Caries is a chronic, transmissible, progressive, diet-dependent, and consequential disease that is extremely prevalent in the United States. Caries form due to the initial accumulation of biofilm on our teeth and the caries process is a continuum resulting from many cycles of demineralization and remineralization. Normally, the pH of saliva is an average of 6.7; however, an accumulation of biofilm from poor oral hygiene and/or a sugary diet will result in a pH drop below 5.5, creating dissolution of enamel. Biofilm accumulation leads to caries, periodontal disease, or calculus, requiring intervention to avoid systemic diseases.
Personally, this topic fascinates me, because as a child I have had multiple carious lesions and I believe that many people do not understand the process of demineralization and how it plays against the enamel pellicle. As a child, my mom would always tell me to eat less sugar to avoid the dentist. She, like many other people, was under the perception that it’s the amount of sugary and soft drinks we consume that causes caries, but it’s actually the exposure time that really makes the difference.
So what is the caries process? A few moments after a professional cleaning, saliva touches your teeth and you get a layer of proline rich proteins on the surface, which is also known as the enamel pellicle. The succession of different proteins and peptides aggregating influences the binding of other components - creating a succession of different proteins and peptides binding to modify the surface of the enamel. Like many other proteins, Statherin is a primary crystal growth inhibitor which binds directly to the hydroxyapatite crystals and protects against extra calcium phosphate. While, the acquired enamel pellicle protects binding sites on hydroxyapatite, if a patient is eating a diet high in carbohydrates and not practicing proper oral hygiene, the enamel pellicle and its associated proteins will not be able to protect the tooth and the tooth will be subject to caries and decay. Once the pellicle is formed, the early colonizers, S. mutans will begin attaching, and in the presence of sucrose, produce glucosyltransferases and glucans. The metabolic activities of these homofermentative masses produce lactic acid which demineralizes the tooth and the pellicle degrades. As it breaks down, the pellicle film and calcium phosphate start to deposit on the surface resulting in either a subsurface lesion with intact enamel or an open surface lesion; however, in some cases, the subsurface lesion can remineralize. In general, smooth surfaces can replenish proteins, but the pockets cannot. Furthermore, calculus forms in gingival pockets because it cannot be buffered.
Calculus is associated with gingival inflammation, bleeding upon probing, and halitosis (bad breath). Plaque and calculus retentive factors include malposed teeth, open contacts, and bacterial accumulation. Treatment may sometimes include scaling and root planing in the quadrants in question. Scaling and root planning creates a microbial shift from gram negative to gram positive bacteria, decreases probing depth, increases clinical attachment, and decreases disease progression. Overall, calculus is dicalcium phosphate and tricalcium phosphate and at pH above 6.2, dicalcium phosphate will start to convert back to hydroxyapatite.
Altogether, as dentists, it is important to understand the science and progression associated with caries so we can intervene and re-establish the patient's oral and overall health. Now, being a dental student, I realize mom was right.
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