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Are Sleep Studies Prudent Before Placing Implants?

About 10% of the adult population in the world suffers from obstructive sleep apnea or sleep disordered breathing and about 90% of those have not been diagnosed.1  7% of men are living with sleep apnea and 5% of women. According to the American Academy of Sleep Medicine the Frost and Sullivan report from 2016, approximately 12% suffer from obstructive sleep apnea, at least 29.4 million adults in the United States - 80% of which go undiagnosed. Statistically that is about 1 in 12 people in the US.

There are three types of sleep apnea:

  1. Obstructive Sleep Apnea when the episodes of apnea and hypopnea occur more than five times a night and are due to an obstruction of the airway.
  2. Central Sleep Apnea is caused by a person’s oxygen saturation decreases because the brain fails to send the signal to breathe.
  3. Complex Sleep Apnea is a combination of OSA and central sleep apnea.

Bruxism

Years of dentistry has taught us one huge lesson. The industry is always evolving, and things that we knew years ago may not have been the completely accurate or the treatment protocols we would do today.  Take serial extractions. With the collapse of arch’s and airways you would be hard pressed to find many clinicians jumping on that bandwagon. Another fascinating topic is bruxism. Bruxism has been underdiagnosed, over-diagnosed and even misdiagnosed. The phenomenon of bruxing has been talked about for what seems like forever. The Bible references the “gnashing of teeth” being associated with anger and frustration but dentistry for one are still trying to get a handle on all the triggers for grinding and clenching.  Reports of prevalence ranges from 8%-31% of the general population.

Clinicians have developed a wide variety of treatments for bruxism, many with no real scientific evidence. There have been occlusal adjustments, appliances with limited data, biofeedback, acupuncture and even medications. Dentistry has in general told patients the cause of their grinding or bruxing was stress. Some medications such as the antidepressant Fluoxetine or even an imbalance in brain neurotransmitters have been implicated.

Sleep bruxism was a medical term coined in 1901 by Marie Pietkiewicz. It is included under a “parafunctional” behavior which really means making use of a body part in a manner in which it wasn’t intended for. Nocturnal bruxism is clearly different from daytime bruxism. Estimates land at about 10% of people sleep brux but that number is quite low considering most people don’t realize they do it. Tooth grinding is not necessarily abnormal but it is the frequency and intensity that has the issues. Bruxism is associated with arousals and autonomic activation during sleep and can also occur with swallowing during sleep.

Medicine and Dentistry already understood how caffeine, smoking and alcohols relationship to sleep bruxism, and the compelling evidence regarding gastroesophageal reflux disease or GERD to grinding at night. Science also shows the correlation with epilepsy, night terrors, and attention-deficient/hyperactivity disorder (ADHD). Mayo clinic offers a hereditary component with rates as high as 50%.  

In 2019 a study was released that found of over 100 subjects 86% had an AHI > 5 and a 50% incident of sleep bruxism. The study also found a relationship between diabetes and sleep bruxism. Some researchers believe that upper airway resistance causes an arousal, which leads to a stress response throughout the body. The heart rate and respiration increase, and stress hormones are released. This leads to an increase in the activity of the muscles of mastication, resulting in bruxing. The movement of the jaw forward opens the airway, and the person is able to take a breath. This process repeats multiple times each night. Another theory is that when the tissues of the upper airway collapse during episodes of snoring, partial or complete apnea, the brain signals the jaw muscles to tighten, which will stiffen the sides of the throat, preventing the collapse of the airway tissues.2  Sleep bruxism in an apnea patient is a sympathetic response to a choking event. A sort of auto protection mechanism. Sleep bruxism is secondary to sleep related micro arousals. "The relationship between obstructive sleep apnea and sleep bruxism is usually related to an arousal response. The ending of an apneic event may be accompanied by a number of mouth phenomena, such as snoring, gasps, mumbles, and teeth grinding," said Shyam Subramanian, MD, FCCP, Baylor College of Medicine, Houston, TX. "Men typically have more severe sleep apnea, and perhaps may have more arousal responses, which may explain the higher prevalence of teeth grinding in men. Besides, men characteristically tend to report more symptoms of sleep apnea than women, such as snoring, loud grunting, and witnessed apneas." American College of Chest Physicians.3

A common misconception about sleep apnea is that is can be treated with any night guard. A typical flat plane night guard or splint tends to make your lower jaw move a little backward that could make the airway close more which increases the rate of snoring and degree of sleep apnea by over 40%. The unfortunate truth is that simply wearing a night guard is not going to help the patient. In a small study 1/2 the patients showed an increase in the apnea-hyponea index of 50% when wearing a flat plane splint vs. not wearing anything.4. Clearly, it is not advisable to use upper flat plane maxillary splints in patients who snore or have sleep apnea.

