Malocclusion complexity and orthodontic treatment need in children with autism spectrum disorder.

OBJECTIVES This study aimed to investigate the malocclusion complexity and orthodontic treatment need among children with and without autism spectrum disorder (ASD) referred for orthodontic treatment by quantifying the Discrepancy Index (DI) and Index of Orthodontic Treatment Need (IOTN). MATERIALS AND METHODS Dental records of 48 ASD and 49 non-ASD consecutive patients aged between 9 and 18 years (median age 13.0 years) referred for orthodontic treatment were reviewed and compared. The Discrepancy Index (DI) was quantified to determine the malocclusion complexity, and the Index of Orthodontic Treatment Need (IOTN), including the Dental Health Component (IOTN-DHC) and Aesthetic Component (IOTN-AC), was quantified to determine the orthodontic treatment need. Statistical analysis included descriptive analysis, Pearson chi-square tests, Fisher's exact test, Mann-Whitney U tests, and several univariate and multivariate regression analyses. The statistical analysis used descriptive analysis, Pearson chi-square test, Fisher's exact test, and multivariate logistic regression. RESULTS The results show that both malocclusion complexity (DI, p = 0.0010) and orthodontic treatment need (IOTN-DHC, p = 0.0025; IOTN-AC p = 0.0009) were significantly higher in children with ASD. Furthermore, children with ASD had a higher prevalence of increased overjet (p = .0016) and overbite (p = .031). CONCLUSIONS Malocclusion complexity and orthodontic treatment need are statistically significantly higher among children with ASD than children without ASD, independent of age and sex. CLINICAL RELEVANCE Children with autism may benefit from visits to a dental specialist (orthodontist) to prevent, to some extent, developing malocclusions from an early age

Developmental characteristics of the permanent upper lateral incisor in unilateral cleft lip and palate

Objectives: This study aims to provide insights into the developmental characteristics of the upper lateral incisor in individuals with unilateral clefts. Materials and methods: Panoramic radiographs of a consistent group of Caucasian children taken over time (ages 6, 9, and 12) were extensively reviewed. The study assessed the distribution pattern, eruption path, tooth development, and crown size of the upper lateral incisor within the cleft region. Results: The most commonly observed distribution pattern was the lateral incisor located distal to the cleft, accounting for 49.2% of cases. Furthermore, a significant delay in tooth development of the upper lateral incisor on the cleft side was noted at ages 6 and 9 (p &gt; 0.001). Compared with the non-cleft side, these incisors often erupted along the alveolar cleft and exhibited microdontia (88.3%, p &lt; 0.041). Conclusion: Lateral incisors on the cleft side display unique distribution patterns, microdontia, and delayed tooth development. Careful monitoring of the cuspid eruption is essential, as it can influence the eruption of the lateral incisor. Clinical relevance: A comprehensive understanding of the development of the upper lateral incisor relative to the cleft is vital for determining its prognosis over time. The position of the upper lateral incisor can also influence the timing and prognosis of secondary alveolar bone grafting. Preserving the upper lateral incisor favors arch length, perimeter, and symmetry in individuals with unilateral clefts.</p

Strategies to improve regeneration of the soft palate muscles after cleft palate repair

Children with a cleft in the soft palate have difficulties with speech, swallowing, and sucking. These patients are unable to separate the nasal from the oral cavity leading to air loss during speech. Although surgical repair ameliorates soft palate function by joining the clefted muscles of the soft palate, optimal function is often not achieved. The regeneration of muscles in the soft palate after surgery is hampered because of (1) their low intrinsic regenerative capacity, (2) the muscle properties related to clefting, and (3) the development of fibrosis. Adjuvant strategies based on tissue engineering may improve the outcome after surgery by approaching these specific issues. Therefore, this review will discuss myogenesis in the noncleft and cleft palate, the characteristics of soft palate muscles, and the process of muscle regeneration. Finally, novel therapeutic strategies based on tissue engineering to improve soft palate function after surgical repair are presented

Strategies to improve regeneration of the soft palate muscles after cleft palate repair

