Pediatric Dentistry Epidemiology Case Study

Cross-Sectional Study: To Assess the Prevalence of Dental Diseases and Treatment Needs of Pediatric Patients Attending Dental Clinics at Ajman University

The WHO Global Oral Health Program emphasizes that although countries have made substantial progress in their effort to improve community health in general, there is still a lot to be done in relation to oral health – particularly among minority and economically-disadvantaged groups1. Oral diseases such as orodental trauma, oropharyngeal cancers, oral lesions, tooth loss, periodontal disease, and dental caries continue to be a thorn in the flesh for governments in the world over even though reports have shown declines in their prevalence and severity. Despite their endemic nature, these diseases impact negatively on the health of the general population and put a strain on the global economy1. Having damaged, discolored or missing teeth affects patients’ well-being and daily lives, just as the time taken to tend to the same restricts activities at home, school, and at the workplace; causing dozens of work and school hours to be lost annually. Anderson 2 points out that the reason why interceptive and preventive interventions have repeatedly failed is because policy-makers have focused on expending resources to the entire population rather than concentrating on the at-risk populations. He advises that in cases where disease is increasingly skewed, “and there are effective interventions, risk-assessment can play a significant role in the treatment of infectious diseases”2(p 377).

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This study presents the researcher’s current knowledge of the epidemiology and risk assessment elements of dental diseases with an increased focus on the adolescent and pediatrician population in the city of Ajman. Ajman was selected for this analysis, first because of its cosmopolitan nature, and secondly, because its average-income status makes it an attractive basis for studying the effect of risk factors other than socio-economic disadvantage. Not many studies have been initiated to assess the oral health status of school-going children in Ajman area, and even the few that have seem to concentrate more on the characteristics of the population as a whole, as opposed to specific demographic cohorts3, 4, 5. In light of this, the current analysis seeks to provide baseline data on the prevalence of dental diseases and treatment needs among 4 to 18-year-old school-going children attending dental clinics in Ajman University. It is based on Moses and his colleagues’6 four-step plan for improving oral health in the community, which involves i) collection of data on oral diseases; ii) evaluation of data to identify community needs; iii) identification of at-risk groups, and iv) formulation of informed treatment plans; and is geared towards guiding oral health planners in Ajman, and the greater Saudi towards developing effective preventive strategies and treatment plans for their communities

Background of the Study

Periodontal disease and dental caries are considered the most burdensome oral health conditions worldwide, alongside malocclusion and enamel fluorosis. Dental caries has persisted as a serious global health concern, with a prevalence rate seven times that of hay fever and five times that of asthma7. The disease currently affects between 60 and 90% of the school-going children population, and a significant proportion of the adult population8. The WHO, in its 2003 annual health report9, points out that although there are significant disparities in the severity and distribution of dental caries between continents and even regions within the same country, the overall prevalence rates of the disease among school-going children have fallen substantially from those reported in the closing decades of the 19th century. Fos and Hutchison 7 attribute this decline to higher levels of education among parents, increased dental insurance coverage, and increased procedure use by dental care providers.

The WHO report 9 shows dental caries prevalence rates, measured by the Decayed, Missing, and Filled Teeth index (DMFT), as being relatively high in the European region (DMFT=2.6) and the Americas (DMFT=3.0), and considerably low (DMFT =1.2-2.6) in Asia and the Middle East. The trend, however, appears to have changed over the last decade, at least for Saudi Arabia. A 2014 review by Al-Ansari 10of the University of Damman in Saudi Arabia, which brought together the findings of multiple cross-sectional studies conducted on the Saudi Arabian populace between 1981 and 2012, found the dental caries prevalence rate to have averaged 7.34 in DMFT for the population aged between 3 and 7; 7.35 for the population aged between 12 and 19; and 14.53 for the adult population between the ages of 30 and 45. This represented a 95% prevalence rate for children aged between 3 and 7; 91% for adolescents between ages 12 and 19; and a massive 98% for adults aged between 30 and 4510. The rising prevalence rates in recent years have been attributed to the rising consumption of sugary foods and increased non-exposure to fluorides8.

It is estimated that approximately 84.37% of school-going children in Asia suffer from gingivitis, and that another 36.42% and 36.36% suffer from malocclusion and enamel fluorosis respectively11. Clinicians and health specialist further estimate that 62 million children in the Asian region are at risk of developing fluorosis, and that the risk is higher for females (DMFT=1.83) compared to males (DMFT=1.3)11. Children with special needs and those from low-income backgrounds have also been found to run higher risks of getting infected and a two times greater likelihood of having untreated tooth decay7. These are worrying statistics, especially because the effects of dental diseases spread far beyond the oral cavity and its supporting structures, and have a pronounced effect on the well-being of the entire body system7. Periodontal disease, for instance, has been found to be a risk factor for a number of serious health complications – including obesity, rheumatoid arthritis, insulin resistance, peripheral arterial diseases, and cardiovascular diseases 12, 7-8.

In light of all these factors, the Saudi Arabian economy is deemed to lose billions of shillings in treatment in coming years; and not only that, the general well-being of the population stands to be compromised. Arigbede and his colleagues 12 (p 487) caution against treating oral health as a “separate, distant, and less important area of health, which is totally unrelated to lifespan and its quality.” Thus, in order for comprehensive healthcare to be achieved, oral health needs to be give the attention it deserves; and this requires clinicians and policy makers alike to first understand the epidemiology and risk assessment elements of dental diseases and other oral health conditions. This understanding provides a sound rationale for the current study.

Aim: To assess the prevalence of dental diseases and treatment needs among pediatric patients attending dental clinics in Ajman University

Study Design: Retrospective study using the records of pediatric patients of Ajman University

2.0 Literature Review

This review comprises of two sections. The first section covers literature on the pathobiology of four selected diseases that have been found to be most common among the population of interest — dental caries, periodontal diseases, enamel fluorosis and malocclusion. It explores definitions, epidemiology, pathobiology, and infectious agents in relation to each of the select diseases. The second section covers literature on the impact of dental diseases on morbidity and general health. It assesses the health effect of dental diseases on various body systems.

