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Lupine Publishers | Cleft Lip and Palate: The Unsolicited Streak

 Lupine Publishers | Journal of Pediatric Dentistry

Abstract

Cleft palate is the third most common congenital deformity subsequent to clubfoot and the cleft lip. It may be either unilateral or bilateral and is either complete or incomplete. A multidisciplinary team approach is important to accomplish the various façades pretentiously observed by orofacial cleft. The optimum time of surgical repair is based on the surgeon’s preference, anesthetic risks, co-morbid congenital anomalies, and the apparent psychological impact on the family. Most surgeons repair the cleft lip around 10–12 weeks of age. Cleft palate and lip need early care and attention with a long-term follow-up which requires a team approach involving many specialties.

Introduction

Cleft palate is the third most common congenital deformity subsequent to clubfoot and the cleft lip [1]. It is seen as anatomical changes which involves the upper lip, nose, and the palate [2]. It represents roughly about 65% of the malformations of the craniofacial section [3]. In this, unilateral cleft lip and palate have been found to have the majority at 46%, followed by isolated cleft palate accounting for 33% of cases. These two being the most common diagnosis among the cleft lip and palate population followed by the others [1].Cleft lips show racial unpredictability, with the highest incidence seen among Asian and Native Americans (1:450 live births) and the lowest incidence seen in the African Americans (1:2,000 live births) [4]. Isolated cleft palate is seen more commonly in females (57%) than in males (43%), with gender differences attributable to the differences in the timing of the embryologic development [4]. About 50% of the isolated cleft palates are found to be in relation with a malformation syndrome, in comparison 15% of combined cleft lip and palate patients without any syndrome [5]. Velocardiofacial syndrome (VCFS) has been found to be the most common syndrome, which is associated with isolated cleft palate [6]. Other etiological factors associated with cleft palate are gestational exposures to alcohol, cigarette smoking, steroids, rubella, anticonvulsants, retinoids, advanced paternal age, folate deficiency and hypoxia [7-9]. An affected parent having a child with a cleft palate is 7%. If one sibling has a palatal cleft with no parental clefts, then future siblings have 2% jeopardy of developing a cleft. That risk upsurges to about 17% if there is one affected sibling and a parent with a cleft [10].

Anatomy

The palate is divided into the primary and the secondary palate. The primary palate comprises of the alveolar arch and secondary palate comprises of the hard and the soft palate. The hard palate is formed by the palatine processes of the maxillae and by the horizontal lamina of the palatine bones. It is covered by oral and nasal mucosa [11].

Cleft classification

A cleft palate may be either unilateral or bilateral and is either complete or incomplete [12]. The Veau System classifies orofacial clefting into four classes by whether the secondary and/or primary palates are affected and by laterality [13].
a) Veau Class I: Incomplete cleft, soft palate only (no unilateral/ bilateral designation)
b) Veau Class II: Hard and soft palate, secondary palate only (no unilateral/bilateral designation)
c) Veau Class III: Complete unilateral cleft including lip (primary and secondary palates)
d) Veau Class IV: Complete bilateral cleft

Clinical manifestations

a) Cleft palate is difficulty with feeding [14].
b) Velopharyngeal Insufficiency.
c) Speech distortion especially is the consonant /s/ [15].
d) Hyper-nasality—the perception of excessive nasal resonance during the production of vowels.16
e) Reduced loudness.
f) Monotone quality.
g) Strangled voice quality - an attempt to be non-nasal in the presence of VPI.

Management

A multidisciplinary team approach is important to accomplish the various façades pretentiously observed by orofacial clefting. The reconstructive surgeon, otolaryngologists, dentists, orthodontists, speech pathologists, audiologists, geneticists, psychiatrists, maxillofacial surgeons, prosthodontists, and social workers form the most important crucial members of the team treating the patients [17]. The procedure of cleft palate repair has been suggested and gained popularity over many years and is not a one-day ideology. These techniques have undergone numerous modifications that are practiced today. The task of contemporary palatoplasty is not just the closure of the cleft palate but also is to enable optimal speech without compromising the maxillofacial growth [18]. The optimum time of surgical repair is based on the surgeon’s preference, anesthetic risks, co-morbid congenital anomalies, and the apparent psychological impact on the family. Most surgeons repair the cleft lip around 10–12 weeks of age. The rule of 10’s was endorsed by Wilhelmsen and Musgrave that repair of cleft lip should take place when the patient reaches the ensuing cut-offs: weight 10lbs, hemoglobin 10g/dL, and white blood cell count <10,000mm3 [19]. It was Mallard who proposed the commonly used “rule of order 10” for the timing of repair stated as weight over 10lbs, hemoglobin over 10g/dL and over 10 weeks [20].

