Children Bruxism (Grinding) Related to Obstructive Sleep Apnea, Enlarged Tonsils and Adenoids, Snoring and Failure to Grow


New research has emerged that shows the significance of children gridningfacial development, bruxism (grinding), enlarged tonsils and adenoids, snoring and obstructive sleep apnea. It show the importance of ENT, dentists, pediatric dentist, orthodontists, and sleep medicine doctors need to work together

Bruxism is usually detected at night, during sleep, when parents can hear their child grinding, clenchingand/orgritting their teeth. It is something the child is not able to control, and, most of the times, bruxism may be caused by obstructive sleep apnea or an upper airway restriction.

If you believe that your child’s bruxism might be caused by and underdeveloped upper or lower jaw, feel free to contact us for an appointment with one of our skilled dentists at Oasis Dental Milton in Ontario.


  • (A) Guilleminault C, Monteyrol PJ, Huynh NT, Pirelli P, Quo S, Li K. “Adenotonsillectomy and rapid maxillary distraction in pre-pubertal children, a pilot study.” Sleep Breath. 2011.


    When both narrow maxilla and moderately enlarged tonsils are present in children with obstructive sleep apnea, the decision of which treatment to do first is unclear. A preliminary randomized study was done to perform a power analysis and determine the number of subjects necessary to have an appropriate response. Thirty-one children, 14 boys, diagnosed with OSA based on clinical symptoms and polysomnography (PSG) findings had presence of both narrow maxillary complex and enlarged tonsils. They were scheduled to have both adeno-tonsillectomy and RME for which the order of treatment was randomized: group 1 received surgery followed by orthodontics, while group 2 received orthodontics followed by surgery. Each child was seen by an ENT, an orthodontist, and a sleep medicine specialist. The validated pediatric sleep questionnaire and PSG were done at entry and after each treatment phase at time of PSG. Statistical analyses were ANOVA repeated measures and t tests.


    The mean age of the children at entry was 6.5 ± 0.2 years (mean ± SEM). Overall, even if children presented improvement of both clinical symptoms and PSG findings, none of the children presented normal results after treatment 1, at the exception of one case. There was no significant difference in the amount of improvement noted independently of the first treatment approach. Thirty children underwent treatment 2, with an overall significant improvement shown for PSG findings compared to baseline and compared to treatment 1, without any group differences.


    This preliminary study emphasizes the need to have more than subjective clinical scales for determination of sequence of treatments.

  • (B) Guilleminault C, et al. “Pediatric sleep-disordered breathing: New evidence on its development.”Sleep Med Review. December 2015; 24:46-56.


    Sleep-disordered breathing (SDB) in children could be resolved by adenotonsillectomy (T&A). However, incomplete results are often noted post-surgery. Because of this partial resolution, long-term follow-up is needed to monitor for reoccurrence of SDB, which may be diagnosed years later through reoccurrence of complaints or in some cases, through systematic investigations.Children undergoing T&A often have small upper airways.. Genetics play a role in the fetal development of the skull, the skull base, and subsequently, the size of the upper airway.In non-syndromic children, specific genetic mutations are often unrecognized early in life and affect the craniofacial growth, altering functions such as suction, mastication, swallowing, and nasal breathing. These developmental and functional changes are associated with the development of SDB. Children without genetic mutations but with impairment of the above said functions also develop SDB. When applied early in life, techniques involved in the reeducation of these functions, such as myofunctional therapy, alter the craniofacial growth and the associated SDB. This occurs as a result of the continuous interaction between cartilages, bones and muscles involved in the growth of the base of the skull and the face. Recently collected data show the impact of the early changes in craniofacial growth patterns and how these changes lead to an impairment of the developmental functions and consequent persistence of SDB. The presence of nasal disuse and mouth breathing are abnormal functions that are easily amenable to treatment. Understanding the dynamics leading to the development of SDB and recognizing factors affecting the craniofacial growth and the resulting functional impairments, allows appropriate treatment planning which may or may not include T&A. Enlargement of lymphoid tissue may actually be a consequence as opposed to a cause of these initial dysfunctions.