Section One

i) Dental Caries

Definition and Etiology: Dental caries is tooth decay that causes enamel breakdown, often resulting in clinical damage to the overall structure of the tooth7, 12. Three different hypotheses have attempted to explain the etiology of dental caries13. The three agree on the physiological mechanisms involved, and only differ in regard to the etiological agent responsible. The specific plaque hypothesis postulates that caries results from the over-infestation of the Streptococcus mutans bacterium, often denoted as S. mutans, whose bacterial cells colonize the tooth structure, inhibiting glucan action, and creating a thick, sticky intraoral bacterial film referred to as dental plaque 2, 13. This plaque reacts with metallic substrates in food to produce organic acids that gradually dissolve the calcium component present in the tooth enamel, leading to cavitation2. The severity of the infection is determined by the degree of bacterial infestation. Smooth surface caries is associated with S. mutans infestation levels exceeding 500,000cfu/ml (colony-forming units per milliliter of saliva); whereas fissure caries is associated with lower infestation levels (Anderson, 2002).

The ecological hypothesis and the non-specific plaque hypothesis do not, however, seem to be in agreement with this view. The ecological plaque hypothesis postulates that caries develops when unexpected changes in the local environment of the oral cavity interfere with the bacterial balance therein, spurring an overgrowth of disease-causing microflora14. The non-specific plaque hypothesis, on the other hand, casts doubt on the implication of S. mutans as the primary etiological agent in caries development. It suggests that caries is not caused by the action one particular species, but rather is the product of the overall activity of multiple bacterial species found in the oral cavity, including Lactobacilli, Propionibacterium, and Atopobium14. Aas and his colleagues 14 sought to find out how true this claim is. They analyzed 243 samples of dental plaque obtained from primary and permanent teeth; and found that although the S. mutans bacteria was extensive in caries-infected primary teeth, it was less common in subjects with permanent teeth14. As a matter of fact, a significant”10% of subjects with rampant caries in permanent teeth” were found not to have detectable levels of the bacteria14 (p 1407). This finding supports the conclusion that bacterial profiles i) differ between permanent and primary dentitions; and ii) change as the disease progresses14, 2. Nonetheless, there is consensus that all these other bacterial species are associated more with disease progression, and do not play as conspicuous a role in the initiation of dental caries14, 2.

Epidemiology: researchers have differed on the actual prevalence rate of dental caries among school-going children. Al-Ansari10, for instance, assessing the prevalence of caries among Saudi Arabian children, places the prevalence of the same at a massive 90-97%, positing that caries accounts for more than 50% of tooth loss among children the world over. Other researchers, however, believe the rate to be substantially lower than this, specifically, between 60 and 90%7-8. There is consensus, nonetheless, that contrary to what has been reported in Europe and the Americas, the dental caries prevalence rates in Saudi Arabia and the greater Continent of Asia have risen substantially in recent years 10, 6, 11. This has largely been attributed to the increased prominence of risk factors associated with dental caries, including inappropriate feeding habits, low socio-economic status, non-exposure to fluorides, and high magnitudes of cariogenic bacterium2, 10.

Risk Factors and At-Risk Populations

The role of Genetics

The fact that a mother can essentially pass on the S. mutans bacteria to their child (vertical transmission) establishes valid grounds for the existence of genetic risk factor relationships between an individual’s phenotypic profile and their likelihood of getting infected with dental caries2. Whether or not one harbors a clinical infection depends on how well their immune system is able compete with the S. mutans strain resident in their oral cavity. The disease is only judged significant if its effects are visible; and its effects are only visible if the resident strain of bacteria is able to compete successfully with the immune system2. Secretory Immunoglobulin A (sIgA), present in saliva, is the chief immunologic response against the S. mutans organism; and is believed to work by binding to the tooth surface to prevent the attachment of the bacteria2. Part of this immunity is passed on to the child through lactation products (or the placenta for the unborn child), but since the child’s immunity is still considerably weak, it is unable to fight the strain of bacteria resident in the mother; and the child runs a significantly high risk of acquiring the disease2.

Inherited conditions such as octodermal dysplasia, which wear down the mineral component in enamel, and other inherited conditions such as xerostomia, which affect immune system competency and salivary flow, also predispose an individual to dental caries2.

The Role of the Environment

Anderson 2 categorizes the environmental factors associated with dental caries in terms of i) fluoride exposure, ii) socioeconomic status, iii) sugar consumption, iv) family history in relation to caries, and v) the nature, sealant status, and caries history of the teeth present. In a study seeking to assess how the nature of teeth increased or reduced the risk of acquiring dental caries, he2 found that the risk of harboring the S. mutans bacteria increases with increasing surface area of the oral cavity or dentition. His findings mirror those of Caufield and his colleagues15, who sought to examine the proportion of disease-causing bacteria in the oral cavity at different stages after birth; and found that the proportion of such bacteria in saliva increased as new teeth emerged.

Anderson 2 further found that people with past histories of dental caries, or existing restorations for that matter, are more predisposed to caries; and that similarly, people with smooth surface caries are more predisposed to future caries than those who exhibit only pit and fissure caries. He contends with Anuradha’s 11 view that owing to the high risk of reoccurrence associated with caries, the specific location of previous or current caries could be crucial in guiding practitioners to make accurate predictions on the possible incidence of future caries.

The absence of sealants has also been identified as a key risk factor for dental caries. In their study seeking to assess the effectiveness of sealants and varnish in reducing the incidence of dental caries, Bravo and his colleagues 16 found both products to be significantly effective, although sealants had a higher level of efficacy, covering approximately 68% of the tooth’s smooth surface, compared to 38% covered by varnish. Various studies have sought to establish why the rate of sealant usage has remained low despite its high level of efficacy in reducing the risk of dental caries. Fos and Hutchison’s7 is one such study – in their review seeking to assess the differences in the risk of exposure to dental caries between children in urban areas and their counterparts in rural areas, the researchers linked sealant use to socioeconomic status, positing that compared to their peers in urban areas, children in rural areas had higher likelihoods of being exposed to sealant usage as owing to uneducated parents, decreased dental insurance coverage, and less use of the procedure by dental care providers.