Contains fulltext : 109604.pdf (publisher's version ) (Open Access)Children with a cleft in the soft palate have difficulties with speech, swallowing, and sucking. These patients are unable to separate the nasal from the oral cavity leading to air loss during speech. Although surgical repair ameliorates soft palate function by joining the clefted muscles of the soft palate, optimal function is often not achieved. The regeneration of muscles in the soft palate after surgery is hampered because of (1) their low intrinsic regenerative capacity, (2) the muscle properties related to clefting, and (3) the development of fibrosis. Adjuvant strategies based on tissue engineering may improve the outcome after surgery by approaching these specific issues. Therefore, this review will discuss myogenesis in the noncleft and cleft palate, the characteristics of soft palate muscles, and the process of muscle regeneration. Finally, novel therapeutic strategies based on tissue engineering to improve soft palate function after surgical repair are presented

Excisional wounding of the soft palate.

<p>Excisional wounds (1 mm ø) were made in the soft palate, 7 mm behind the 9th palatal ruga. W: excisional wound, R: 9th ruga.</p

Regeneration of the soft palate after wounding.

<p>Control and wound tissues from the soft palate were stained with AZAN, and with antibodies against myofibroblasts (ASMA) and fast muscle fibers (Fast MyHC). After 7 days, extensive granulation tissue with collagen and myofibroblasts had formed. (A) AZAN staining. Connective tissue is stained blue, muscle tissue red. Black arrows indicate muscle fibers, white arrows indicate initial regeneration of salivary glands. SG: Salivary glands. (B) ASMA (Brown). Myofibroblasts were not present in the controls, except in blood vessels and salivary glands. In contrast, large numbers of myofibroblasts were present in the wound area at 7 days in the experimental group. (C) Fast MyHC (brown). In both groups, almost all myofibers were of the fast-twitch type. Wound margins are indicated by the dotted lines. The bar represents 200 µm.</p

Anatomy of levator veli palatini and tensor veli palatini.

<p>Left: Schematic representation of the levator veli palatini and tensor veli palatini muscles. Right: (A) The levator veli palatini muscle arises from the inferior surface of the temporal bone, lateral and posterior from the tympanic bulla. The tympanic bulla is a bony projection of the temporal bone containing the tympanic cavity. (B) Posterior to the pterygoid process, the levator veli palatini continues towards the soft palate. The glossopharyngeal, vagus and hypoglossal nerves are visible between the levator veli palatini and the skull base. (C) The tensor veli palatini originates from the inferior surface of the sphenoid bone, the lateral surface of the perygoid plate, and the auditory tube. (D) The tendon of the tensor veli palatini turns around a curved process; the pterygoid hamulus. It continues medially towards the soft palate and forms the palatine aponeurosis. LVP: levator veli palatini muscle, TVP: tensor veli palatini muscle, IX: glossopharyngeus nerve, X: vagus nerve, XII: hypoglossus nerve, Ty: Tympanic bulla, At: auditory tube, H: pterygoid hamulus, Pt: pterygoid process, PNS: posterior nasal spine, S: soft palate.</p

Satellite cells and myofibers after wounding.

<p>Control and wound tissues were stained with antibodies against Pax7, MyoD, and Myogenin. Large numbers of activated satellite cells and regenerating myofibers are present in the experimental group. (A) Satellite cells (arrows) express the transcription factor Pax7. (B) The myogenic determination factor 1 (MyoD, arrows) is expressed during satellite cell proliferation. (C) Differentiation is marked by a decline in Pax 7 expression, and the induction of myogenin (MyoG, arrows). Pax7-, MyoD-, and MyoG positive cells are stained brown. The bar represents 50 µm.</p

General aspect of the soft palate in rats.

<p>Left: Schematic representation of the soft palate (intraoral view). Right: The soft palate in the rat extends from the posterior edge of the hard palate (9^th ruga) towards the nasopharyngeal sphincter. In adult rats, the length of the soft palate is about 11 mm. Ns: nasopharygeal sphincter, R: 9th ruga, M: molar. The red circle indicates the location of the excisional wound (1 mm ø). The dotted lines indicate the location of the histological sections shown in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0059193#pone-0059193-g004" target="_blank">Figure 4</a>. S: midsagittal section. B1, B2, and B 3 coronal sections.</p