A recommendation by Dallas operative protocol for treatment of cleft lip and palate cases is that at three months of age, primary unilateral cleft lip and nose should be treated and at six to nine months, palatoplasty should be performed in a single stage; At the age of five years, lower secondary cleft lip and nose; from seven to nine, cancellous bone graft from the iliac to the alveolar cleft; after full growth, orthognathic surgery; from 12 to 18, soft tissue surgery, rhinoplasty or other should be done [21]. However, in developing countries there is a significant risk of neglect of palatoplasty procedure after lip repair. Cleft palate should be initially repaired at the age of 6-9 months of age, as suggested by Agrawal et al, whereas cleft lip should be fixed three to six months after the first operation [22]. Further, all-in-one (AIO) closing procedure includes the repair of the lip, hard and soft palate within a single stage. De Mey et al. in his study has shown the AIO surgical protocol offers many benefits, such as a single anesthesia, less hospitalization, less snooping during the growth process, lower amount of scar tissue, no secondary operations, being an ideal alternative for countries that do not have a health system able to afford the costs of a multistage, multidisciplinary treatment [23]. The operative schedule plays an important role in the prognosis of patients with cleft lip and palate, so that the timing of the primary palate closure can influence the indication for orthognathic surgery. According to Broome et al. Children who had conventional repair of primary cleft palate during the first year of life need orthognathic surgery more than those who underwent repair of the soft palate at three months of age, and hard palate at six [24]. To ensure the proper development of speech, the Protocol of Marburg (Germany) establishes the closure of the soft palate at six months of age and hard palate not before 13 years of age. Likewise, the Malek operating protocol anticipates the closure of the soft palate to allow speech without compensatory mechanisms and delays the closure of the hard palate to minimize iatrogenic effects in the face [25].

Nonsurgical treatment of the cleft palate is attempted with prosthodontic devices designed to correct velopharyngeal incompetence. Indications for use of prosthodontic devices are rare and largely of historical interest. Candidates who may benefit from prosthodontic devices are those who do not want or are too high risk for surgery, those in whom surgery has failed, or patients who would benefit from better alignment of the maxillary segments prior to definitive surgery [26]. The major drawback is that the prosthesis must be realigned every 2 weeks until growth is finished. Additionally, the device may be irritating to the fragile mucosal surface, difficult to clean, and require cooperation on the child’s behalf. Obturation is practical beginning at ages 3 to 4 years. The principle advantage is achieving as high or a higher rate of velopharyngeal competence than with surgery while avoiding potential surgical complications, such as restricted maxillary growth. Cleft patients are capable of normal facial skeleton development, but corrective surgical procedures are known to impair maxillary growth and may lead to midface retrusion [27]. Optimal timing of cleft palate repair must consider other medical conditions and speech development. Early repair has been shown to benefit speech development but may inhibit facial growth to a greater extent as transverse facial growth is not complete until 5 years of age. In the past, surgery on the palate was often delayed until maxillary growth was completed or when deciduous molars achieved proper occlusion. Recently, speech outcomes have taken precedence and as a result, most experts repair cleft palates beginning at 10 months of age [25-28]. Some advocate waiting until 2 years of age to operate on large cleft palates. Surgery on isolated soft palate clefts has been advocated as early as 3 months of age. The most common surgical techniques for repair of the soft palate are the Furlow doubleopposing Z-plasty and the intralveolar veloplasty. The bony palate is often repaired using the Von Langenbeck palatoplasty, the Veau- Wardill- Kilner palatoplasty, or a Bardach two-flap palatoplasty. Vomer flaps are used in conjunction with the above hard palate repairs to repair the nasal mucosa [29,30]. Rhinoplasty in cleft lip and nose patients can lead to the formation of inclusion cysts, which can be either epidermoid or the mucous cysts, which is based on the type of the epithelium seen [31].

