Prevalence and risk factors of tooth discolouration after orthognathic surgery: a retrospective study of 1455 patients.

This study was conducted to evaluate the prevalence of tooth discolouration and to examine the factors that may pose a higher risk for tooth discolouration after orthognathic surgery. This was a retrospective study of 1455 orthognathic surgeries. The following data were collected for analysis: presence of discoloured teeth, sex, age at operation, the extent of the surgical displacement of the maxilla, and whether patients had undergone genioplasty, zygomaplasty, or descending palatine artery (DPA) ligation. Out of 1339 patients who underwent double-jaw surgery, 49 received root canal treatment due to tooth discolouration. No tooth discolouration was found in the 116 patients undergoing single-jaw surgery. DPA ligation, genioplasty, and mandibular sub-apical osteotomy were associated with a significant risk of tooth discolouration. Patients should be informed preoperatively of the possibility of tooth discolouration. Additionally, the DPA should be preserved during Le Fort I osteotomy to reduce the risk of tooth discolouration.

A randomized controlled clinical and radiological trial about outcomes of navigation-assisted TKA compared to conventional TKA: long-term follow-up.

PURPOSE: Well balanced knees with good alignment are essential for a well-functioning TKA with long survival of its implants. This prospective randomized study comparing navigation-assisted TKA and conventional TKA reported the clinical and radiological outcomes at a follow-up of 9 years. The purpose of this study was to compare the clinical and radiological outcomes for patients who underwent navigation-assisted TKA or conventional TKA after long-term follow-up. METHODS: A total of 80 patients (88 knees) were available for physical and radiological examination 9 years after TKA. Clinical outcomes were evaluated using HSS, WOMAC, and KS function and pain scores. And radiological outcomes of the component loosening and its survivorship during 9-year follow-up were also evaluated. RESULTS: There were no significant differences in the field of clinical outcomes between the two groups. In terms of radiological outcomes, the navigation group had fewer alignment outliers (7.3 vs 20 %, p = 0.006). Although the clinical outcomes showed no differences between the two groups, the survival rate was slightly better in the navigation group than in the conventional group without statistical significance (best-case scenario 100 vs 95.3 %, n.s., worst-case scenario 95.6 vs 88.4 %, n.s.). CONCLUSION: Navigation-assisted TKA produced better alignment outcomes and better survival rates than conventional instruments although some of the differences were not statistically significant. LEVEL OF EVIDENCE: I.

Phospholipase D1 decreases type I collagen levels in hepatic stellate cells via induction of autophagy.

Hepatic stellate cells (HSCs) are major players in liver fibrogenesis. Accumulating evidence shows that suppression of autophagy plays an important role in the development and progression of liver disease. Phospholipase D1 (PLD1), which catalyzes the hydrolysis of phosphatidylcholine to yield phosphatidic acid (PA) and choline, was recently shown to modulate autophagy. However, little is known about the effects of PLD1 on the production of type I collagen that characterizes liver fibrosis. Here, we examined whether PLD1 regulates type I collagen levels in HSCs through induction of autophagy. Adenovirus-mediated overexpression of PLD-1 (Ad-PLD1) reduced type I collagen levels in the activated human HSC lines, hTERT and LX2. Overexpression of PLD1 in HSCs led to induction of autophagy as demonstrated by increased LC3-II conversion and formation of LC3 puncta, and decreased p62 abundance. Moreover, inhibiting the induction of autophagy by treating cells with bafilomycin or a small interfering (si)RNA for ATG7 rescued Ad-PLD1-induced suppression of type I collagen accumulation in HSCs. The effects of PLD on type I collagen levels were not related to TGF-ß/Smad signaling. Furthermore, treatment of cells with PA induced autophagy and inhibited type I collagen accumulation. The present study indicates that PLD1 plays a role in regulating type I collagen accumulation through induction of autophagy.