A plethora of other studies have focused on assessing how family history determines one’s risk of acquiring dental caries. Familial history has been found to be a considerably weak factor, given that caries has more to do with one’s own lifestyle and feeding habits2. There, however, is consensus that infected mothers risk transferring the S. mutans bacteria to their unborn children and infants2, 10-11. The higher the proportion of bacteria present in the mother’s saliva, the greater the risk of the same being passed on to the child2. Moreover, the more resistant the strain of bacteria present in the mother, the greater the risk of transmission 7. For these reasons, Anderson advises that it is “in the clinician’s and the child patient’s best interest to sample the mother for the presence and severity of a S. mutans infection” 2 (p 379). Al-Ansari 10 however, cautions against understating the role of the mother in the development of dental caries in older children. In his view, a mother’s perception about their own oral health status is a crucial risk factor for older children between the ages of three and fifteen because it determines whether or not a mother will seek dental care for herself and her children10.

Age plays out as another crucial risk factor for dental caries. Al-Ansari10 and Anuradha and his colleagues 11, for instance, report extremely high infection and prevalence rates among the elderly population. This has largely been attributed to changes in diet, as well as mental and physical inability to observe oral hygiene11. This inability to maintain appropriate hygiene has also been found to be a significant factor in the high prevalence rates reported among children with special needs17. In her study involving 61 autistic and an equal number of non-autistic children aged between 4 and 16, Jaber (2011) found that autistic children ran higher risks of acquiring dental caries due to increased use of anticonvulsants or psychoactive drugs, inadequate dental hygiene instructions from those taking care of them, difficulties in flossing and brushing, a pronounced preference for sweetened foods, and the fact that autistic children “tend to pouch food inside the mouth instead of swallowing it due to poor tongue coordination” 2 (p 216).

Researchers concur that reducing the risk of caries infection among autistic persons would require dental and pedopsychiatric teams to work together towards increasing the promotion of oral health activities for caregivers and parents so that they are able to formulate effective prevention techniques for their children 7, 17. Jaber17 proposes that the parental and caregiver education include guidance and information on among other things, benefits of early attendance to a dental specialist for care and advice, benefits of fluoride toothpaste, strategies of maintaining proper hygiene, and the benefits and strategies of reducing the amount of sugars in the diet. Visual pedagogy is one specific strategy that has proven quite useful in teaching people with mental illnesses how to maintain proper oral hygiene18. Pilebro and Backman18 conducted a prospective study where they exposed fourteen autistic children with visible plaque to a 12-month intervention program, in which they were taught how to brush effectively through a number of images indicating or demonstrating a structured technique and method of tooth brushing. At the completion of the program, the amount of visible plaque was found to have reduced considerably.

ii) Periodontal Diseases

The term ‘periodontium’ is derived from two Greek words with ‘peri’, being used to denote ‘around’ and ‘odons’, representing ‘tooth’19. It basically refers to the tissues and any other supportive structures around the tooth19. These include the alveolar bone, the periodontal ligaments, the cementum, and the gingiva. Periodontal diseases is a term used to collectively refer to the acquired or inherited disorders that cause damage to the aforementioned tissues, and inhibit their ability to perform their supportive functions effectively19. Rhee and his colleagues (2013) define periodontal diseases differently – as “inflammatory disorders most commonly initiated by microorganisms; if untreated, they reduce a patient’s quality of life”13(p 127). The first definition focuses on the physiological processes involved whereas the second definition places more emphasis on the etiological agent(s) responsible for the same. Regardless of the definition adopted, researchers have contended that some periodontal diseases are more common, and have significantly higher prevalence rates than others13, 19. Studies have shown gingivitis and chronic periodontitis to be the more common forms of periodontal diseases; and aggressive periodontitis, autoimmune gingival diseases, and combined endodontic-periodontic infections to be the rarer forms13, 19.

Epidemiology: Rhee and his colleagues 13 assessed the overall prevalence of periodontal diseases in the U.S. using data collected from 2,137 subjects scattered across different age groups and found the prevalence rate to be significantly higher (53%) than the national estimate suggested by the American Academy of Periodontology (47%). They found the rare forms of the disease to have a low prevalence rate of 4%13. Combined endodontic-periodontic infections were the commonest form of the three, with a prevalence rate of 2.6% 13. Chronic periodontitis and gingivitis were, however, found to have significantly high prevalence rates, especially among the older populations13. This finding was replicated by multiple other studies, which found the prevalence rate of periodontal diseases to be substantially low among American children20-21.

Females were also found to have higher prevalence rates of gingival diseases (83%) compared to males’ at 17% 13, 21. 0.007% of the subjects were found to have combined forms of periodontal diseases, with chronic periodontitis and periodontal-endodontic infections being the most common combination13. In a separate study, Albandar and his colleagues20, assessing the prevalence of juvenile periodontitis among U.S. subjects, found 2.75% of teenagers between ages 16 and 17 to have chronic periodontitis, and 0.6% of those between ages 13 and 15 to have juvenile periodontitis. All the same, researchers have found that despite children having greater amounts of plaque compared to adults, they still reported lower levels of inflammation and health complications; and their conditions were more easily reversible13, 19.

Causes: periodontal diseases are caused by overgrowth of the pathogenic microorganisms present in dental plaque that forms around the tooth as a result of poor oral hygiene. Specifically, they are caused by increases in the numbers of Gram-negative anaerobes and bacteria present in subgingival plaque19. The most common disease-causing bacteria in plaque include Treponema denticola, Tannarella forsynthesis, Porphyromonas gingivalis, and Aggregatibacter19. Recent studies have, however, implicated systemic diseases; fungi such as Herpes viruses and Candida albicans; and metabolic, developmental, and genetic factors in the etiology of periodontal diseases13.

Classification and Nomenclature: the nomenclature and classification of periodontal diseases has changed severally over the last few decades. Presently, the common forms of periodontal diseases are classified as either reversible and non-destructive or irreversible and destructive19. Periodontitis is the destructive form of the disease. It causes irreversible inflammation of the tissues surrounding the tooth, leading to breakdown of the alveolar bone19. If left untreated, periodontitis progresses to expose the roots of the tooth, causing tooth rigidity, and severe pain that ultimately leads to removal19. Periodontitis could take various forms; the different forms are distinguished through a six-item criteria set by the American Academy of Periodontology in 1989 — i) presence (absence) of specific microbial elements; ii) how the disease responds to treatment; iii) the rate at which the disease progresses; iv) the presence (absence) of systemic diseases identified as risk factors; v) the manner in which the affected sites are distributed; and vi) the patient’s age at onset of symptoms.