In case of repair involving the patients with bilateral cleft lip and palate, a deformity in the central portion of the upper lip is seen which usually requires multiple revisions throughout childhood. The other deformities seen are the lack of redness in the midline, with relative excess laterally (whistle deformity); incompatibility of the lip vermilion color when compared with the hypoplastic prolabium vermilion; enlargement and absence of depression in the philtrum; straight lateral columns; absence or deformation of the cupid’s bow and philtrum landmarks [32]. In case of secondary deformity associated with bilateral clefts, Abbe flap technique is the surgical method with the initial phase of the technique being the evaluation of bilateral cleft lip and palate and rotation of a pedicle flap of the lower lip in a defect created in the center of the upper lip. The pedicle should remain in place for two to three weeks to neovascularization and posterior section with safely. To ensure proper extension, this procedure should be performed with the premaxilla in the correct position. The cases in which the premaxilla is deficient should undergo Le Fort I surgery before the Abbe flap. In the Texas Children’s Hospital, Koshy concluded that this flap is effective for replacing structural components and functional defects of the total thickness of the upper and lower lips resulting from the resection of cancer, birth defects or traumatic amputation [32]. Vertical excess of the premaxilla has been a challenge for orthodontists and surgeons according to Meazzini et al. constituting a serious cosmetic problem that does not improve spontaneously with growth [33]. Orthodontic intrusion during the growth phase offers advantages such as the use of low-intensity forces, improves the relationship between the front teeth and upper lip due to control of the premaxilla, and allows further growth of the impaired maxilla in patients with bilateral cleft. In severe cases, such as 7-8 mm superior bulge, orthodontics alone is not enough to achieve the intended objectives and should not be indicated because of the risk of root resorption and, considering the expected mandibular growth, the good positioning of the premaxilla is important [33]. The two most common abnormalities after primary lip repair according to Koh are the loss of the philtrum setting and the obliteration of the cupid’s bow [34]. Cleft lip and palate patients are at higher risk for chronic middle ear disease, hearing loss, hypochromic anemia, and hypoproteinemia, [35] particularly individuals from lower social classes. Patients undergoing Millard lip repair are at increased risk for development of cholesteatoma and tympanic membrane perforation. However, the type of palatoplasty and age did not influence the otologic and audiologic indicators of children of 5-6 years with unilateral cleft [36].

Conclusions

Cleft palate and lip need early care and attention with a longterm follow-up which requires a team approach involving many specialties. However, there are many complications associated with the cleft palate and lip, therefore a systematic approach is, was and always will be the need of the hour.

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Lupine Publishers | Periodontal Infections in Children

 Lupine Publishers | Journal of Pediatric Dentistry

Abstract

Periodontal infections are very common in children and should be properly diagnosed and treated after obtaining proper history. They can arise due to multiple factors, of which an important role is played by various bacteria. Familial and genetic factors are also important. Timely treatment is essential for best outcome. In this review article authors have tried to summaries available information about the condition.

Keywords:Periodontal disease; infection; gingivitis; plaque

Introduction

In medical dictionaries, the word periodontium is said to be derived from the Greek term’s peri-, which means “around,” and -odons, which means “tooth.” Hence, literally, it means that which is around the tooth. Periodontium includes the tissues that surround and support the teeth. Those tissues are gingiva, cementum, periodontal ligaments, and alveolar bone [1]. Periodontal diseases consist of a group of conditions that are considered nowadays ubiquitous among children, adolescents, and adults [2] . The term “periodontal diseases” includes any inherited or acquired disorders of the tissues that are investing and supporting the teeth (gingiva, cementum, PDL, and alveolar bone) [2]. Another researcher defined periodontal diseases as chronic infectious disorders caused primarily by bacteria . Also, destructive forms or type of lesions are lesser in younger children than older children or adults [3]. Children and adolescents can have any of the several forms of periodontitis as discussed in the proceedings of the 1999 International Workshop for a Classification of Periodontal Diseases and Conditions (like aggressive periodontitis, chronic periodontitis, and periodontitis as a manifestation of systemic diseases) [3]. However, aggressive periodontitis is more commonly seen in younger children and chronic lesions in younger children [3].

Classification and Types

An up-to-date classification of the periodontal diseases allows the clinician to consider the full range of periodontal disorders that can affect the patient and provides a basis for their diagnosis and subsequent management [4]. Hence, nowadays researchers classify the following types of periodontitis in children:
a) Gingival diseases, Plaque-induced gingivitis, Gingival diseases associated with dental plaque only (without/with local factors which predispose to plaque retention), Gingival diseases modified by systemic factors, Gingival diseases modified by medications, Gingival diseases modified by malnutrition, Non-plaque induced gingival lesions, including: those of specific bacterial, viral, fungal or genetic origin; lesions of systemic conditions; traumatic lesions or foreign body reactions
b) Chronic periodontitis.
c) Aggressive periodontitis.
d) Periodontitis as a manifestation of systemic diseases, associated with hematological disorders, Associated with genetic disorders.
e) Necrotising periodontal diseases, Necrotising ulcerative gingivitis, Necrotising ulcerative periodontitis.
f) Abscesses of the periodontium, Gingival abscess, Periodontal abscess, Peri coronal abscess
g) Periodontitis associated with endodontic lesions.
h) Developmental or acquired deformities and conditions, Localised tooth-related factors that modify or predispose to plaque-induced gingival diseases/periodontitis, Mucogingival deformities and conditions around teeth, including gingival recession and gingival overgrowth, Mucogingival deformities and conditions on edentulous ridges
i) Occlusal trauma

