|Year : 2019 | Volume
| Issue : 1 | Page : 47-52
Trisha Das Sarma, Abhishek Mandal, Shabnam Zahir, Gautam Kumar Kundu
Department of Pedodontics and Preventive Dentistry, Guru Nanak Institute of Dental Sciences and Research, Kolkata, West Bengal, India
|Date of Web Publication||15-Mar-2019|
Trisha Das Sarma
157/F, Nilganj Road, Sahid Colony, Panihati, Kolkata - 700 114, West Bengal
Bruxism is diurnal or nocturnal parafunctional habits which includes repetitive jaw-muscle activities, clenching or grinding of the teeth and/or bringing forward the mandible. Psychological components, genetic components, peripheral and patho-physiological components are the main Etiology of bruxism. Treatment options include occlusal rehabilitation, behavioural and pharmacological therapy. We perform a scientific paper search by using ebscohost, pubmed, and Google search engines. The searched item 'Bruxism' showed total 1125 papers, among which 250 were review papers. Most of them were published between 1990 to 2017 and some of them before 1990. Through this review an overview about childhood bruxism and its various treatment options and outcomes will be provided.
Keywords: Bruxism, children, etiology, management
|How to cite this article:|
Sarma TD, Mandal A, Zahir S, Kundu GK. Childhood bruxism. SRM J Res Dent Sci 2019;10:47-52
| Introduction|| |
Parafunction denotes occlusal habitual exercises which are not the normal functions. Bruxism is “parafunctional grinding of teeth or an oral habit consists of involuntary rhythmic or spasmodic nonfunctional gnashing, grinding, or clenching of teeth in other than chewing movements of the mandible which may lead to occlusal trauma” – Glossary of Prosthodontic Terms.
According to international classification of sleep disorder (ICSD), bruxism is the third most common form of sleep disorder following sleep talking and snoring. Some authors suggested the connection of obstructive sleep apnea (OSA) with bruxism and concluded that assessment of head posture should be included in the evaluation of children with bruxism.
| Nomenclature|| |
- In 1901, Karolyi M coined the term – “traumatic neuralgia”
- 1907: Marie Pietkiewicz – “bruxomania”
- 1931: Frohman – “bruxism”
- 1971: Ramjford Ash – “centric and eccentric bruxism”
- In 1972, Drum gives the name – “emotional loaded parafunction”
- In 1983, the difference between clenching and grinding is explained as – Clenching is termed as centric bruxism and grinding is called eccentric bruxism.
| Materials and Methods|| |
A computerized literature search was conducted using EBSCOhost Database of Central Library heading Dentistry and Oral Sciences Source, PubMed, and Google search engines. The research descriptors used were “bruxism,” “Bruxism in children,” “Bruxism therapy and children,” “Bruxism pharmacology children,” “Bruxism dopamine inhibitor children,” “Bruxism psychologic techniques children,” “Bruxism cognitive therapeutics children,” “Bite plates bruxism,” “Occlusal plates bruxism,” and “Airway bruxism.” The searched component “Bruxism” gave 1125 papers, among which 250 were review papers. The number of papers headed “Childhood Bruxism” was 145.
- Review articles which primarily focus on sleep bruxism (SB) in children
- 0–13 years aged individuals considered as children
- Reviews published between 1990 and 2017 without language restrictions. Very few of them were published before 1990. The period was chosen due to an attempt to retrieve reviews with more precise and accurate methodological criteria and new discoveries about SB over the past few years and to compare the effectiveness of old and new diagnostic methods.
The following exclusion criteria were also applied:
- Articles based on bruxism in adults
- Articles published before 1990.
About 25, 52, and 250 articles were evaluated for the title, abstract, and the final review write-up, respectively.
| Classification of Bruxism|| |
According to time
- Awake bruxism/diurnal bruxism (AB) occurs when individual is awake and usually occurs due to stress and anxiety
- SB occurs when an individual is sleeping. Rhythmic masticatory events are seen with arousals most of the time
- Combined occurs in both conditions.
