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I need to know this information about Streptococcus mutans (tooth decay)  please. PLEASE BE CLEAR AND ABLE...

I need to know this information about Streptococcus mutans (tooth decay)  please. PLEASE BE CLEAR AND ABLE TO UNDERSTAND IT I WILL RATE.

-ETIOLOGY:

Reservoir:  

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Answer) Etiology of Streptococcus mutans (tooth decay)

Early colonizers of the tooth surface are mainly Neisseria spp. and streptococci, including S. mutans. They must withstand the oral cleansing forces (e.g. saliva and the tongue movements) and adhere sufficiently to the dental hard tissues. The growth and metabolism of these pioneer species changes local environmental conditions (e.g., Eh, pH, coaggregation, and substrate availability), thereby enabling more fastidious organisms to further colonize after them, forming dental plaque. Along with S. sobrinus, S. mutans plays a major role in tooth decay, metabolizing sucrose to lactic acid. The acidic environment created in the mouth by this process is what causes the highly mineralized tooth enamel to be vulnerable to decay. S. mutans is one of a few specialized organisms equipped with receptors that improve adhesion to the surface of teeth. S. mutans uses the enzyme glucansucrase to convert sucrose into a sticky, extracellular, dextran-based polysaccharide that allows them to cohere, forming plaque. S. mutans produces dextran via the enzyme dextransucrase (a hexosyltransferase) using sucrose as a substrate in the following reaction: n sucrose → (glucose)n + n fructose
Sucrose is the only sugar that bacteria can use to form this sticky polysaccharide.

However, other sugars—glucose, fructose, lactose—can also be digested by S. mutans, but they produce lactic acid as an end product. The combination of plaque and acid leads to dental decay

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The reservoir of Streptococcus mutans (tooth decay)-

the oral cavity is the Reservoir of Streptococcus mutans (tooth decay).  oral infections and poor oral health can provoke the introduction of oral microorganisms into the bloodstream or the lymphatic system. The subsequent attachment and multiplication of these bacteria on tissues or organs can lead to focal oral infections. Pathogenic agents may also remain at their primary oral site but the toxins liberated can reach an organ or tissue via the bloodstream and cause metastatic injury. Finally, metastatic inflammation may result from an immunological injury caused by oral bacteria or their soluble products that enter the bloodstream and react with circulating specific antibodies to form macromolecular complexes.


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