In a recent commentary in the Journal of Periodontology, Merchant and Josey (2016) had suggested directed acyclic graphs to better comprehend the partly conflicting results from randomized controlled trials (RCT) on diabetic control after periodontal treatment in diabetic patients. In particular the influence of obesity caught their attention.
As a matter of fact, a remarkable number of systematic reviews (whose varying quality have recently been reviewed in at least two further SRs of SRs) have shown that numerous small-scale, single-center, often poorly designed RCTs had shown that the marker for diabetic control, HbA1c, might be reduced by, say 0.4% 3 months after in essence non-surgical periodontal therapy. The only large-scale, multi-center trial (DPTT) by Engebretson et al. (2013) couldn’t confirm that, though, which sparked harsh criticism of a large number of our thought leaders. A professor in the Department of Epidemiology and Biostatistics at the University of South Carolina, Columbia, Dr. Anwar Merchant himself had written a letter to the editors of JAMA pointing first to the fact that most participants in the paper by Engebretson et al. were utterly obese. He had further noticed that, “[i]n RCTs conducted among mostly nonobese individuals, periodontal treatment has been shown to reduce systemic inflammation2,4 and improve glycemic control among those with type 2 diabetes.2 However, periodontal treatment has not been shown to affect glycemic control in RCTs conducted among predominantly obese individuals with type 2 diabetes.1,3”
Obesity is positively correlated with inflammatory markers in the blood and strongly related to insulin resistance and metabolic dysregulation mediated by chronic systemic inflammation.5 These findings, taken together with results from RCTs evaluating the effects of periodontal treatment, suggest that the lack of effect of periodontal treatment on glycemic control observed in the study by Engebretson et al may be attributed to the high level of obesity in the study population. Therefore, the findings may be generalizable only to predominantly obese populations with type 2 diabetes.
Any dental student in Germany would certainly fail his/her final exam if carelessly talking about the role of “fluor” in preventive dentistry. An assumed power of environmentalist pressure groups is very much feared among cariologists who want to make sure that it is fluoride, not fluorine, which has its most important part in the prevention and early treatment of dental caries. One possible accident of a child ingesting several fluoride tablets would suffice to provide environmentalists with further arguments. Elemental fluorine is highly toxic, in contrast to fluoride which is not so toxic, and environmentalist propagandists have used the public’s lack of knowledge to differentiate for manipulating public opinion against water fluoridation and further application and wide distribution of fluorides which have certaily resulted in most of the observed post WWII caries decline in all industrialized countries. So, dental students are advised to be precise. Fluorides are used in preventive dentistry, not highly toxic fluorine (“fluor”). As table salt is not chlorine!
The frenzy about fluorides in cariology appears to be based on the concept that dental caries is a result of fluoride deficiency. While it is undisputed that modern oral hygiene includes daily toothbrushing with fluoridated toothpaste (1450 ppm), additional application of, for instance, fluoride mouthwash may be restricted, based on current evidence, to caries-active individuals, in particular between 6 and 18 years. Most recently, 0.5% to 1% chlorhexidine gel alone or in combination with fluoride or 0.12% chlorhexidine mouthwash alone or with fluoride for prevention of coronal caries was not recommended, based on expert opinion in the former and strong experimental evidence in the latter case. Continue reading