findings from the population-based case-control COLDENT study suggest.
The rate of new CRC diagnoses among individuals in the study who had a history of PD was nearly 50% higher than in those with no such history, after adjustment for a host of medical and demographic factors, the investigators noted.
This isn’t the first time PD has been linked with extra-oral health outcomes, including gastrointestinal cancers. It has been shown to be associated with several major systemic diseases, such as cardiovascular, respiratory, chronic kidney, and metabolic diseases. Evidence also suggests a link between PD and Alzheimer’s disease.
However, prior studies that looked at the connection between PD and CRC have relied on secondary analyses of data from other studies and are limited by other methodologic shortcomings, noted the researchers, led by Amal Idrissi Janati, DDS, University of Montreal.
To better assess the etiologic role of PD in the development of CRC, Dr. Janati and colleagues analyzed 348 histologically confirmed cases of colon or rectal cancer diagnosed from January 2013 to December 2019 and compared them to 310 matched controls.
The rate of new CRC diagnoses among individuals with a history of PD was 1.4 times higher than among those with no PD history after adjustment for age and gender. It increased to 1.45 times higher when the researchers also adjusted for body mass index, education, income, diabetes, family history of CRC, regular use of aspirin and non-aspirin nonsteroidal anti-inflammatory drugs, and lifetime cumulative smoking, consumption of red and processed meats, alcohol consumption, and total physical activity score.
The findings were published online Jan. 26 in Cancer Causes and Control.
“Our results support the hypothesis of an association between PD and sporadic CRC risk,” the researchers said, adding that further epidemiologic studies are recommended.
They speculated that the “putative mechanism of PD and cancer association involves the spread of periodontal pathogens to extra-oral sites, dissemination of bacteria endotoxins, and release of inflammation products directly into the bloodstream.”
The chronic inflammation associated with PD “promotes carcinogenesis by induction of gene mutations, inhibition of apoptosis, stimulation of angiogenesis, cell proliferation, and epigenetic alterations,” they added.
The COLDENT study was supported by the Cancer Research Society. The authors have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.