The non-destructive form of periodontal diseases is gingivitis, which is “the inflammation of the marginal gingiva” but which is often unaccompanied by attachment loss19 (n.pag). It could take one of two forms — infectious gingivitis or non-infectious gingivitis. The specific classifications are, however, beyond the scope of this review; and since children are the main subjects of the current study, the researcher will only focus on the gingival and periodontal problems facing juveniles and infants, and the risk factors as well as treatment mechanisms for responding to each one.

a) Gingivitis

Gingival problems can either be chronic or acute in nature. In children, diagnosis of gingivitis relies on clinical manifestations including bleeding, edema, and redness of the marginal gingiva, or bulbous and enlarged interdental papilla and a rolled gingival margin in case the condition has remained untreated 19, 21. Researchers have observed that in adolescents, gingivitis manifests itself as B-cell (plasma cells) infiltrate, as opposed to the T-lymphocyte filtrate predominant in younger children19. The most common gingival problems among juveniles are as follows.

Pubertal Gingivitis: this form of gingivitis is caused by rising levels of the gonadotrophic hormone during poverty19. Exacerbation of gingivitis is also common in women taking oral contraceptives 13 and during pregnancy owing to rapidly rising levels of HCG, and the hormones estrogen and progesterone 19. It is believed that increases in the hormonal level of the gingival margin induce vascularity, causing proliferation and vasodilatation, and making the gingiva more susceptible to inflammation19. Pubertal gingivitis is treated through professional prophylaxis, and the removal of local factors responsible for the gingiva’s increased susceptibility19.

Eruption Gingivitis: this is gingival inflammation that occurs as a direct result of tooth eruption19. It is aggravated by teeth malalignment and poor oral hygiene, and will normally subside once the erupting tooth reaches normal occlusion. It is treated through plaque-control medication.

Drug-Induced Gingivitis: certain medication classes, including calcium channel blockers, phenytoin, and cyclosporine have been observed to aggravate gingival inflammations as well as cause gingival overgrowth in the presence of facilitative local factors19. Three separate studies studying the effect of the three medication classes above found 15% of patients taking calcium channel blockers, 50% of patients medicated with phenytoin, and 30% of patients taking cyclosporine to have substantial gingival overgrowth, compared to the control population19. Although the pathogenesis is still unclear, it is believed that these drugs interact with fibroblast and metabolites in the gingival margin, causing fibroepithelial overgrowth12.

Gingival Complications Resulting from Mouth-Breathing: mouth breathing, in essence, promotes the desiccation of the oral tissue, and makes the gingiva more susceptible to inflammation19. This form of gingivitis can be prevented through the utilization of oral screen to cover the oral tissues when sleeping, lubrication of the oral tissues, and the maintenance of proper oral hygiene. Elimination of the problem is, however, a more complex process requiring the input of both an otolaryngologist and an otolaryngologist19.

Acute Necrotizing Ulcerative Gingivitis (ANUG): this is gingival inflammation that is caused specifically by the Borrelia vincentii bacterial species22. The risk factors for this form of gingivitis include HIV infection, decreased host resistance, stress, and poor oral hygiene19, 22. It is characterized by fetid odor (resulting from the tissue necrosis and bacterial toxins produced as end-products of bacterial action), malaise, low-grade fever, and a pseudomembrane covering a punched-out interdental papilla19. The treatment of ANUG is a combination of both systemic and local therapy22. First, gentle scaling is performed to remove necrotic tissue and any local deposits from the oral cavity. Oxidizing mouthwash is then used to restore normal bacterial balance, and the patient is then subjected to a daily oral hygiene regimen19.

Gingival Complications Resulting from Malnutrition: deficiencies of critical minerals could increase the gingiva’s vulnerability to inflammation19. Lack of vitamin C, for instance, causes scurvy, which inhibits the production of collagen, leading to hemorrhage, gingival edema, and gingival swelling19. When combined with poor oral hygiene, scurvy exacerbates into ‘Scorbutic gingivitis’, which is “characterized by ulcerative gingivitis, fetid odor, rapid development of periodontal pocket, and tooth loss”19 (p 3).

Primary Herpetic Gingivitis: this is gingival inflammation caused by the Type 1 Herpes Simplex virus19. It is characterized by malaise, fever, and yellow-gray ulcers on the gingiva, hard palate, and tongue19. It is more common in children between the ages of two and four; and is treatable through symptomatic interventions only19.

b) Periodontitis

Like gingivitis, periodontitis can either be chronic or aggressive19,21. It is termed as the destructive form of periodontal disease owing to the fact that it leads to breakdown of the alveolar bone19, 21.

Aggressive Periodontitis: Albandar and Tinoco21 make use of the six-item criteria set by the American Academy of Periodontology to distinguish between the two forms of periodontitis. Their criteria for aggressive periodontitis included:

i) Onset age between the ages of 11 and 13 (circumpubertal period)

ii) A familial occurrence pattern

iii) No evidence of significant correlation between the disease’s occurrence and local etiological factors

iv) A higher prevalence risk in females (3:1)

v) Disease only affects the permanent teeth (molars and incisors) and has no substantial effect in deciduous teeth

vi) A high rate of progression (three to four times that of chronic periodontitis)

vii) Disease not an oral manifestation of the patient’s systemic diseases

viii) Results in alveolar bone loss characterized by arc-shaped or vertical bone defects in the incisors and molars

Ghutaimel 19 notes that aggressive periodontitis can further be categorized into localized aggressive (LAgP) periodontitis and generalized aggressive periodontitis (GAgP). LAgP affects no more than two teeth other than the first permanent incisors and molars, whereas GAgP affects three teeth at the very least, apart from the first permanent incisors and molars19, 21. It is still not clear what specific microorganisms are responsible for either; however, researchers have found Eubacterium sp., bacteroides-like sp., and Aggregatibacter to be more common in LAgP; and Treponema denticola and Porphyromonas gingivalis more common in GAgP cases19. Treatment of aggressive periodontitis combines systemic antibiotic therapy with non-surgical periodontal therapy19. Tetracycline has been found to be an effective antibiotic for the treatment of aggressive periodontitis19. Amoxicillin, in combination with metronidazole, has also been found to be quite effective in case tetracycline is unavailable or becomes resistant19,21.

