ObjectiveThe present study aimed at investigating whether non-surgical periodontal treatment can reduce the Haemoglobin A1c (HbA1c) % level in type 2 diabetic patients.MethodsA search of the literature on English publications was performed in Cochrane Central, Medline, ISI Web of Knowledge and EMBASE (until 06 February 2014). An RCT was selected if the subject was type 2 diabetic patients diagnosed with chronic periodontitis, and compared HbA1c% change after non-surgical periodontal treatment alone for at least three months of the study duration. Weighted mean difference for pooled data and large sample size strata were calculated. Heterogeneity and publication bias were explored.ResultsAfter the study selection process, only 9 RCTs were suitable. Compared to the control group, the pooled analysis (n=1082) showed −0.27 % (95 % CI:-0.46 % to −0.07 %, p= 0.007) absolute difference in HbA1c % with treatment while studies with sufficient sample size had HbA1c % change of −0.014 % (95 % CI:-0.18 % to 0.16 %, p= 0.87). Publication bias was marginally significant with Egger’s teat (p=0.045) but not with Begg’s test (p=0.72).ConclusionThe moderate reduction in HbA1c after the non-surgical therapy in patients with type 2 diabetes is consistent with previous systematic reviews. However, more large scale and high-quality RCTs are necessitated to confirm these results.Electronic supplementary materialThe online version of this article (doi:10.1186/s13063-015-0810-2) contains supplementary material, which is available to authorized users.

In order to investigate whether Yinchenhao decoction (YCHD) attenuates hepatic fibrogenesis in the bile duct ligation (BDL) model via recovering and restoring the self-regulation and balance of the renin-angiotensin system (RAS), 33 specific-pathogen-free (SPF) male Sprague-Dawley rats with common BDL and scission were randomly divided into five groups as follows: G1, the sham group (n=4); G2, BDL 7-day group (n=5); G3, BDL+YCHD 430 mg/mL (n=8); G4, BDL+losartan 0.65 mg/mL (ARB group, n=8); G5, model group (BDL without any treatment, n=8). YCHD and losartan (10 mL·kg(-1)·day(-1)) were given by gastric gavage for 16 days following BDL in G3 and G4 groups, respectively. The effect of YCHD on liver fibrosis and the detailed molecular mechanisms were assessed by liver function including total bilirubin (TBIL), direct bilirubin (DBIL), indirect bilirubin (IDBIL), alanine aminotransferase (ALT), and aspartate aminotransferase (AST). Histological changes were observed by transmission electron microscopy (TEM) and Masson trichrome staining. Western blotting was used to detect the protein expression level of the renin-angiotensin system (RAS) components including angiotensin converting enzyme (ACE), angiotensin II type 1 receptor (AT1R), ACE2, angiotensin II (AngII) as well as transforming growth factor β1 (TGFβ1). The experimental data were analyzed by principle component analytical method of pattern recognition. The results showed that biochemically, serum TBIL, DBIL, IDBIL, ALT and AST levels were markedly increased following BDL as compared with the sham group (P<0.05). Serum TBIL, IDBIL and DBIL levels in G3 group were dramatically decreased as compared with G5 and G4 groups (P<0.05). Serum AST level in G3 was significantly lowered than in G5 group (P<0.05), but there was no significant difference in ALT among G3, G4 and G5 groups (P>0.05). Histologically, livers in G3 group showed less hepatocytes necrosis, less bile duct hyperplasia and less collagen formation than in G4 and G5 groups. The protein expression levels of ACE2, ACE, AngII, AT1R and TGFβ1 in G2, G3 and G4 groups were significantly higher than in sham group (P<0.05), and lower than in G5 group (P<0.05). However, the differences among G2, G3 and G4 groups were not significant (P>0.05). ACE2 protein expression in G3 group was significantly higher than in G2 group (P<0.05) and there was no significant difference in comparison with G4 group (P>0.05). Moreover, the protein expression of TGFβ1 in G3 group was significantly lower than in G5 and G4 groups (P<0.05). Our findings suggest that the antifibrotic effects of YCHD may be associated with the decreased classical RAS pathway components and TGFβ1 downexpression so as to recover and rebuild self-regulation of the RAS by elevating the protein expression of ACE2.