According to motor activity
- Tonic – Muscular contractions lasting >2 s
- Phasic – Brief repeated muscular contractions with at least three consecutive electromyographic bursts of 0.25 and 2 s long
- Combined – Variation of tonic and phasic type of motor activity.
Ninety percent of SB shows phasic or combined, but AB mostly shows tonic activity.
- Nonactive – Bruxism presents before but absent at the time he/she came to the physician
- Active – Bruxism is currently present.
- Mild – No damage to teeth or psychological impairment
- Moderate – Mild impairment of psychological functioning
- Severe – Affects the teeth, temporomandibular joint (TMJ), and severe psychological deterioration.
| Prevalence|| |
Starting time of SB coincides with the eruption of deciduous incisors. SB is most commonly seen in the children. The prevalence of SB was around 8% in the adults and 14%–20% in children. After observing the result of questionnaires and polysomnography, the prevalence slightly lowers in adults and becomes 5.5%. Only 3% of geriatric population are aware of frequent grinding.
The prevalence of AB was around 16%–20% of the general population. Females are more commonly affected by AB, while SB is equally distributed among males and females. Among all bruxism episodes, 80% are not accompanied by noise.
SB patients show 67% more microarousals/hour of sleep (5/h) than normal individuals. Normal individuals have approximately one rhythmic masticatory muscle activity/hour of sleep, while individuals with SB may have up to 12 rhythmic masticatory muscle activities/hour of sleep.,
| Etiology|| |
Pathophysiological factors and disturbances in central neurotransmitter system
In 86% of bruxism episodes, arousal response along with involuntary leg movements is seen. Arousal response is arrival in the lighter sleep stage or waking up in the response to sudden shift in the depth of the sleep. Heart rate and muscle activity are increased, and changes in respiratory rates and gross movements of the body are seen during this arousal response.
Most SB episodes occur in the light stages of non-rapid eye movement (REM) sleep (i.e., Stages 1 and 2 sleep) and occasionally (<10%) during REM sleep in association with sleep arousals.
Direct and indirect pathways of the basal ganglion consist of five subcortical nuclei which coordinate movements and do not work properly in bruxism.
Pathways of action potential transmission, where dopamine is the main controlling agent, are defective in these patients. Short- and long-term use of L-dopa (dopamine precursors) decreases and increases bruxism activity, respectively.
Bruxing children are more anxious. Elevated levels of urinary catecholamine and salivary cortisol is seen in their body due to stress, anxiety, fear, frustration, or poor social support.
- If the harmony between maximum intercuspation and centric relation is lost, it results in bruxism episodes
- Pacifier sucking, lip biting, and thumb sucking have association with bruxism among which relation between pacifier sucking and bruxism is statistically significant. The exact cause of this connection is explained as all parafunctional habits have the same roots
- Genetic factors – Researchers have got an association between C allele carrier of HTR2A single-nucleotide polymorphism rs6313 and SB
- Pathogenic parasites – mainly Enterobius vermicularis and Giardia lamblia – kill probiotic bacteria and release toxins, may cause the initiation of bruxism among children. One of the ways of entrance of these parasites in human body is through nail biting.
Dopamine agonists, dopamine antagonists, tricyclic antidepressants, selective serotonin reuptake inhibitors (SSRIs), alcohol, cocaine, and amphetamines stimulate dopaminergic system and can result in developing bruxism after chronic use. Bruxism is two times more common in cigarette smokers than the nonsmokers.,
- Occlusal interferences occur due to either a premature contact or a deflective interference. Deflective contact is, when the jaws are brought into occlusion in overerupted upper third molar, the mandibular posterior teeth contact first to the prominent third molar, and then the individual has to push forward his/her lower jaw so that rest of the teeth can contact
- Angle Classes 2, 3 malocclusions, deep bite, anterior and postcrossbite, and increased overjet may be associated with bruxism
- Recent literature findings report a relationship between intraesophageal acidity, gastroesophageal reflux disease (GERD), and SB in adults.