Chronic Periodontitis: Rhee and his colleagues13 found chronic periodontitis to be more prevalent in elderly populations, with extremely low rates in juveniles. Unlike aggressive periodontitis, chronic periodontitis exhibits a low to moderate disease progression rate21. It can be divided into i) localized chronic periodontitis (affecting less than 30% of the dentition) and generalized chronic periodontitis, which affects more than 30% of the dentition19; and ii) mild chronic periodontitis (1-2CAL), moderate chronic periodontitis (2-4 CAL) and severe chronic periodontitis (>4 CAL) 19.

iii) Malocclusion

Definition: Malocclusion is a dental condition characterized by the departure of teeth from normal occlusion23. Edward Angle, in 1899, introduced a standard system for classifying malocclusion cases, where he defined normal occlusion “based on the relationship between the position of the mesiobuccal cusp of the maxillary first molar to the lower first molar”23 (p 12). Normal occlusion is said to exist if i) the mandibular first molar buccal groove (mandible) occludes with the mesiobuccal cusp of the first upper molar (maxilla); and ii) the teeth formed a smooth, curvy line of occlusion23. Based on this definition, three classes of malocclusions have been derived:

Class 1: where there is occlusion between the mandible and the maxilla, but the line of occlusion has some discrepancy and is not smoothly-curved as it would be under normal occlusion24. Bi-maxillary protrusion, where there is occlusion between the mandible and the maxilla, but the arches (both upper and lower) appear forwardly in relation to the profile of the face, falls under this class23.

Class 2: where there is a distal relationship between the mandible and maxilla24. The mesiobuccal groove of the first molar occludes after the upper first molar mesiobuccal cusp, such that i) the upper incisors are more pronounced (projected) than they would be under normal occlusion (division one); or ii) the central incisors on the upper jaw are almost in their anteroposterior normal position, but the lateral incisors on the same jaw have a mesial and labial inclination (division two) 24.

Class 3: where there is a mesial relationship between the mandible and the maxilla, such that the mesiobuccal groove of the first molar on the lower jaw occludes previously to the mesiobuccal cusp of the first permanent molar on the upper jaw 24.

Angle’s classification has a number of shortcomings, including the failure to consider malpositions of individual teeth, failure to emphasize the etiology of malocclusion, failure to differentiate between dental and skeletal malocclusions, and more conspicuously, failure to provide an alternative criterion for determination in case the first permanent molars are missing or have been extracted25. Nonetheless, it still remains the standard classification framework for malocclusion and other orofacial irregularities25.

The current study will focus primarily on literature that touches on the occurrence of class III malocclusion. Studies have observed that class III malocclusion is the least prevalent of the three (with a rate of approximately 3%). For this reason, the condition has remained largely understudied. Most researchers have chosen to focus on the other two classes; and this explains why when it comes to class III malocclusion, “early diagnosis, prognosis, and the definition of appropriate time and therapeutic modalities suitable for treatment remain a challenge to the orthodontist”26 (n.pag).

Class III Malocclusion

As mentioned in the previous section, class III malocclusion is characterized by a mesial relationship between the mandible and the maxilla, such that the mesiobuccal groove of the first molar on the lower jaw occludes previously to the mesiobuccal cusp of the first permanent molar on the upper jaw24.

Epidemiology: modern societies are estimated to have a class III malocclusion prevalence rate of between 3 and 7% 23. The rate is higher in African and Asian countries, and considerably lower in the more developed economies of Europe and America. A 2010 study conducted by Garbin and his colleagues on Brazilian subjects found the prevalence rate of the condition to be relatively uniform at a rate of 2% across different age groups between the ages of three and five24. However, the risk of occurrence was seen to peak around the age of six (rising to 4%), and then falling slightly, but maintaining a progressive rate of 3% up to the age of 1524. This spike at age six has been associated with the eruption of permanent incisor teeth, which normally takes place around this age24. The subsequent progressive rate, on the other hand, is thought to result from “the so-called natural dental compensation of skeletal discrepancies”24(p 49). Huge deviations have also been reported in the prevalence rates of people in different socio-economic statuses, and races. Burns23, for instance, found black Americans to have a prevalence rate of 6.3% compared to the national average of 1%. Further, Oliveira and his colleagues27 observed that persons with special needs had extremely high prevalence rates for malocclusion (21% for AOB, 21.5% for posterior crossbite, and 20.4% for anterior crossbite). They attribute this high prevalence to non-nutritive sucking habits and prolonged use of bottle feeding.

Etiology: class III malocclusion is a product of multiple factors, ranging from jaw and tooth size discrepancies to genetics, oral habits such as tongue thrusting and conditions such as cleft lip. Burns 23 also notes that reverse overjet and other such occlusal functions can cause alterations in the shape and direction of the mandible. He is, however, quick to point out, that this is only so if the functional alteration is exacerbated by the presence of other environmental effects and inherited traits23. Cases of class III malocclusion can be divided into three divisions. Individuals in division A have an overgrown mandible and a rather normal maxilla, such that the anterior crossbite is a direct result of the mandible; whereas those in division B. have both the mandible and the maxilla exaggerated, but the excess in the mandible exceeds that in the maxilla, giving rise to an anteriorly positioned point and an acute nasolabial angle23. Division C. individuals, unlike the other two, have a maxilla hypoplasia, characterized by a concave facial profile with an exaggerated nasolabial angle23.

Causes: although it may be caused by local factors such as discrepancies between tooth and jaw size or different sizes of the upper and the lower jaw, malocclusion is most often inherited from an individual’s family line25. Other key causes of the condition include tumors of the jaw and the mouth; jaw fractures resulting from injury; ill-fitting braces, retainers, appliances, crowns or dental fillings; abnormally-shaped teeth, impacted teeth, lost teeth, or extra teeth; prolonged use of the drinking bottle during infancy; birth defects such as palate and cleft lip, prolonged pacifier use, and such childhood habits as tongue-thrusting and thumb-sucking, all of which result in abnormal bite patterns or overcrowding28. Sidlauskas and Lopatiene28, for instance, in their analysis involving Brazilian subjects, found that children with mouth-breathing habits had a ten times greater likelihood of exhibiting malocclusion compared to their peers with nasal breathing habits.

