The Tooth’s Response to the Caries Process Essay
The Tooth’s Response to the Caries Process Essay
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 Tooth’s Response to the Caries Process Essay. 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 Tooth’s Response to the Caries Process Essay.
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.
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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. The Tooth’s Response to the Caries Process Essay.
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.
Abstract
Dental caries (decay) is an international public health challenge, especially amongst young children. Early childhood caries (ECC) is a serious public health problem in both developing and industrialized countries. ECC can begin early in life, progresses rapidly in those who are at high risk, and often goes untreated. Its consequences can affect the immediate and long-term quality of life of the child’s family and can have significant social and economic consequences beyond the immediate family as well. ECC can be a particularly virulent form of caries, beginning soon after dental eruption, developing on smooth surfaces, progressing rapidly, and having a lasting detrimental impact on the dentition. Children experiencing caries as infants or toddlers have a much greater probability of subsequent caries in both the primary and permanent dentitions. The relationship between breastfeeding and ECC is likely to be complex and confounded by many biological variables, such as mutans streptococci, enamel hypoplasia, intake of sugars, as well as social variables, such as parental education and socioeconomic status, which may affect oral health. Unlike other infectious diseases, tooth decay is not self-limiting. Decayed teeth require professional treatment to remove infection and restore tooth function. In this review, we give detailed information about ECC, from its diagnosis to management.
Dental caries is the most common chronic infectious disease of childhood, caused by the interaction of bacteria, mainly Streptococcus mutans, and sugary foods on tooth enamel. S. mutans can spread from mother to baby during infancy and can inoculate even pre-dentate infants. These bacteria break down sugars for energy, causing an acidic environment in the mouth and result in demineralization of the enamel of the teeth and dental caries.[1] Early childhood caries (ECC) is a serious public health problem in both developing and industrialized countries.[2] ECC can begin early in life, progresses rapidly in those who are at high risk, and often goes untreated.[3,4] Its consequences can affect the immediate and long-term quality of life of the child and family, and can have significant social and economic consequences beyond the immediate family as well.[5]
DESCRIPTION
Dental caries in toddlers and infants has a distinctive pattern. Different names and terminology have been used to refer to the presence of dental caries among very young children.[6] The definitions first used to describe this condition were related to etiology, with the focus on inappropriate use of nursing practices. The following terms are used interchangeably: Early childhood tooth decay, early childhood caries, baby bottle-fed tooth decay, early childhood dental decay, comforter caries, nursing caries, maxillary anterior caries, rampant caries, and many more.[7,8] Some of these terms indicate the causes of dental caries in pre-school children.The Tooth’s Response to the Caries Process Essay. [8] Baby bottle-fed tooth decay refers to decay in an infant’s teeth, associated with what the baby drinks.[9] However, some authors use the term “nursing caries” because it designates inappropriate bottle use and nursing practices as the causal factors.[7,10] However, the term “early childhood caries” is becoming increasingly popular with dentists and dental researchers alike.[8,11]
The term “early childhood caries” was suggested at a 1994 workshop sponsored by the Centers for Disease Control and Prevention in an attempt to focus attention on the multiple factors (i.e. socioeconomic, behavioral, and psycho-social) that contribute to caries at such early ages, rather than ascribing sole causation to inappropriate feeding methods.[12] ECC is defined as “the presence of one or more decayed (non-cavitated or cavitated lesions), missing teeth (due to caries), or filled tooth surfaces in any primary tooth in a child 72 of months age or younger. In children younger than 3 years of age, any sign of smooth-surface caries is indicative of severe early childhood caries (S-ECC). From ages 3 through 5, one or more cavitated, missing teeth (due to caries), or filled smooth surfaces in primary maxillary anterior teeth, or decayed, missing, or filled score of ≥4 (age 3), ≥5 (age 4), or ≥6 (age 5) surfaces constitutes S-ECC.[13]
In the initial phase, ECC is recognized as a dull, white demineralized enamel that quickly advances to obvious decay along the gingival margin.[14] Primary maxillary incisors are generally affected earlier than the four maxillary anterior teeth which are often involved concurrently.[15] Carious lesions may be found on either the labial or lingual surfaces of the teeth and, in some cases, on both.[16] The decayed hard tissue is clinically evident as a yellow or brown cavitated area. In older children, whose entire primary dentition is fully erupted, it is not unusual to see considerable advancement of the dental damage. The Tooth’s Response to the Caries Process Essay.