Other possible associations
- Condylar asymmetry Sleep disturbance/arousals
- Dental arch form Allergies
- Parkinson's diseases Rett syndrome
- Torus mandibularis Trauma
- Oromandibular dystonia Atypical facial pain.
Nutritional deficiencies (e.g., calcium and magnesium).
| Consequences|| |
Any individual gives a load of over 20 g on a tooth over a period of 2.5 s per clenching which is much greater than the load occurred in normal functional swallowing and chewing.
This affects the viscoelastic property of periodontal ligament (PDL) and causes distortion of alveolar bone, from which the tissue recovering properties become delayed.
Affect the proprioceptive nerve endings – The protective reflex mechanism decreased – leading to abnormal muscle activity.
Tooth and periodontal structures
Hypersensitivity, hypermobility, hypercementosis, periodontal damage, pulpitis, pulpal necrosis, tooth wear (0-degree cusps), abfraction cavities, tooth or cusp fracture, restoration fracture or dislodgement, implant failure, ridge resorption, and torus mandibularis.
Masticatory muscle and temporomandibular joint
Masticatory muscle pain or discomfort, TMJ pain or degeneration, TMJ disc displacement temporomandibular disorder-related headache, jaw function disabilities, deviation of the lower jaw on opening, and limitation of mouth opening ability.
Tongue/cheek indentation or scalloping; lip, cheek, or tongue biting.
Reduced facial vertical dimension and masticatory muscle hypertrophy (characteristic square jaw).
Widened PDL space and trabeculation of the alveolar bone.
Mercury release from amalgam restorations causes reduction in salivary flow and/or xerostomia.
| Diagnosis|| |
Bruxism risk patients can be diagnosed by (1) various questionnaire, (2) individual tooth wear index, and (3) different intraoral appliances. (4) Electromyographic and (5) polysomnographic records help in definitive diagnosis.
- Has anyone heard the sound of grinding of your teeth when you sleep?
- Did you ever feel fatigue or soreness in your jaw when you wake up in the morning?
- Did you feel soreness in your teeth or gums?
- Did you ever sense temporal headache when you wake up in the morning?
- Do you realize that you grind your teeth during day time?
- Can you realize that you clench your teeth during day time?
Individual (personal) tooth wear index
To investigate the prevalence and severity of incisal or occlusal wear.
- 0: No wear or negligible wear is seen in enamel
- 1: Wear of enamel or wear proceeds through the enamel to dentine in single area
- 2: Wear of the dentin affects up to the one-third height of the crown
- 3: Wear of the dentin affects more than one-third height of the crown; or excessive wear of the restorative material or dental material in the crown and bridgework affects more than one-third height of the crown.
The individual (personal) tooth wear index (IA) =10 × G1 + 30 × G2 + 100 × G3/G0 + G1 + G2 + G3.
- G0 – Numbers of teeth which score 0
- G1 – Numbers of teeth which score 1
- G2 – Numbers of teeth which score 2
- G3 – Numbers of teeth which score 3.
- After multiple readjustments of the occlusal splints, if wear pattern appears repetitively in the same area with a similar pattern and direction, bruxism is diagnosed
- Bruxcore Bruxism-Monitoring Device (BBMD) – it counts how many abraded microdots appear on its surface and measures the volumetric magnitude of abrasion. It consists of a polyvinyl chloride plate (thickness – 0.51 mm) which is made of four layers of two alternative colors and a halftone dotted topmost surface. By observing how many microdots are missing, we can recognize the abraded area and the uncovered number of layers equivalents to the depth of force applied at the time of bruxism episodes
- Intrasplint force detector (ISFD) – 1–2 mm below the occlusal surface of the splint, a thin, deformation-sensitive piezoelectric film is installed which can measure the force applied during bruxism episodes. Results of ISFD correlate with the result of masseter electromyogram (EMG).
Portable masticatory muscle electromyogram recording device
Number, duration, and magnitude of force can be calculated by this device.
