Dental caries is a bacterial infection that occurs on organic matter and hard tissues of the teeth such as the dentin, the enamel and the cementum leading to their demineralization which is as a result of the production of acids by the bacteria (Levine et al. 465). The acids accumulate on teeth surfaces until the demineralization process exceeds remineralization factors s including the saliva and calcium, hence progressively break down tissues to result in dental caries, also referred to as cavity or tooth decay. The teeth respond differently to dental caries. This essay explains the tooth’s response to the caries process.
Many morphologic changes occur in the odontoblasts (Robert 889s). These may include enamel lesions which mark the beginning of a pulpal response. Caries lesions that occur after the demineralization of tissues are the initial stage in the process of irreversible pulp inflammation. It has been observed that the pulp can react to signals that traverse the enamel even before the dentin responds to histological caries reactions.
Hypermineralized dentinal tubules are the first observable histological changes that occur in the dentin before the occurrence of any other visible sign of demineralization. This marks the start of odontoblasts activity, though it may resemble physiologic sclerosis of the intratubular which is common during old-age.
Dentin demineralization begins when the enamel lesion comes into contact with the dentin-enamel junction and it occurs in dentin with decreased permeability. A cariogenic biofilm is formed between the dentin and the tooth due to the change of the ph gradient that originates from the demineralization process (Levine et al. 465). If the enamel tissue is not strong enough to separate the dentin from the biofilm, then bacteria gain access into the dentin. The enamel may break due to mechanical stress posed by the biofilm.
The environment around the dentin changes and teeth respond by forming a lesion. The dentin becomes demineralized and this time, plaque is apparent as the lesion progresses actively inside the dentine. According to Sylvester and Ian (138), lesions of the demineralized tissue only occur where the enamel has been cavitated but not in areas where it is intact. Under heavy bacterial infection in the dentin, the tooth reacts by forming a necrotic zone that is soft, moist, and disintegrated. It is possible to separate the enamel from the carious dentin at this stage.
Increased demineralization of the dentin leads to a decrease in the moisture content which leads to shrinking of the dentin. A gap is now visible between the enamel and the dentin. The cariogenic biofilm has sufficient growth conditions hence there is progressive lateral growth of retrograde caries. Eventually, the enamel breaks down if the condition is left untreated for several weeks. This results in irreversible pulpal changes that further lead to infection and necrosis of the pulps. The pulps become infected with apical pathosis (Robert 886s).
In cavitated lesions, tertiary dentin may be formed in response to external stimuli including the cariogenic biofilm. The tertiary dentin prevents further advancement of bacteria. This may result in reversible pulpal infections. Treatment with anesthetics or use of fluoridated toothpaste may kill the bacteria hence give teeth enough immunity to fight further infection through the production of antibodies. Some studies have found that some useful bacteria such as Actinomyces naeslundii have been found to increase teeth with microbial biofilms (plaques) (Levine et al. 467). These bacteria have been associated with increased Actinomyces antibody A-Ab around the infected teeth due to their response to serum immunoglobulin G (IgG) antibody.
It is evident from this essay that there are reversible and irreversible pulp inflammations that represent pulpal response to caries. The teeth may also form antibodies while some helpful bacteria such as the Actinomyces naeslundii may increase tooth immunity response to caries.
Works Cited
Levine, Martin et al. “Antibody Response to Actinomyces Antigen and Dental Caries Experience: Implications for Caries Susceptibility.” Clinical and Diagnostic Laboratory Immunology 2.6 (2005): 764–769. Print.
Robert, Tougher-Decker. “Sugars and dental caries”. The American journal of clinical nutrition 78.4 (2003): 881S-892S. Print.
Sylvester, Fure and Ian Zickert. “Incidence of tooth loss and dental caries in 60-, 70 and 80-year-old Swedish individuals”. Community dentistry and oral epidemiology 25.2 (1997): 137-142. Print.