Tooth wear presents as a significant challenge for many reasons, not the least of which is attempting to identify the etiology of the wear, which in turn has a significant impact on the future prognosis of any treatment.
The common causes of tooth wear can be identified as, Attrition, Erosion, Abrasion, and Abfraction. In this article I will focus on Attrition, discussing the other causes in detail in future articles.
Attrition – wear on the teeth from opposing occlusal contacts on the incisal or occlusal surfaces during mandibular movement. The hallmark of attrition is the creation of flat shiny wear facets in locations where the teeth are in occlusal contact. (Figs. 1-4)
Of all the causes, Attrition has potentially the worst prognosis for the restorative dentist and patient, as it has the highest risk of future wear or fracture of any restorative treatment, especially implant related restorations due to their lack of a pdl. (Figs. 5-7)
The major question about attrition is why are the teeth rubbing against each other, said differently, why is the mandible moving in such a way that the teeth are running into each other.
Three major theories exist to explain the mandibular movement:
1. Functional wear, the teeth are rubbing against each other during normal function, such as mastication. Research on chewing has shown that there are two major categories which describe how people masticate, a chopping pattern, in which the teeth never come into contact except when the mandible closes into the intercuspal position during chewing, and therefore, the teeth do not rub against each other, and a grinding pattern of chewing, in which the mandible has much broader horizontal movements during mastication, in which case the teeth do rub against each other. The grinding pattern is associated with more tooth wear and mobility.1
2. Occlusal interferences, the classic concept that interferences in the occlusion, such as a shift from centric relation to the intercuspal position, interferences in the intercuspal position, such as a high restoration, or interferences in excursive movements, such as working or non-working interferences trigger the grinding behavior.
Beliefs among clinicians on occlusal interferences is very divided as to whether they initiate tooth grinding, however multiple researchers have intentionally placed interferences in the occlusion to see if they can initiate tooth grinding, and while several negative effects are seen, such as tooth mobility, tooth sensitivity, muscle pain, and sometimes TMD symptoms, rarely if ever does the patient start grinding.2
3. Bruxism, wear that is initiated as an event from the Central Nervous System. Typically bruxism is thought of as a micro-arousal of the sympathetic nervous system, the micro-arousal triggers a cascade of events including increased brain activity, heart rate, respiratory rate, and finally RMMA’s, or rhythmic masticatory muscle activity, in which the individual rhythmically closes and grinds their teeth.3
The initiation of the micro-arousals has been associated with Sleep Apnea, Gastric Reflux, and Psychologic stress, to name a few possibilities. When associated with apnea or airway issues the bruxism is thought to be the body’s mechanism for opening the airway and increasing oxygenation.4,5 The incidence of nocturnal bruxism decreases with age, going from a high of 14-20% in children 11 and younger, to 13% among young adults from 18-29 years of age, to 3% among adults over 60, meaning those patients who say they used to grind but don’t anymore may be accurate.6 Daytime bruxism in contrast, rises from 12% in children to 20% in adults.7
Other facts concerning bruxism that differ from what many were taught in dental school relate to the actual force applied during the bruxing event, most clinicians believing that the forces applied during nocturnal bruxism are significantly higher then the forces that can be applied while awake. Yet research shows the average force applied during nocturnal bruxism to be less then half what can be applied during maximal clenching during the day.8 With regards to children and bruxism, Carllson et.al. followed 402 seven, eleven, and fifteen year olds over twenty years to see if they could predict what occlusal factors in children may lead to bruxism and tooth wear in adulthood. The only occlusal factor with statistical significance was having a Class II occlusion and tooth wear as a child.9 In contrast there is strong evidence that children exposed to second hand smoke affecting their respiratory system have a much higher incidence of bruxism.10
Further evidence of the role airway plays in childhood bruxism can be seen after the removal of tonsils and adenoids in children diagnosed with sleep apnea, reducing the incidence of bruxism from 45.6% to 11.8% following the surgery.11
And finally, it is also important to recognize in children and adults the increased incidence of bruxism that occurs in individuals taking SSRI’s, the serotonin uptake inhibiting antidepressants. This increase in bruxing activity can be mediated by lowering the dose of the SSRI, or the use of Buspirone in addition to the SSRI.12
The significance of identifying the etiology of tooth wear is critical to predicting the outcome of any future treatment. But the possibility of helping a patient discover undiagnosed apnea or airway issues by recognizing the signs of uncontrolled attrition can be life saving and life altering.