Miniature self-contained electromyogram detector analyzer with a biofeedback function
They are useful for the patients who have moderate-to-high level of bruxism. Masseter and anterior temporalis muscle activities can be recorded by this device.
It consists of electroencephalogram, EMG, electrocardiogram, and thermally sensitive resistor (monitoring air flow) signals combined with audio–video recordings simultaneously. Other sleep disorders such as sleep apnea, insomnia, and diseases related to orofacial activities such as myoclonus, swallowing, and coughing can be ruled out as clenching and grinding causes heavy horizontal forces as opposed to predominantly vertical forces during chewing and swallowing.
| Management|| |
Eliminate the causative factors – Quitting smoking, alcohol, and coffee uptake.
Occlusal rehabilitation – By increasing the vertical dimension in occlusion and create interocclusal space. According to the Dahl's concept, “partial bite raising appliance” can be used which will help in intrusion of the anterior teeth which are in contact with the appliance and extrusion of the separated posterior teeth simultaneously.
The “neuro-occlusal rehabilitation” theory hypothesizes that for the proper development and evolution of the components of stomatognathic system (alveolar bone, the mucosa, dentoperiodontal components, muscles, TMJ, and position of the teeth on the dental arch), masticatory function plays an important role, and defective mastication may hamper this system.
Any malocclusion that prevents or hinders lateral movements, causing a functional problem at TMJ level, is one of the etiological factors of bruxism. To resolve this alteration, the nervous system induces the generation of this functional habit since the wear of the occlusal tooth surface would favor laterality mandibular movements.
To provide neuro-occlusal rehabilitation, Pedro Planas proposes the therapy based on selective carving, the placement of flat direct or indirect tracks, and in more extreme cases, the placement of aparatology, with the intention to functionalize the stomatognathic system.
Direct tracks added composite to certain teeth to increase the height and to make the occlusal plane parallel to camper plane. Along with these tracks, functional masticatory angles should be made almost equal in the right and left sides – which cause a stimulus occurs to the masticatory apparatus, similar to that of natural chewing, and help to naturally establish a balanced occlusion.,
Occlusal splint – Another names are occlusal bite guard, bruxism appliance, bite plate, night guard, occlusal device. Hard splints are more favorable as it is very difficult to adjust a soft splint.
- Hard acrylic resin and composite resins or soft vinyl
- Stabilization splints are nowadays universally used as it provides full coverage and consists of a flat plane with balanced contacts with all opposing teeth in centric relation. Different studies conclude that canine ramps may reduce elevator muscle activity and so can be added to the stabilization splints. “Nociceptive Trigeminal Inhibition Clenching Suppression System” is a chairside adjustment of small anterior splint which is much more effective than other methods
- ”Bruxism 'S' Splint” – Prefabricated splint and can be adjusted chair side, used in conjunction with fixed orthodontic treatment.
Ventilatory stimuli that activate the genioglossus during OSA also engage the masseter muscles. Mandibular advancement devices correct OSA as well as SB.,
Biofeedback – Psychological approaches to manage SB include biofeedback, hypnotherapy, cognitive therapy, behavioral therapy, stress, and relaxation management.
Patients should be enough trained so that they can control their jaw muscle activities through auditory or visual commands from a surface EMG, when they are aroused. When patients are asleep, auditory, electrical, vibratory, and even taste stimuli (bruxism activities rupture the capsules which were filled with an aversive substance) can be used for feedback.
Pharmacological management – Drugs which inhibit release of acetylcholine at the neuromuscular junction:
- Botulinum toxin produces motor weakness to the point of paralysis – specifically used in severe cases of bruxism
- Acute use of catecholamine precursor L-dopa decreases SB activities
- selective alpha-2 agonist clonidine and low dosage of dopamine D1/D2 receptor agonist pergolide can be used in a severe bruxism case
- Antidepressant drugs – SSRI and tranquilizers (i.e., a dose of 10 mg hydroxyzine 1 h before bedtime).
| Conclusion|| |
Bruxism is considered as a parafunctional habit, and the pediatric population is mostly affected by it. Pediatric dental surgeons should be well informed about the etiology, treatment of bruxism, and how to rehabilitate such patients. At present, there is no such effective treatment to eliminate bruxism permanently. The therapeutic approach mainly focuses to prevent further damage and to treat the pathological effects of bruxism on the structures of the masticatory apparatus.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Shetty S, Pitti V, Satish Babu CL, Surendra Kumar GP, Deepthi BC. Bruxism: A literature review. J Indian Prosthodont Soc 2010;10:141-8.