Associated Problems: there are multiple reasons why an individual should seek orthodontic treatment for malocclusion. To begin with, malaligned teeth can be a source of psychosocial problems such as discrimination and low self-esteem23. Moreover, they increase one’s susceptibility to periodontal diseases and interfere with the normal functioning of the oral cavity, often causing speech and chewing difficulties and unnecessary pain in the temporomandibular joint28.

Treatment: treatment for class III malocclusion often aims at correcting the way the teeth are positioned in the oral cavity3, 25. It could take the form of i) braces, which are attached to the tooth surface to push them it into the proper position; ii) tooth removal, especially if the malalignment is due to overcrowding; iii) tooth repair, where the irregular or rough teeth are capped, bonded, reshaped, or adjusted down; or iv) orthognatic surgery, where a procedure is performed to reshape, lengthen or shorten the jaw.

iv) Enamel Fluorosis

Definition: the term dental fluorosis has been defined differently by different researchers. The current study, however, adopts Masceranhas’ 29 (p 269) definition, which caps fluorosis as “a chronic fluoride-induced, in which enamel development is disrupted and the enamel is hypomineralized.” In other words, fluorosis is a dental condition resulting from the excessive diffusion of fluorides into the tooth enamel during tooth development30.

Etiology: the occurrence and severity of fluorosis is based on the absolute quantity of “fluoride consumed from all possible sources during the tooth development” phase29. Fluoride weakens the enamel by increasing its degree of porosity. The degree of damage is dependent upon the fluoride concentration in the tissues surrounding the tooth during tooth development29. Microscopically, the width of the crystals forming the tooth enamel is seen to increase, and so is the size of the intercrystalline spaces between them29. These widening intercrystalline spaces cause pores, whose degree of severity increases as the fluoride concentration in the tissues surrounding the tooth rises29. Studies have observed that the most critical periods for fluorosis development are the early maturation and the post-secretory phases of tooth development, which naturally translates to the period between birth and age eight 11, 29-30.

Fluorosis manifests as either white spots or brown pits and stains on the tooth surface, depending on the severity of the disease 11, 29. Brown stains are imminent in moderate or severe fluorosis, whereas white flecks are representative of less severe fluorosis and lower levels of damage to the enamel29. Anuradha and his colleagues11, in their study seeking to assess the prevalence of dental fluorosis in India, found that ingestion of water with fluoride concentrations two to three times the recommended safety dosage of 1 ppm led to chalky opaque areas and white spots on the tooth surface; whereas fluoride concentration four times greater than this dosage led to a brown pitted appearance on the tooth enamel.

Studies have shown that fluoride levels in the diet and self-applied gels can also lead to fluorosis 11, 29. Historically, it was believed that diets with fluoride concentration levels exceeding 0.07 mgF/kg body weight caused noticeable changes in teeth in children and infants29. More recent studies have, however, found the threshold to be much lower – 0.03 mgF/kg body weight which is approximately 0.75mgF per day for developed nations and approximately 0.01mgF/kg of body weight in less-developed economies, especially in Africa29. The high susceptibility in African nations has largely been associated with malnutrition, renal insufficiency and low altitude29.

Epidemiology: Anuradha and his colleagues11, in their study on Indian teenagers between the ages of 13 and 15 living in a fluoridated community, reported a 41% overall prevalence rate for fluorosis, with the mild form of the disease being more prevalent than the severe form. Data from the 1986-1987 National Survey of Oral Health in U.S. School Children and the National Health and Nutrition Examination Survey conducted between 1999 and 2004 showed that almost a quarter of the U.S. population between the ages of 6 and 49 had dental fluorosis, and that the prevalence rate rose significantly between 1999 and 200431. For instance, the prevalence rate among adolescents aged 12 to 15 rose from 22.6% in 1987 to 40.7% in 200431.

The data also showed that, like is the case in many other countries, the disease was less prevalent among the elder populations, and adolescents between the ages of 12 and 15 had higher fluorosis prevalence rates (40.6%) compared to other age brackets (33.4% for children between the ages of 6 and 11; and 8.7% for adults between ages 40 an 49)31. The rates were slightly higher in girls compared to boys (DMFT=1.83 for girls and DMFT=1.3 for boys) 11. The high rates among adolescents between the ages of 12 and 15 has been attributed to the fact that children at this age usually have an incomplete set of permanent teeth given that posterior permanent second molars and premolars mostly erupt between the ages of 11 and 1231.

Parallel studies have also shown that the prevalence of dental fluorosis increases as that of dental caries decreases11, 32; and that teeth that erupt later in life such as the posterior premolars and second molars are more severely affected11, 31.

Risk Factors: recent fluorosis studies have identified four fundamental risk factors in the development of fluorosis. The four and their associated risks have been discussed in the subsections that follow.

Fluoridated Drinking Water: 1 ppm is the recommended safety dosage of fluoride in drinking water11. The estimated prevalence rate at this dosage is a low 10% for very mild fluorosis29. Data from the 1986-1987 National Survey of Oral Health in U.S. School Children and the National Health and Nutrition Examination Survey conducted between 1999 and 2004 showed higher prevalence rates in communities whose water sources contained higher levels of fluoride concentration31. The overall rates of fluorosis prevalence range from 7.7 to 69% in fluoridated communities, compared to 2.9% to 42% in their non-fluoridated counterparts29.

Fluoride Supplements: the use of fluoride supplements is recommended as a caries-preventive measure in fluoride-deficient areas11, 29-30. However, studies have shown that these supplements pose a high risk for fluorosis among children (24% in fluoridated communities and between 1.7 and 8% in non-fluoridated communities) 29. For this reason, countries are advised to revise their safety dosage guidelines so that rather than blindly follow a fixed prescription formula, clinicians are allowed to “consider the fluoride content of the water consumed, and the caries risk of the child” when making their prescription decisions involving fluoride supplements 29 (p 272)

Infant Formula: historically, infant formula was regarded as a key risk factor for fluorosis in both fluoridated and non-fluoridated communities29. Recent studies such as that conducted by Pendrys and Katz30 have, however, shown that owing to countries’ attempts to reduce fluoride concentration in infant formula to optimum levels, infant formula no longer is a significant risk factor for non-fluoridated communities although it remains a key factor “in the development of fluorosis in fluoridated communities,” with a relatively high odds ratio of 10.77% (Masceranhas, 2000). These findings have led to the conclusion that concentrated infant formula only causes noticeable damage to the enamel if used together with fluoridated water29. Reducing the significance of infant formula as a risk factor for fluorosis in fluoridated communities would, therefore, involve among other things, recommending the use of bottle water in the dilution of infant formula, or advocating for the use of ready-to-feed infant formulas as opposed to their dilution-based equivalents29.