EPIDEMIOLOGY
Despite the decline in the prevalence of dental caries in children in the western countries, caries in pre-school children remains a problem in both developed and developing countries. ECC has been considered to be at epidemic proportions in the developing countries.[4,17]
A comprehensive review of the occurrence of the caries on maxillary anterior teeth in children, including numerous studies from Europe, Africa, Asia, the Middle East, and North America, found the highest caries prevalence in Africa and South-East Asia.[18] The prevalence of ECC is estimated to range from 1 to 12% in infants from developed countries.[19]
Prevalence of ECC is a not a common finding relative to some European countries (England, Sweden, and Finland), with the available prevalence data ranging from below 1% to 32%.[20,21] However, this figure is rising by as much as 56% in some eastern European countries.[22] In US, pre-school children data from a more recent study indicate that the prevalence of dental caries of children 2–5 years of age had increased from 24% in 1988–1994 to 28% in 1999–2004.The Tooth’s Response to the Caries Process Essay. Overall, considering all 2–5-year olds, the 1999-2004 survey indicates that 72% of decayed or filled tooth surfaces remain untreated.[14,23,24] The prevalence of ECC children in the general population of Canada is less than 5%; but in high-risk population, 50–80% are affected.[25,26,27] Studies reveal that the prevalence percentage of ECC in 25- to 36-month olds[28] is 46% and the reported prevalence in Native Canadian 3-year-olds[29] has been as high as 65%.
Published studies show higher prevalence figures for 3-year-olds, which ranges from 36 to 85%[30–32] in Far East Asia region, whereas this figure is 44% for 8- to 48-month olds[33] reported in Indian studies. ECC has been considered at epidemic proportions in the developing countries.[34] Studies conducted in the Middle East have shown that the prevalence of dental caries in 3-year-olds is between 22% and 61%[35–37] and in Africa it is between 38% and 45%.[38,39]
ETIOLOGY
The etiology of ECC is multifactorial and has been well established. ECC is frequently associated with a poor diet[40] and bad oral health[14] habits.
Microbiological risk factors
S. mutans and Streptococcus sobrinus are the main cariogenic micro-organisms.[41,42] These acid-producing pathogens inhabiting the mouth cause damage by dissolving tooth structures in the presence of fermentable carbohydrates such as sucrose, fructose, and glucose.[43,44] Most of the investigations[15,45,46] have shown that in children with ECC, S. mutans has regularly exceeded 30% of the cultivable plaque flora. These bacterial masses are often associated with carious lesions, white spot lesions, and sound tooth surfaces near the lesions. Conversely, S. mutans typically constitutes less than 0.1% of the plaque flora in children with negligible to no caries activity.[47] It is well known that initial acquisition of mutans streptococci (MS) by infants occurs during a well-delineated age range that is being designated as the window of infectivity.[48] Most of the long-term studies also demonstrated that the individuals with low infection levels in this period are less likely to be infected with MS, and subsequently have the lowest level of risk of developing caries.[49,50] This may be explained by the competition between the oral bacteria, resulting in the invasion of the niches, where MS can easily colonize, by less pathogenic species.[51]
Vertical transmission, also known as mother-to-child transmission, is the transmission of an infection or other disease from caregiver to child. The major reservoir from which infants acquire MS is their mothers.The Tooth’s Response to the Caries Process Essay. The early evidence for this concept comes from bacteriocin typing studies[52–54] where MS isolated from mothers and their infants demonstrated identical bacteriocin typing patterns. More advanced technology that utilized chromosomal DNA patterns or identical plasmids provided more compelling evidence to substantiate the concept of vertical transmission.[55–58]
Feeding practices
Inappropriate use of baby bottle has a central role in the etiology and severity of ECC. The rationale is the prolonged bedtime use of bottles with sweet content, especially lactose. Most of the studies have shown significant correlation between ECC and bottle-feeding and sleeping with a bottle.[59–61] Breastfeeding provides the perfect nutrition for infant, and there are a number of health benefits to the breastfed child, including a reduced risk of gastrointestinal and respiratory infections.[62] However, frequent and prolonged contact of enamel with human milk has been shown to result in acidiogenic conditions and softening of enamel. Increasing the time per day that fermentable carbohydrates are available is the most significant factor in shifting the re-mineralization equilibrium toward de-mineralization.[63] There appears to be a clinical consensus amongst dental practitioners that prolonged and nocturnal breastfeeding is associated with an increased risk of ECC, especially after the age of 12 months. These conditions explained by less saliva production at night result in higher levels of lactose in the resting saliva and dental plaque for longer than would be expected during the day. Thereby, balance is shifted toward de-mineralization rather than re-mineralization during the night because of the insufficient protection caused by reduced nocturnal salivary flow.[64,65]
Sugars
In general, perspective dental caries is accepted as primarily a microbial disease, but few would disagree that dietary features play a crucial and a secondary role. Numerous worldwide epidemiologic studies, laboratory and animal experiments, as well as human investigations after the World War II have contributed to much of the knowledge on the etiology and natural history of caries.[66]
Fermentable carbohydrates are a factor in the development of caries. The small size of sugar molecules allows salivary amylase to split the molecules into components that can be easily metabolized by plaque bacteria.[67] This process leads to bacteria producing acidic end products with subsequent de-mineralization of teeth[68,69] and increased risk for caries on susceptible teeth. Some authors[70,71] found a positive relationship between sugar intake and the incidence of dental caries where fluoridation was minimal and dental hygiene was poor. The length of time of exposure of the teeth to sugar is the principal factor in the etiology of dental caries; it is known that acids produced by bacteria after sugar intake persist for 20–40 min. The Tooth’s Response to the Caries Process Essay. Some authors[72] studied the clearance of glucose, fructose, sucrose, maltose, and sorbitol rinses, as well as chocolate bars, white bread, and bananas, from the oral cavity. Sucrose is removed the quickest, while sorbitol and food residues stay in the mouth longer. Retentiveness of the food and the presence of protective factors in foods (calcium, phosphates, fluoride) are considered as other factors that contribute to de-mineralization.
