Recent advances in the pathogenesis and prevention strategies of dental calculus.

Dental calculus severely affects the oral health of humans and animal pets. Calculus deposition affects the gingival appearance and causes inflammation. Failure to remove dental calculus from the dentition results in oral diseases such as periodontitis. Apart from adversely affecting oral health, some systemic diseases are closely related to dental calculus deposition. Hence, identifying the mechanisms of dental calculus formation helps protect oral and systemic health. A plethora of biological and physicochemical factors contribute to the physiological equilibrium in the oral cavity. Bacteria are an important part of the equation. Calculus formation commences when the bacterial equilibrium is broken. Bacteria accumulate locally and form biofilms on the tooth surface. The bacteria promote increases in local calcium and phosphorus concentrations, which triggers biomineralization and the development of dental calculus. Current treatments only help to relieve the symptoms caused by calculus deposition. These symptoms are prone to relapse if calculus removal is not under control. There is a need for a treatment regime that combines short-term and long-term goals in addressing calculus formation. The present review introduces the mechanisms of dental calculus formation, influencing factors, and the relationship between dental calculus and several systemic diseases. This is followed by the presentation of a conceptual solution for improving existing treatment strategies and minimizing recurrence.

Bacteria-mediated resistance of neutrophil extracellular traps to enzymatic degradation drives the formation of dental calculi.

Dental calculi can cause gingival bleeding and periodontitis, yet the mechanism underlying the formation of such mineral build-ups, and in particular the role of the local microenvironment, are unclear. Here we show that the formation of dental calculi involves bacteria in local mature biofilms converting the DNA in neutrophil extracellular traps (NETs) from being degradable by the enzyme DNase I to being degradation resistant, promoting the nucleation and growth of apatite. DNase I inhibited NET-induced mineralization in vitro and ex vivo, yet plasma DNases were ineffective at inhibiting ectopic mineralization in the oral cavity in rodents. The topical application of the DNA-intercalating agent chloroquine in rodents fed with a dental calculogenic diet reverted NET DNA to its degradable form, inhibiting the formation of calculi. Our findings may motivate therapeutic strategies for the reduction of the prevalence of the deposition of bacteria-driven calculi in the oral cavity.

[Monitoring the prevalence of schistosomiasis in Erlang Village, Yueyang County from 2005 to 2012].

OBJECTIVE: To understand the dynamics of schistosomiasis situation so as to provide the evidence for formulating the prevention and control scheme in Erlang Village, Yueyang County, Hunan Province. METHODS: The schistosomiasis prevalence and Oncomelania snail status were investigated from 2005 to 2012. RESULTS: The schistosome infection rates of the residents decreased from 2.76% in 2005 to 0.54% in 2012 and the decline rate was 80.43%; the infection rates of the livestock decreased from 8.70% in 2005 to 0 in 2012. No snails were found in the inner embankment over the eight-year period. The density of the infected snails was 0.0005 per 0.1 m(2) in 2005, but no positive snails were found from 2009 to 2012 outside the embankment. CONCLUSION: The schistosome infections of people and livestock and the status of the intermediate host snails have achieved the criteria of schistosomiasis transmission control.