Management of type IIIb dens invaginatus using a combination of root canal treatment, intentional replantation, and surgical therapy: A case report.

BACKGROUND: Type Ⅲb dens invaginatus (DI) with a lateral canal located at the mid-third of the root is rarely reported. Here, we report a rare case of type Ⅲb DI in the left upper anterior tooth with a lateral canal that led to persistent periodontitis. CASE SUMMARY: A 15-year-old female patient presented with a chief complaint of pain associated with recurrent labial swelling in the area of the left anterior tooth. A diagnosis of type Ⅲb DI and chronic periodontitis was made. Intentional replantation was performed after conventional endodontic treatment failed. After 6 mo, the patient was asymptomatic, but a sinus tract was observed. Cone-beam computed tomography images showed bone loss in the mesial of the mid-root. Based on methylene blue staining and microscopy images, the lateral foramen located at the middle third of the root was surgically treated. After 3 years of follow-up, the clinical findings and radiographic assessment presented a favorable prognosis of bone healing without root absorption or ankylosis. CONCLUSION: Type Ⅲb DI with a lateral canal can be successfully treated by root canal treatment, intentional replantation, and surgical therapy.

Local Inflammation Alters MMP-2 and MMP-9 Gelatinase Expression Associated with the Severity of Nifedipine-Induced Gingival Overgrowth: a Rat Model Study.

Nifedipine-induced gingival overgrowth (NIGO) is characterized by cell proliferation and extracellular matrix (ECM) component accumulation in gingival connective tissues, with varying degrees of inflammation and fibrosis. Impaired collagen and ECM homeostasis may be among the underlying molecular mechanisms that lead to the fibrotic changes that occur in drug-induced gingival overgrowth (DIGO). Because matrix metalloproteinases (MMPs) play vital roles in regulating collagen and ECM metabolism, many studies have been performed to reveal the relationship between MMPs and DIGO. It is thought that the gelatinases MMP-2 and MMP-9, both type IV collagenases, are involved in the development of tissue inflammation and organ fibrosis. However, the few studies regarding gelatinase expression in DIGO are controversial. Recent studies have demonstrated the inhibitory effect of cyclosporine A (CsA) on gelatinase expression and/or activity; however, similar changes have yet to be detected in Nif-treated gingival tissues. In this study, we verified that Nif treatment could lead to gingival overgrowth in rats and that gingival inflammation played a pro-proliferative role in NIGO development. Additionally, we examined the temporal expression of gelatinases on days 0, 7, 14, 21, 30, and 40 during NIGO development. The aim was to investigate whether MMP-2 and MMP-9 played significant roles in regulating NIGO development and progression. MMP-2 gene expression was not altered by Nif treatment alone but was significantly inhibited by Nif treatment for 30 days in the presence of local inflammation. However, no significant alterations in MMP-2 protein expression were detected in the Nif-treated gingival tissue, regardless of the presence or absence of local inflammation. Moreover, Nif treatment could lead to transient and significant increases in MMP-9 gene and protein expression levels in the presence of local inflammation. In particular, active MMP-9 expression increased significantly in the gingival tissue that received the combined effect of Nif and ligation treatment; besides, a temporal, but not significant, change was also observed in the gingival tissue that received Nif treatment alone. Taken together, these results provided evidence that temporal changes in MMP-2 and MMP-9 expression occurred during NIGO development. Nif treatment accompanied by local inflammation regulated MMP-2 and MMP-9 expression, primarily MMP-9, which was most likely associated with NIGO severity. Thus, MMP-9 is a potential contributing factor in the process of NIGO development.

[A novel mutation of MSX1 gene in a Chinese pedigree with oligodontia].

OBJECTIVE: To detect the MSX1 gene mutation in a Chinese family with oligodontia. METHODS: Blood samples were obtained from seven affected and seven unaffected individuals in the pedigree. All exons and flanking intronic boundaries of the MSX1 gene were amplified with polymerase chain reaction technique and then directly sequenced. The website of bioinformatics was used to predict the effect of the mutation on the function. RESULTS: A splicing mutation (IVS1-2A > G) was found at position -2 near the 3' end of the IVS1 of MSX1, which made a change of the intron 1 splice acceptor site. None of the mutation was found in normal individuals of the family and in 100 unrelated healthy matched control individuals. CONCLUSIONS: IVS1-2A > G was a novel splicing mutation identified in the MSX-1 gene and it might be responsible for nonsyndromic oligodontia in this family.