Gingivitis in children

Gingivitis of varying severity is found very commonly in children and adolescents [3]. Gingivitis was added as a new category of periodontal infections in 1999. Plaque-induced gingivitis is common in young as well as older age groups and modifying factors can be identified from the history and examination that can influence the natural course and management [4]. Plaque displays typical properties of biofilms or microbial communities ; the plaque ecology is a very important determinant in disease development [5]. People now opine that gingivitis may be more important than previously thought. From the Fifth European Workshop in Periodontology in 2005, it was concluded that gingivitis and periodontitis are an extension of the same broad inflammatory disease [6]. However, there is a wide range in individual susceptibility and not all individuals with gingivitis will progress to destructive periodontitis. It is also significant that the terminology has changed from ‘adult periodontitis’ to ‘chronic periodontitis’ because this highlights the increased international awareness that periodontitis is not just confined to adults over the age of 35 years, but can begin in early teenage years and progress slowly throughout the teens [6,7]. A subgingival calculus, smoking and Diabetes mellitus are plausible predisposing factors (6). A diverse microbial flora can be found in the subgingival plaques in this condition, and a bacterium, Tannerella forsythensis has been significantly associated with loss of attachment and the conversion of periodontally healthy sites to diseased sites over a three year period in adolescents, in a study [8].

Aggressive periodontitis

The term ‘ Early onset periodontitis’ is now replaced with ‘Aggressive periodontitis’. It is a rapidly developing disease with family history, and mainly occurs in people lesser than 30 years [6]. Aggressive periodontitis can be localized or generalized. Localized aggressive periodontitis (LAgP) patients have interproximal attachment loss on at least two permanent first molars and incisors, with attachment loss on no more than two teeth other than first molars and incisors. Generalized aggressive periodontitis (GAgP) patients show generalized interproximal attachment loss including at least three teeth that are not first molars and incisors [3]. LAgP occurs in children and adolescents without clinical evidence of systemic disease and is characterized by the severe loss of alveolar bone around permanent teeth. Linkage studies of the Brandywine population (a segregated group of people in Maryland that represents a relatively closed gene pool) have found a gene conferring increased risk for LAgP on chromosome 4 [3]. A number of functional defects have been reported in neutrophils from patients with LAgP. These include anomalies of chemotaxis, phagocytosis, bactericidal activity, superoxide production, FcgIIIB (CD16) expression, leukotriene B4 generation, and Ca2+–channel and second messenger activation [3]. The defect in chemotaxis is considered to be an intrinsic defect by some investigators.

Plaque associated gingivitis

In children, the most common form of infection belonging to the classification of periodontal disease, is plaque-associated gingivitis , which is usually reversible when the plaque is removed but, in a few cases, leads to a more serious teeth destruction with bone loss [9]. Chronic gingivitis is common in children. It usually causes gum tissue to swell, turn red and bleed easily. Gingivitis is both preventable and treatable with a usual routine of brushing, flossing and professional dental care in children. However, if left untreated, it can finally progress to more serious forms of periodontal disease [10].

Microbial aetiology

Microbial dental plaque and the presence of periodontal pathogens are required for the beginning of periodontal disease, but the host defense mechanism is also an important factor that affects the progression and severity of periodontitis in individuals affected by systemic diseases [6]. Some of the periodontal pathogens present in periodontal pockets in children are Actinobacillus actinomycetemcomitans, Prevotella intermedia, Eikenella corrodens and Capnocytophaga sputigena [11]. Aggressive form of periodontal infection with tooth loss is uncommon in children, and generally indicates a systemic illness [11]. Such diseases are usually hematological and genetic disorders. The types of hematological disorders are:

a) Acquired neutropenia
b) Leukemias
c) Other
The types of genetic disorders are:
a) Familial and cyclic neutropenia
b) Down syndrome
c) Leukocyte adhesion deficiency syndrome
d) Papillon-Lefèvre syndrome
e) Chédiak-Higashi syndrome
f) Histiocytosis syndromes
g) Glycogen storage disease
h) Infantile genetic agranulocytosis
i) Cohen syndrome
j) Ehlers-Danlos syndrome (Types IV and VIII)
k) Hypophosphatasia
l) Others.

