who complained of moderate occlusal abnormalities and TMDs such as mouth-opening limitation, underwent occlusal treatment by prosthodontic repair and temporomandibular joint treatment instead of surgery. Results: One patient who underwent orthognathic surgery had complete loss of open bite and TMD after surgery. One patient who underwent reconstruction using an iliac bone graft had a good healing process. Other patients were treated with splint, injection, and physical therapy for mouth-opening limitation and temporomandibular joint pain. After treatment, the TMDs were resolved, but the remaining occlusal abnormalities were resolved with prosthetic restoration. Conclusions: Considering the severity of malocclusion and TMJ symptom and the feasibillity of reoperation, nonsurgical methods such as orthodontic and prosthodontic treatments and splint therapy can be used to manage the dental and TMD complication after the trauma surgery. However, reoperation needs to be strongly considered for severe malocclusion and TMD problem.
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