The best available evidence indicates that the level of dental caries is low in countries where the consumption of free sugars is below 40–55 g per person per day.[73] Caries risk is greatest if sugars are consumed at high frequency and are in a form that is retained in the mouth for long periods.[74] Non-milk extrinsic sugars (NMES) have also been widely implicated as the cause of caries, while milk sugars are not.[75] However, consumption of milk-based formulas for infant feeding, even without sucrose in their formulation, proved to be cariogenic.[76] The relationship between diet and dental caries has become weaker in contemporary society and this has been attributed to the widespread use of fluoride.[77] There is evidence to show that many groups of people with habitually high consumption of sugars also have levels of caries higher than the population averages.
Socioeconomic factors
Association between ECC and the socioeconomic status (SES) has been well documented. Studies suggested that ECC is more commonly found in children who live in poverty or in poor economic conditions,[35,40,44,78,79] who belong to ethnic and racial minorities,[80] who are born to single mothers,[81] whose parents have low educational level, especially those of illiterate mothers.[35,82,83] In these populations, due to the prenatal and perinatal malnutrition or undernourishment, these children have an increased risk for enamel hypoplasia and exposure to fluorine is probably insufficient,[80] and there is a greater preference for sugary foods.[84] The Tooth’s Response to the Caries Process Essay.
The possible influence of SES on dental health may also be a consequence of differences in dietary habits and the role of sugar in the diet.[85] In their review on inequalities in oral health, Sheiham and Watt indicated that the main causes of inequalities in oral health are differences in patterns of consumption of non-milk sugars and fluoride toothpaste.[86] Weinstein[4] emphasizes the discrepancy in ECC prevalence rate: 1–12% in developed countries, whereas it as high as 70% in developing countries or within select immigrant or ethnic minority populations. Authors in Ref.[23] confirm that children with parents in the lowest income group had mean Decayed, Missing, and Filled Teeth (dmft) scores four times as high as children with parents in the highest income group.
DIAGNOSIS
ECC is initially recognized as a dull, white hand of de-mineralized enamel that quickly advances to obvious decay along the gingival margin.[31] The decay is generally first seen on the primary maxillary incisors, and the four maxillary anterior teeth are often involved concurrently.[87] Carious lesions may be found on either the labial or lingual surfaces of the teeth and, in some cases, on both.[40] The decayed hard tissue is clinically evident as a yellow or brown cavitated area. In the older child whose entire primary dentition is fully erupted, it is not unusual to see considerable advancement of the dental damage.
Furthermore, the expression S-ECC was adopted in lieu of rampant caries in the presence of at least one of the following criteria:
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Any sign of caries on a smooth surface in children younger than 3 years.
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Any smooth surface of an antero-posterior deciduous tooth that is decayed, missing (due to caries), or filled in children between 3 and 5 years old.
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The dmft index equal to or greater than 4 at the age of 3 years, 5 at the age of 4 years, and 6 at the age of 5 years.[88]
CONSEQUENCES OF UNTREATED DENTAL CARIES IN CHILDREN
Although largely preventable by early examination, identification of individual risk factors, parental counseling and education, and initiation of preventive care procedures such as topical fluoride application, the progressive nature of dental disease can quickly diminish the general health and quality of life for the affected infants, toddlers, and children.[89] Failure to identify and prevent dental disease has consequential and costly long-term adverse effects [Table 1]. The Tooth’s Response to the Caries Process Essay. As treatment for ECC is delayed, the child’s condition worsens and becomes more difficult to treat, the cost of treatment increases, and the number of clinicians who can perform the more complicated procedures diminishes.
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Table 1
A summary of the consequences of leaving untreated carious primary teeth
Oral health means more than just healthy teeth. Oral health affects people physically and psychologically, and influences how they grow, look, speak, chew, taste food, and socialize, as well as their feelings of social well-being.[90] Children’s quality of life can be seriously affected by severe caries because of pain and discomfort which could lead to disfigurement, acute and chronic infections, and altered eating and sleeping habits, as well as risk of hospitalization, high treatment costs, and loss of school days with the consequent diminished ability to learn.[91] In most small children, ECC is associated with reduced growth and reduced weight gain due to insufficient food consumption to meet the metabolic and growth needs of children less than 2 years old.[91] Children of 3 years of age with nursing caries weighed about 1 kg less than control children[92] because toothache and infection alter eating and sleeping habits, dietary intake, and metabolic processes. Disturbed sleep affects glucosteroid production. In addition, there is suppression of hemoglobin from depressed erythrocyte production. Early tooth loss caused by dental decay has been associated with the failure to thrive, impaired speech development, absence from and inability to concentrate in school, and reduced self-esteem.[92–94]
The Tooth’s Response to the Caries Process Essay