Fluoride Toothpaste: studies have yielded differing conclusions on the significance of the association between fluoride toothpaste and the risk of fluorosis. Ripa, for instance, in a 1991 review of fluorosis studies, found nine of the ten studies chosen for review not to have established any significant association between the two, with only one yielding a significant association, and a high odds ratio of 11% for fluorosis when the use of fluoride began before age two33. The study by Pendrys and Katz30 also failed to establish a positive association between fluoridated toothpaste and the risk of enamel fluorosis. Conspicuously, however, a significant 46% of the subjects in the ‘positive’ study reviewed by Ripa 33 were below seven years of age, implying that there may be considerable risk of fluorosis if fluoride toothpaste is used for children below the age of six. For this reason, low-fluoride toothpaste is recommended for children below the age of six; and even so, parents need to play an increased role to ensure that they supervise their children’s tooth brushing, and that the children expectorate and rinse appropriately29.

Well, there are other risk factors involved in the development of fluorosis, including socio-demographic variables, feeding practices during infancy, and parents’ income and educational level29. Black Americans are more at risk of developing fluorosis compared to their white counterparts; and so are children weaned before the recommended nine months, and those whose parents are more educated, with higher levels of income29.

Section Two

Health Effects of Dental Diseases

Dental diseases, if inadequately treated or worse still, left untreated, have been associated with a range of systemic diseases12. This section reviews literature focusing on the health impacts of dental diseases on various systems within the body.

Effects on the Cardiovascular System: periodontitis has been associated with the risk of cardiovascular heart disease in younger populations that would, under normal circumstances, run no significant risk of the same34. Although it is still not clear whether periodontal disease is a direct cause of CVD in this case, researchers have shown that periodontitis increases the levels of neutrophils, interleukin, and C-reactive protein, thereby increasing the inflammatory activity in the lesions present in the arteries, and increasing the risk of heart attack 11, 35. More general studies have associated disease-causing bacteria present in the oral cavity such as S. mutans, Lactobacilli, Propionibacterium, and Atopobium with platelet aggregation, one of the key elements of thrombosis11.

Effects on the Respiratory System: studies have shown a significant association between an individual’s oral health status and their risk of respiratory diseases11. There is sufficient evidence to support the claim that regular professional dental care and high standards of oral hygiene can significantly reduce the risk of respiratory diseases among the elderly11, 36. Azarpazhooh & Leake36 demonstrate that increased periodontal attachment loss increases lung infection and the occurrence of pulmonary infections such as nosocomial pneumonia36. In a separate study, Anil 37 found the risk of chronic respiratory diseases to be five times higher in individuals with poor oral health compared to those with high standard of oral hygiene. A number of views have been advanced to explain this link. They include i) bacteria in the oral cavity alter the mucus surface in the local environment, making it more favorable for respiratory pathogens; ii) the bacteria destroy salivary pellicles allowing for the release of cytokines that facilitate the destructive action of respiratory pathogens11.

Effect on the Musculoskeletal System: periodontal diseases have been found to increase the risk of rheumatoid arthritis11. Such diseases have been found to play a significant role in the “initiation and maintenance of the autoimmune inflammatory response that occurs in rheumatoid arthritis”11 (p 488).

Effect on the Endocrine System: it is a widely-accepted fact that diabetes increases the risk of developing dental diseases. Studies have nonetheless managed to show that dental diseases in turn increase the risk of type II diabetes38. Dental diseases provide a pathway for harmful bacteria to enter the blood stream and stimulate immune cells to produce cytokines; these cytokines could accumulate to levels capable of damaging the insulin-producing cells in the pancreas, thereby inducing Type II diabetes 38.

Effect on the Reproductive System: periodontitis has been observed to increase the risk of poor pregnancy outcomes 11, 39. According to Arigbede and his colleagues11, when pathogenic bacteria in the oral cavity enter the bloodstream, they stimulate the cells to produce such cytokines as prostaglandins (PDE2), tumor necrosis factor (TNF-a), and interleukins (IL-1, IL-6), which are believed to i) interfere with the mechanisms of the normal parturition mediators, thereby increasing the likelihood of low birth weight; and ii) induce labor on reaching a certain concentration threshold.

From the existing body of literature, it is evident that little research has been done on the prevalence pattern of dental diseases in Saudi Arabia. Existing studies have focused on the developed economies of Europe and America, and even the few that have focused on less developed countries have devoted most of their attention to the emerging economies of India, China, and Brazil. This has created huge knowledge gaps that have made it challenging for clinicians and policy makers in Saudi Arabia to identify and respond effectively to the dental treatment needs of their populations. The current study is geared towards assessing the prevalence of dental diseases in this understudied group, and consequently, guiding oral health planners in Ajman, and the greater Saudi towards developing effective preventive strategies and treatment plans for their communities.


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2. Anderson M. Risk Assessment and Epidemiology of Dental Caries: Review of the Literature. Pediatric Dentistry 2002; 24(5):377-385.

3. Anis R, Gaballah K. Oral Cancer in the UAE: A Multicenter, Retrospective Study. Libyan Journal of Medicine 2013; 8(10):217-222.

4. Jaber MA. Dental Caries Experience, Oral Health Status and Treatment Needs of Dental Patients with Autism. Journal of Applied Oral Science 2011; 19(3): 212-217.

5. Jayakumary M, Jayadevan S, Ranade AV, Matthew E. Prevalence and Pattern of Dokha Use among Medical and Allied Health Students in Ajman, United Arab Emirates. Asian Pacific Journal of Cancer Prevention 2010; 11(1): 1547-1549.