Pathogenesis of periodontitis

Dental plaque in LgAP has predominantly A actinomycetemcomitans ,releasing virulence factors like leukotoxin, lymphocyte suppression factor, fibroblast and keratinocyte inhibitor, collagenase, and lipopolysaccharides [12]. P gingivalis also has host specific proteases called gingipains that causes its virulence [12]. In CP (Chronic periodontitis) and GAgP, the plaque bacteria are more in variety and diversity, and consists of P gingivalis, P intermedia, T forsythia, Eubacterium sp and F nucleatum [12]. Generalized AP shows equal number of A actinomycetemcomitans, Campylobacter rectus, and Spirochetes [13]. The serum level of antibody IgG2 reactive against A. actinomycetemcomitans is generally higher in LAP than in GAP and CP patients [12]. Hence the bacterium definitely plays a role. Gingival problems that are commonly seen in children and adolescents, and their pathogenesis are as follows:

Eruption Gingivitis: Some gingival inflammation normally accompanies eruption process . Poor oral hygiene by neglect or as a consequence of malalignment of the erupting teeth will aggravate gingival inflammation . Usually, the condition will subside as the oral hygiene improves and the tooth reaches normal occlusion . Plaque control regimen is the treatment of eruption gingivitis [14].

Pubertal Gingivitis: Pubertal gingivitis , which is also called steroid hormone-related gingivitis is defined as exacerbation of gingivitis by fluctuation in gonadotrophic hormone levels during puberty . A similar condition is seen during pregnancy and in females taking contraceptives. The phenomenon of this condition can be explained as any increase in the levels of oestrogen and progesterone in the gingival tissues resulting in vasodilatation and proliferation, increase in gingival vascularity, and increase in susceptibility of inflammation in the presence of local factors [14].

Acute necrotising ulcerative gingivitis is somewhat rare in children. It is illustrated in Figure 2. Generalized Aggressive periodontitis is highlighted in Figure 3.

Diagnosis

Diagnosis of periodontitis in children is mainly clinical based on appearance of lesions and family illness. However, radiographic investigation should be performed when it is clinically required iand affects patient prognosis and management [12]. Although panoramic radiography gives important information on unerupted permanent and missing teeth, the alveolar bone levels are best assessed and viewed by intraoral periapical and Bitewing radiography [12]. Figure 1 illustrates Bitewing radiograph.

Figure 1: Bitewing radiography.

Figure 2: Acute Necrotising Ulcerative gingivitis.

Figure 3: Generalized Aggressive periodontitis.

Treatment

Plaque control program can be planned based on the chronological age and manual dexterity of the child and can be done by caregiver if necessary [12]. Scrub technique of tooth-brushing technique has been found to be useful in children, but the modified Bass technique can be taught to adolescents with expertise [15]. Periodontal lesions predominantly are interdental, and older individuals can be advised use of interdental cleaning aids [16]. Nowadays, Triclosan with copolymer and dentifrices containing Fluoride have been documented to significantly reduce attachment loss in adolescents aged 11–13 years [12]. Keyes’s technique involving a paste of baking soda, salt, and hydrogen peroxide as a dentifrice and subsequent irrigation with saturated salt solution carried out with a regimen of tetracycline hydrochloride orally, is old and has been prescribed to patients having AgP ;it has shown good results also [17]. Scaling and root planning can definitely reduce microbial load and bring down Cytokine levels, but not in Aggressive periodontitis where motile bacteria are involved and recolonization with reinfection is very common [12,18]. Systemic antibiotics are indicated where A. actinomycetemcomitans is involved and recolonization occurs very frequently. The dosage should be adjusted as per the child’s weight and age. As per adult doses and individuals weighing 40 kg and more, Tetracycline in 250 mg qid and doxycycline in 100 mg od doses have the ability to concentrate in the gingival crevice fluid and inhibit the growth of A. actinomycetemcomitans. It exhibits anticollagenase effect also, which can thereby inhibit tissue destruction and aid in bone regeneration.