As to what treatment to render in patient’s with attrition, those topics will be covered in future articles, but when tooth wear is present, the first step is always to attempt to identify the etiology of the wear.
(Click this link to read more dentistry articles by Dr. Frank Spear.)
1) J Oral Rehabil. 2001 Nov;28(11):1048-55.
A study of the effects of chewing patterns on occlusal wear.
Kim SK, Kim KN, Chang IT, Heo SJ.
Department of Prosthodontics, College of Dentistry, Seoul National University, 28 Yeongundong, Jongrogu, Seoul, South Korea.
2) J Prosthet Dent. 1999 Dec;82(6):704-13.
Sixty-eight years of experimental occlusal interference studies: what have we learned?
Clark GT, Tsukiyama Y, Baba K, Watanabe T.
School of Dentistry, University of California, Los Angeles, CA 90095-1668, USA.
3) 1: J Oral Rehabil. 2008 Jul;35(7):476-94.
Bruxism physiology and pathology: an overview for clinicians.
Lavigne GJ, Khoury S, Abe S, Yamaguchi T, Raphael K.
Faculty of Dentistry, Surgery Department, Pain, Sleep and Trauma Unit, Université de Montréal, Hôpital du Sacré-Coeur de Montréal, Montréal, Canada.
4) Sleep Med. 2002 Nov;3(6):513-5.
Sleep bruxism related to obstructive sleep apnea: the effect of continuous positive airway pressure.
Oksenberg A, Arons E.
Sleep Disorders Unit, Loewenstein Hospital-Rehabilitation Center, P.O. Box 3, Raanana, Israel. email@example.com
5) 1: Chest. 2008 Aug;134(2):332-7. Epub 2008 May 19.
A significant increase in breathing amplitude precedes sleep bruxism.
Khoury S, Rouleau GA, Rompré PH, Mayer P, Montplaisir JY, Lavigne GJ.
Faculté de Médecine Dentaire, Université de Montréal, CP 6128, Succursale Centre-ville, Montréal, QC, Canada H3C 3J7.
6) Lavgne GJ, Manzini C.
Bruxism. In:Kryger M, Roth T, Dement W (eds)
Principles and Practice of Sleep Medicine. 4th ed. Philadelphia, Pa:
W.B. Saunders Company; 2005: 946-959
7) Dent Clin North Am. 2012 Apr;56(2):387-413. doi: 10.1016/j.cden.2012.01.003.
Sleep bruxism: a comprehensive overview for the dental clinician interested in sleep medicine.
Carra MC, Huynh N, Lavigne G.
8) J Oral Rehabil. 2001 May;28(5):485-91.
Quantitative study of bite force during sleep associated bruxism.
Nishigawa K, Bando E, Nakano M.
Department of Fixed Prosthodontics, The University of Tokushima, School of Dentistry, Tokushima, Japan. firstname.lastname@example.org
(9) 1: J Orofac Pain. 2003 Winter;17(1):50-7.
Predictors of bruxism, other oral parafunctions, and tooth wear over a 20-year follow-up period.
Carlsson GE, Egermark I, Magnusson T.
Department of Prosthetic Dentistry/Dental Materials Science, Göteborg University, Box 450, SE 405 30, Göteborg, Sweden.
10) Tob Control. 2012 Jan 13. Association between exposure to secondhand smoke and sleep bruxism in children: a randomised control study.
Montaldo L, Montaldo P, Caredda E, D'Arco A.
Department of Dentistry, Second University of Naples, Naples, Italy.
11) Int J Pediatr Otorhinolaryngol. 2004 Apr;68(4):441-5.
Improvement of bruxism after T & A surgery.
DiFrancesco RC, Junqueira PA, Trezza PM, de Faria ME, Frizzarini R, Zerati FE.
Division of Otolaryngology, São Paulo University Medical School, Rua Guarará 529 cj. 121, São Paulo CEP 01425-001, Brazil. email@example.com
12) J Clin Psychiatry. 1993 Nov;54(11):432-4.
SSRI-associated nocturnal bruxism in four patients.
Ellison JM, Stanziani P.
Department of Psychiatry, Tufts/New England Medical Center, Boston, Mass. 02111.