Byproducts of periodontal bacteria may induce oral cancer growth
CLEVELAND, USA: Periodontal pathogens such as Porphyromonas gingivalis and Fusobacterium nucleatum produce five different short chain fatty acids as metabolic byproducts. Researchers at Case Western Reserve University in the U.S. have found that these acids might trigger the growth of lesions and tumors in the mouth.*
The findings may have important implications for HIV-positive and AIDS patients in particular because about 20 percent of HIV patients develop Kaposi's sarcoma (KS) lesions in the oral cavity, which can develop into malignant tumors.
Although it is not known what role the oral microenvironment plays in oral KS tumor development, the study demonstrated that short chain fatty acids from P. gingivalis and F. nucleatum promote replication of KS-associated herpesvirus (KSHV), the etiological agent associated with KS, explained lead investigator Dr. Fengchun Ye.
In the study, the researchers assessed the gingival health of 21 patients and studied their saliva samples. Eleven patients (average age of 50) were diagnosed with severe chronic gum disease and ten participants (average age of 26) had healthy gums. Overall, the researchers detected significantly higher levels of short chain fatty acids in the saliva of patients with severe periodontal disease and observed that the fatty acids allowed KSHV to multiply.
In addition, they found that this process inhibited molecules in the body's immune system from stopping the growth of the virus.
The researchers believe that this discovery could lead to early saliva testing for the bacteria to enable early treatment and monitoring for signs of cancer in at-risk patients.
Alongside HIV patients, KS affects other populations with comprised immune systems, such as people on medication to suppress rejection of transplants, cancer patients on chemotherapy and elderly people, according to the researchers.
The study, titled "Short Chain Fatty Acids From Periodontal Pathogens Suppress HDACs, EZH2, and SUV39H1 to Promote Kaposi's Sarcoma-Associated Herpesvirus Replication," was published online on Feb. 5 in the Journal of Virology ahead of print.