Murali RV, Rangarajan P, Mounissamy A. Bruxism: Conceptual discussion and review. J Pharm Bioallied Sci 2015;7:S265-70.
Yap AU, Chua AP. Sleep bruxism: Current knowledge and contemporary management. J Conserv Dent 2016;19:383-9.
] [Full text]
Sari S, Sonmez H. The relationship between occlusal factors and bruxism in permanent and mixed dentition in Turkish children. J Clin Pediatr Dent 2001;25:191-4.
International Classification of Sleep Disorders. Diagnostic and Coding Manual. Diagnostic Classification Steering Committee, Thorpy, Chairman. Rochester, MN: American Sleep Disorders Association; 1990.
Lavigne GJ, Montplaisir JY. Restless legs syndrome and sleep bruxism: Prevalence and association among Canadians. Sleep 1994;17:739-43.
Lavigne GJ, Rompré PH, Poirier G, Huard H, Kato T, Montplaisir JY, et al.
Rhythmic masticatory muscle activity during sleep in humans. J Dent Res 2001;80:443-8.
Schames SE, Schames J, Schames M, Chagall-Gungur SS. Sleep bruxism, an autonomic self-regulating response by triggering the trigeminal cardiac reflex. J Calif Dent Assoc 2012;40:670-1, 674-6.
Macaluso GM, Guerra P, Di Giovanni G, Boselli M, Parrino L, Terzano MG, et al.
Sleep bruxism is a disorder related to periodic arousals during sleep. J Dent Res 1998;77:565-73.
Bader G, Lavigne G. Sleep bruxism; an overview of an oromandibular sleep movement disorder. REVIEW ARTICLE. Sleep Med Rev 2000;4:27-43.
Lobbezoo F, Lavigne GJ, Tanguay R, Montplaisir JY. The effect of catecholamine precursor L-dopa on sleep bruxism: A controlled clinical trial. Mov Disord 1997;12:73-8.
Monaco A, Ciammella NM, Marci MC, Pirro R, Giannoni M. The anxiety in bruxer child. A case-control study. Minerva Stomatol 2002;51:247-50.
Giffin KM. Mandibular adaptive reposturing: The etiology of a common and multifaceted autodestructive syndrome. Gen Dent 2003;51:62-7.
Gonçalves LPV, Toledo OA, Otero SAM. The relationship between bruxism, occlusal factors and oral habits. Dent Press J Orthod 2010;15:97-104.
Tehrani MH, Pestechian N, Yousefi H, Sekhavati H, Attarzadeh H. The correlation between intestinal parasitic infections and bruxism among 3-6 year-old children in Isfahan. Dent Res J (Isfahan) 2010;7:51-5.
Lobbezoo F, van Denderen RJ, Verheij JG, Naeije M. Reports of SSRI-associated bruxism in the family physician's office. J Orofac Pain 2001;15:340-6.
Ashcroft GW, Eccleston D, Waddell JL. Recognition of amphetamine addicts. Br Med J 1965;1:57.
Ohmure H, Oikawa K, Kanematsu K, Saito Y, Yamamoto T, Nagahama H, et al.
Influence of experimental esophageal acidification on sleep bruxism: A randomized trial. J Dent Res 2011;90:665-71.
Bruxism/Teeth Grinding. Mayo Foundation for Medical Education & Research; 19 May, 2009.