  • (C) Bonuck K et al. Growth failure and sleepdisordered breathing: a review of the literature.Int J PediatrOtorhinolaryngol. 2006 May;70(5):769-78



    While otolaryngologists consider growth failure an absolute indication for tonsillectomy and adenoidectomy (T&A), they may not be accustomed to screening for poor growth, and thus unlikely to consider it when recommending a T&A. This paper will (a) familiarize otolaryngologists with the definition, prevalence, and etiology of growth failure and (b) review the published findings that examine the inter-relationship among sleepdisordered breathing, growth failure, and adentonsillar hypertrophy in children.


    This paper is divided into three sections. The first section presents a brief overview of growth failure for the otolaryngologist. The second section reviews the evidence base linking sleepdisordered breathing, growth failure, and adenotonsillar hypertrophy in children. The anthropometric outcomes of children presenting for T&A, or having sleep symptoms assessed, are presented. The third section presents pilot data (n=28) on the prevalence of growth failure and sleepdisordered breathing among children presenting for T&A at our institution.


    Among children presenting for T&A or having sleep symptoms assessed, growth failure was at least twice the expected rate in six of eight published studies. Across these six studies, this rate ranged from a low of 6% of children <3rd percentile for weight and 6% <3rd percentile for height in one study, to a high of 52% who were <3rd percentile in weight in a second study, and 44% who were or= 5th percentile for height in a third. Among children presenting for T&A at our own institution, 14% were or=5th percentile in height, and 11% were or=5th percentile in weight. Among children under 6 years of age, 21% were either or= 5th percentile in weight and/or height.


    Published studies, as well as our own pilot data support the hypothesis that SDB (Sleep Disorder Breathing), secondary to adenotonsillar hypertrophy increases the risk of growth failure in children.Adenotonsillar hypertrophy and sleepdisordered breathing may be unrecognized risk factors in the etiology of growth failure. Otolaryngologists can play an important role in identifying growth failure, and referring children to the appropriate specialists.

  • (D) Major MP, El-Hakim H, Witmans M, Major PW, Flores-Mir C. Adenoid hypertrophy in pediatric sleep disordered breathing and craniofacial growth: the emerging role of dentistry. Journal of Dental Sleep Medicine 2014;1(2):83–87.

    Study Objectives

    Summarize and synthesize the most recent evidence about adenoid hypertrophy, impact on craniofacial growth,role in sleep disordered breathing, and effects of treatment.


    Literature review of relevant manuscripts from dentistry, orthodontics, otolaryngology, and sleep medicine


    Adenoid hypertrophy is the most common cause of nasopharyngeal obstruction in children; the most common cause of pediatricsleep disordered breathing (SDB); and can be an etiologic cause of altered craniofacial growth characterized by long face, retrusive chin,and narrow maxilla. Early detection and treatment may mitigate or resolve negative effects of adenoid hypertrophy. Adenoidectomyremains a front line treatment for the majority of cases, although alternative treatments must be considered when different SDB etiologiesand co-morbidities are present.. Best available evidence suggests that rapid maxillary expansion and adenoidectomy work synergisticallyto resolve SDB symptoms, and often both treatments are necessary for full treatment effect.


    Primary care dentists, pediatric dentists, and orthodontists have an important role in early detection of adenoidhypertrophy. Emerging evidence continues to demonstrate dental treatments as playing an increasingly important role in multidisciplinarymanagement of pediatric SDB.

  • (E) Ferreira et al. Sleep bruxism associated with obstructive sleep apnea syndrome in children.Cranio. 2014



    Sleep bruxism (SB) and obstructive sleep apnea syndrome (OSAS) are often observed in children and may have several health implications. The aim of this paper is to evaluate their prevalence and to test for possible associations between these two conditions.


    The sample consisted of 496 children randomly selected among the preschoolers of Taubaté, Brazil; 249 (50•2%) were boys and 247 (49•8%) were girls. Diagnoses of SB and OSAS were made by clinical examinations and questionnaires filled out by the children’s parents in a cross-sectional design. Analysis of variance and Chi-square tests were applied to verify possible association among the variables in question.


    The average age was 4•49 years (SD: ±1•04 years). A total of 25•6% were diagnosed with SB, while 4•83% were diagnosed with OSAS, and only 2•82% presented both conditions. A statistical association was found between SB and OSAS (P<0•001; Chi-square test): 11•03% of subjects with SB also presented with OSAS, and 97•18% of subjects without SB did not present with OSAS. No association was found among children's gender and age and the presence of SB or OSAS.


    Within the limits of this study , SB (Sleep Bruxism) was associated with OSAS (Obstructive Sleep Apnea Syndrome).



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