6. Moses J, Rangeeth BN, Gurunathan D. Prevalence of Dental Caries, Socio-Economic Status and Treatment Needs among 5 to 15-year-old School-Going Children of Chidambaram. Journal of Clinical and Diagnostic Research 2011; 5(1): 146-151.

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9. WHO. The world Oral Health Report 2003. The World Health Organization 2003.

10. Al-Ansari A. Prevalence, Severity, and Secular Trends of Dental Caries among Various Saudi Populations: A Literature Review. Saudi Journal of Medicine and Medical Sciences 2014; 2(3): 142-150.

11. Anuradha BR, Laxmi GS, Sudhakar P, Malik VN, Reddy AK, Reddy SN, Prasanna AL. Prevalence of Dental Caries among 13 and 15-year-old School Children in an Endemic Fluorosis Area: A Cross-Sectional Study. The Journal of Contemporary Dental Practice 2011; 12(6): 447-450

12. Arigbede OO, Babatope BO, Bamidele MK. Periodontitis and Systemic Diseases: A Literature Review. Journal of Indian Society of Periodontology 2012; 16(4): 487-491.

13. Rhee ES, Sekhon PK, Boehm TK. Prevalence of Periodontal Disease among Dental School Patients. Journal of Taibah University Medical Studies 2014; 9(2): 126-131.

14. Aas JA, Griffen AL, Dardis SR, Lee, AM, Olsen, I, Dewhirst FE, Leys EJ, Paster BJ. Bacteria of Dental Caries in Primary and Permanent Teeth in Children and Young Adults. Journal of Clinical Microbiology 2008; 46(4): 1407-1417.

15. Caufield PW, Dasanayake AP, Li Y, Pan Y, Hsu J, Hardin JM. Natural History of Streptococcus Sanguinis in the Oral Cavity of Infants: Evidence for a Discrete Window of Infectivity. Infect. Immun 2000; 68(7): 4018-23

16. Bravo M, Garcia-Anllo I, Baca P, Llodra JC. A 48-Month Survival Analysis Comparing Sealant (Delton) with Fluoride Varnish (Duraphat) in 6 to 8-year-old Children. Community Dent Oral Epidemiol 1997; 25(3): 247-250

17. Jaber MA. Dental Caries Experience, Oral Health Status and Treatment Needs of Dental Patients with Autism. Journal of Applied Oral Science 2011; 19(3):212-217

18. Pilebro C, Blackman B. Teaching Oral Hygiene to Children with Autism. International Journal of Pediatric Dentistry 2005; 15(1): 1-9.

19. Ghutaimel HS, Riba H, Al-Kahtani S, Al-Duhaimi S. Common Periodontal Diseases of Children and Adolescents. International Journal of Dentistry 2014.

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21. Albandar JM, Tinoco, EM. Global Epidemiology of Periodontal Diseases in Children and Young Persons. Periodontology 2002; 29(7): 153-76

22. Eversole LR. Clinical Outline of Oral Pathology: Diagnosis and Treatment. 4th ed. Shelton, CT: PMPH — USA; 2011

23. Burns NR. Class III Camouflage Treatment: A Retrospective Study. ProQuest.

24. Garbin AJ, Perin PC, Garbin CA, Lolli LV. Malocclusion Prevalence and Comparison between the Angle Classification and the Dental Aesthetic Index in Scholars in the Interior of State Paulo State-Brazil. Dental Press Journal of Orthodontics 2010; 15(4): 940-102

25. Mitchell L. An Introduction to Orthodontics. 4th ed. Oxford: Oxford University Press; 2013

26. Farias VC, Tesch RS, Danardin OV, Ursi W. Early Cephalometric Characteristics in Class III Malocclusion. Dental Press Journal of Orthodontics 2012; 17(2): 49-54.

27. Oliveira AC, Paiva SM, Martins MT, Torres CS, Pordeus IA. Prevalence and Determinant Factors of Malocclusion in Children with Special Needs. European Journal of Orthodontics 2011, 33(), 413-418.

28. Sidlauskas A, Lopatiene K. Prediction of Malocclusion Development Based on the Evaluation of the Etiologic Factors. Stomatolojia 2003; 5(1): 22-26.

29. Mascarenhas AK. Risk Factors for Dental Fluorosis: A Review of the Recent Literature. American Academy of Pediatric Dentistry 2000; 22(4): 269-277.

30. Pendrys DG, Katz, RV. Risk Factors for Enamel Fluorosis in Optimally Fluoridated Children Born After the U.S. Manufacturers’ Decision to Reduce the Fluoride Concentration of Infant Formula. American Journal of Epidemiology 1998; 148(10): 967-974

31. Beltran-Aguilar ED. Prevalence and Severity of Dental Fluorosis in the United States, 1994-2004. The Center for Disease Control and Prevention 2010.

32. Heller KE, Eklund SA, Burt BA. Dental Caries and Dental Fluorosis at Varying Water Fluoride Concentrations. Journal of Public Health Dentistry 1997; 57(3): 136-143.

33. Ripa LW: A Critique of Topical Fluoride Methods (Dentifrices, Mouthrinses, Operator and Self-Applied Gels) in an Era of Decreased Caries and Increased Fluorosis Prevalence. Journal of Public Health Dent 1991; 51(1): 23-41.

34. Dietrich T, Jimenez M, Kaye EA, Vokonas PS, Garcia RI. Age-Dependent Associations between Chronic Periodontitis/Edentulism and Risk of Coronary Heart Disease. Circulation 2008; 117(1); 1668-74.

35. Lavelle C. Is Periodontal Disease a Risk Factor for Coronary Artery Disease? J. Can Dent Assoc 2002; 68(3): 176-180

36. Azarpazhooh A, Leake JL. Systematic Review of the Association between Respiratory Diseases and Oral Health. Journal of Periodontology 2006; 77(9): 1465-82.

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38. Iacopino AM. Periodontitis and Diabetes Interrelationships: Role of Inflammation. Ann Periodontol 2001; 6(1): 125-137.

39. Bansal J, Bansal A, Kukreja N, Kukreja U. Periodontal Disease as an Emerging Potential Risk Factor for Adverse Pregnancy Outcomes: A Review of Concepts. Journal of the Turkish-German Gynecological Association 2011; 12(3): 176-180.

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