Manfredini D, Poggio CE, Lobbezoo F. Is bruxism a risk factor for dental implants? A systematic review of the literature. Clin Implant Dent Relat Res 2014;16:460-9.
Pintado MR, Anderson GC, DeLong R, Douglas WH. Variation in tooth wear in young adults over a two-year period. J Prosthet Dent 1997;77:313-20.
Ekfeldt A, Hugoson A, Bergendal T, Helkimo M. An individual tooth wear index and an analysis of factors correlated to incisal and occlusal wear in an adult Swedish population. Acta Odontol Scand 1990;48:343-9.
Korioth TW, Bohlig KG, Anderson GC. Digital assessment of occlusal wear patterns on occlusal stabilization splints: A pilot study. J Prosthet Dent 1998;80:209-13.
Forgione A. Simple but effective method quantifying bruxing behavior. J Dent Res 1974;53.
Takeuchi H, Ikeda T, Clark GT. A piezoelectric film-based intrasplint detection method for bruxism. J Prosthet Dent 2001;86:195-202.
Rugh JD, Solberg WK. Electromyographic studies of bruxist behavior before and during treatment. J Calif Dent Assoc 1975;3:56-9.
Minakuchi H, Clark GT, Haberman PB, Maekawa K, Kuboki T. Sensitivity and specificity of a miniature bruxism detection device. OOOOE J 2005;99:440-1.
Lavigne GJ, Khoury S, Abe S, Yamaguchi T, Raphael K. Bruxism physiology and pathology: An overview for clinicians. J Oral Rehabil 2008;35:476-94.
Mengatto CM, Coelho-de-Souza FH, de Souza Junior OB. Sleep bruxism: Challenges and restorative solutions. Clin Cosmet Investig Dent 2016;8:71-7.
Planas P. Rehabilitación Neuro-Oclusal (RNO). 1st
ed., barcelona: Salvat Editores; 1987.
Borţun CM, Rusu LC. Recording of mastication angles by Planas's laws. Stoma Educ J 2014;1:86-91.
Belkhiri A, Zenati L. Neuro-occlusal rehabilitation: Therapeutic by direct and indirect tracks. EC Dent Sci 2017;7:82-91.
Okeson JP. The effects of hard and soft occlusal splints on nocturnal bruxism. J Am Dent Assoc 1987;114:788-91.
Leib AM. The occlusal bite splint – A noninvasive therapy for occlusal habits and temporomandibular disorders. Compend Contin Educ Dent 1996;17:1081-4, 1086, 1088.
Boyd JP. Improving TMD treatment and protecting restorative dentistry. Dent Today 1998;17:144.
Sullivan TC. A new occlusal splint for treating bruxism and TMD during orthodontic therapy. J Clin Orthod 2001;35:142-4.
Landry ML, Rompré PH, Manzini C, Guitard F, de Grandmont P, Lavigne GJ, et al
. Reduction of sleep bruxism using a mandibular advancement device: An experimental controlled study. Int J Prosthodont 2006;19:549-56.
Hollowell DE, Bhandary PR, Funsten AW, Suratt PM. Respiratory-related recruitment of the masseter: Response to hypercapnia and loading. J Appl Physiol (1985) 1991;70:2508-13.
Nissani M. Can taste aversion prevent bruxism? Appl Psychophysiol Biofeedback 2000;25:43-54.
Shim YJ, Lee MK, Kato T, Park HU, Heo K, Kim ST, et al
. Effects of botulinum toxin on jaw motor events during sleep in sleep bruxism patients: A polysomnographic evaluation. J Clin Sleep Med 2014;10:291-8.
Saletu A, Parapatics S, Anderer P, Matejka M, Saletu B. Controlled clinical, polysomnographic and psychometric studies on differences between sleep bruxers and controls and acute effects of clonazepam as compared with placebo. Eur Arch Psychiatry Clin Neurosci 2010;260:163-74.
Amir I, Hermesh H, Gavish A. Bruxism secondary to antipsychotic drug exposure: A positive response to propranolol. Clin Neuropharmacol 1997;20:86-9.