Maintenance

Periodic review is essential to prevent recurrences in such cases, especially AgP (20). Qualitative chair side diagnostic aids for guessing the risk for future attachment loss for severe cases of CP and AP consists of the use of chair-side assays such as ELISA for detecting the presence of A. Actinomycetemcomitans, P. gingivalis and P. intermedia in plaque samples, and Benzoyl-DLarginine- napthylamide assay for trypsin and other end products of proteolytic enzymes in plaque samples containing P. gingivalis, T. forsythia, and Treponema denticola . X ray can also be required for assessment and review.

Discussion

CP usually has a slower progression rate and a better prognosis . It responds to therapy better ,as compared to AgP [12]. Considering the multifactorial aetiology and predisposing factors that lead to the development of AgP in the susceptible host, special care needs to be taken that all facets affecting the diagnosis and therapeutic outcomes are addressed well [12]. AgP affects young individuals with early loss of teeth which influences quality of life. Early diagnosis with meticulous therapeutic intervention and monitoring of the child and adolescent is therefore advised with thorough periodontal examination and early intervention [12].

Conclusions

Periodontitis is very common in children. Knowledge of the different types of periodontitis is optimal for correct diagnosis and therapy.

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Lupine Publishers | Mentoring of SDMUPR Students in Pediatric Dentistry and Academics

 Lupine Publishers | Journal of Pediatric Dentistry

Abstract

The American Association for Dental Education (ADEA) is working on several initiatives to foster an interest in academic careers. One of these strategies is a student fellowship aimed at allowing the student at the School of Dental Medicine to explore early experiences in academia. In 2016, the School of Dental Medicine of the University of Puerto Rico (SDMUPR), Medical Sciences Campus, began this fellowship. A pipeline of SDMUPR students with interest in pediatric dentistry and academics has evolved from this initiative.

Keywords:The pipeline of future pediatric dentists; mentoring in pediatric dentistry

Abbreviations: ADEA:American Association for Dental Education; SDMUPR: School of Dental Medicine of the University of Puerto Rico

Introduction

The School of Dental Medicine of the University of Puerto Rico (SDMUPR), Medical Sciences Campus, began in 2016 an ADEA Fellowship Program in Dental Academic Careers (ADEA/ADCFP) to encourage students to discover and experience the options available in the academic work setting[1]. This initiative began a parallel pipeline. Students with interest in academics and pediatric dentistry applied continuously to the ADEA/ADCFP and achieved successful educational projects in pediatric dentistry with their mentor assistance. This article will relate the SDMUPR4 years’ experience with this pipeline project of future pediatric dentists with interest in academics.

Discussion

ADEA’s Dental Academic Careers Fellowship Program was founded in 2006 to provide students and residents of the USA and Canadian Dental Schools with the opportunity to venture into academia, providing a structured mentoring to be able to observe and reflect on what an academic career requires[1]. The student is required to complete eight components during the ADEA Fellowship Program in Dental Academic Careers. These components include building an action plan, bi-monthly meetings with a mentor, reflective essays before and after an academic experience, interviews with faculty, academic practice, research practice, presenting a poster, and submitting a portfolio with the evidence of all activities made[1]. In 2016, the SDMUPR began with the ADEA/ADCFP with SDM/UPR students. Since then, every year, at least one student applies to the pediatric dentistry track (Table 1). The mentor is a pediatric dentistry faculty at the SDMUPR, and they work together for eight months on a pediatric educational dentistry track project (Figures 1-3). The number of Applications and First-year Enrollment for Advanced Dental Education Programs continues to rise in the USA[2]. With proper guidance and early experiences, the students can learn and explore their areas of interest in dentistry.

Table 1: SDMUPR ADEA/ADCFP Fellows.

Figure 1: Faculty and student participating in academic activities.

Figure 2: Student presenting a poster at ADEA’s Annual Meeting.

Figure 3: Faculty and student in by-monthly meetings.

Conclusions

Twenty-six students have completed the ADEA Academic Dental Careers Fellowship Program at the UPRMSC School of Dental Medicine and one of the students who participated in the Program in 2016, currently is a pediatric dentist, from the 2017-2018 cohort, two are pediatric dentistry residents at the SDMUPR, and from the 2019-2020 cohort, one applied to pediatric dentistry programs and is waiting for interviews invitations.

Acknowledgments

We want to thank Dr. Jocelyn Medina Paneto, professor and co-liaison of the SDMUPR ADEA/ADCFP, Dr. Carla Rodríguez, main mentor of the pediatric dentistry track, and all the faculty of the School of Dental Medicine of the University of Puerto Rico, Medical Sciences Campus, for their collaboration in this Program.

Conflict of Interest

The author of this article has no conflict of interest to disclose.

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