Abstract
Skeletal class II and III malocclusions are craniofacial disorders that negatively impact people’s quality of life worldwide. Unfortunately, the growth patterns of skeletal malocclusions and their clinical correction prognoses are difficult to predict largely due to lack of knowledge of their precise etiology. Inspired by the strong inheritance pattern of a specific type of skeletal malocclusion, previous genome-wide association studies (GWAS) were reanalyzed, resulting in the identification of 19 skeletal class II malocclusion-associated and 53 skeletal class III malocclusion-associated genes. Functional enrichment of these genes created a signal pathway atlas in which most of the genes were associated with bone and cartilage growth and development, as expected, while some were characterized by functions related to skeletal muscle maturation and construction. Interestingly, several genes and enriched pathways are involved in both skeletal class II and III malocclusions, indicating the key regulatory effects of these genes and pathways in craniofacial development. There is no doubt that further investigation is necessary to validate these recognized genes’ and pathways’ specific function(s) related to maxillary and mandibular development. In summary, this systematic review provides initial insight on developing novel gene-based treatment strategies for skeletal malocclusions and paves the path for precision medicine where dental care providers can make an accurate prediction of the craniofacial growth of an individual patient based on his/her genetic profile.
Highlights
Skeletal class II and III malocclusions are disorders with a sagittal discrepancy between the maxilla and the mandible [2,3]: patients diagnosed with skeletal class II malocclusion exhibit an anterior position of the maxilla in comparison with the mandible, which could result from mandibular retrognathism and/or maxillary prognathism [2,4]
FGFR2 mutations have previously been linked to bone development and growth diseases, such as Apert syndrome [86], a genetic syndrome characterized by untimely early fusion of the skull bones during development that displays skeletal class III malocclusion [87,88]
Enrichment results showed that FGFR2 is involved in of the top skeletal class III malocclusion-associated pathways (Table 5), echoing the assertion that this receptor and the associated FGFR pathway play a vital role in the sagittal disharmony of the maxillomandibular complex
Summary
Skeletal class II and III malocclusions are disorders with a sagittal discrepancy between the maxilla and the mandible [2,3]: patients diagnosed with skeletal class II malocclusion exhibit an anterior position of the maxilla in comparison with the mandible, which could result from mandibular retrognathism (reduced lower jaw growth and size) and/or maxillary prognathism (excessive upper jaw growth and size) [2,4]. Skeletal class III malocclusion, characterized by a posterior maxilla position related to the mandible, could be attributed to mandibular prognathism, maxillary retrognathism, or a combination of the two [3,5]. Both skeletal class II and III malocclusions significantly diminish patients’ ability to chew food effectively [6]. Skeletal class II and III malocclusions have been linked to a diversity of maladies that concern oral health, such as myogenic temporomandibular disorders [9], and even extend to other parts of the body, such as myofascial pain [10] and gastroesophageal reflux disease [8]
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