Many patients in a dental practice may present with temporomandibular joint dysfunction that is brought on by the side effects of sleep apnea. Bruxism has been discussed and, in addition to oxygen deprivation, can lead to headaches and muscle pain. Sleep apnea can also deprive patients of their REM sleep. Loss of REM sleep can lead to increased pain levels, including the TM joints and muscles of mastication.5

When treating TMD, it important to screen cautiously for signs and symptoms of OSA. A cohort and case control study both “supported a significant association of OSA symptoms and TMD.” 6  Treating the OSA may help alleviate the TMD symptoms, but it may not. As with anything in dentistry, the more information presented to the patient before treatment, the more the patient begins to understand and take ownership of their condition.

Implant Complications and Sleep Apnea

A systematic review and meta-analysis from 2015 found “In contrast to non-bruxers, prostheses in bruxers had a higher failure rate. It suggests that bruxism is a contributing factor of causing the occurrence of dental implant technical/biological complications and plays a role in dental implant failure.” 7

Although there is no conclusive scientific evidence that bruxism causes overload on dental implants and their superstructure, professionals should proceed cautiously when planning implant supported restorations in bruxers, mainly due to the severity of possible complications. Under normal conditions, the total time when teeth come into contact is about 30 minutes a day. With a parafunctional habit such as bruxing that time can increase considerably. All preventive measures should be aimed at minimizing the forces that are applied to implants.8 A bruxism patient presents an increased risk of implant fracture over time since the magnitude of forces increases as the muscles become stronger. Therefore, when a source of additional load on the implant is identified, the treatment plan must be changed to minimize adverse effects on the alveolar bone, implant and definitive restoration.

In 2018 a 5-year retrospective study was released with several pertinent findings. Excessive occlusal overload caused in bruxism patients is the leading cause of failure such as fracture of implant, loosening of screw, fracture of screw, and fracture of porcelain. Survival rate of dental implants with bruxism habit in males was 90% after 1 year, 87% after 2 years, 85% after 3 years, 75% after 4 years, and 72% after 5 years. Survival rate of dental implants in females with bruxism habit was 92% after 1 year, 90% after 2 years, 85% after 3 years, 75% after 4 years, and 70% after 5 years.9

OSA patients who have implants have a higher incidence of abutment tooth fracture, fracture of the connector component, fracture or loosening of the screw, fracture of the abutment, ceramic chipping prosthesis and implant failure. Another way that bruxism does increase the risk of dental implant failure is that success depends on a process called osseointegration. Integration is gradual and fusion isn’t complete for several months and the pressure from grinding can compromise the bond. Additionally, bruxism effects are compounded by the fact that teeth have a periodontal membrane and implants do not which makes teeth more resilient to pressure.  

Researchers from OSI Araba University Hospital in Victoria, Spain published a study in the Journal of Oral Implantology that looked into how OSA affects implants. The study showed that 81% of OSA patients experienced complications with their prostheses. The average time for a complication to occur was at 73 months post-implantation.10  Past studies revealed that those afflicted with bruxism had a higher instance (6/10) of complications with implant prostheses than those without bruxism (13/75). This shows that people suffering from OSA and/or bruxism have a more difficult time with successful prosthetic implantation.

Patients with OSA can be hyperalgesic, as mentioned above. Therefore, expect more discomfort during implant procedures and post operatively. OSA patients also have more inflammatory markers and therefore higher inflammation levels. Expect longer and more difficult healing. The increased inflammatory load is also interesting when considering implant placement and success.

It’s simple to evaluate sleep disordered breathing and either treat or refer. The complications from sleep apnea as related to bruxism must be addressed for the pursuit of a longer lasting implant.

Please see our other related article Screening for Sleep Disordered Breathing in the Dental Office

1 Young T, et al. Epidemiology of obstructive sleep apnea: a population health perspective. AJRCCM 2002;165:1217-1239

2 American Dental Association Council on Dental Practice. Dentistry’s Role in Sleep Related Breathing Disorders. Retrieved from https://www.ada.org/en/member-center/leadership-governance/councils-commissions-and-committees/dentistry-role-in-sleep-related-breathing-disorders

3 "Teeth Grinding Linked To Sleep Apnea; Bruxism Prevalent In Caucasians With Sleep Disorders." ScienceDaily. ScienceDaily, 5 November 2009 www.sciencedaily.com/releases/2009/11/09110217121

4 Mayer P, Morisson F, Rompré PH, Lavigne GJ. Aggravation of repiratory disturbances by the use of an occlusal splint in apneic patients. Int J Prosthodont. Jul.-Aug. 2004;17(4):447-453.

5 Roehrs T, Hyde M, Blaisdell M, Greenwald M, Roth T. Sleep loss and REM sleep loss are hyperalgesic. SLEEP 2006;29(2).

6 Sanders AE, Essick GK, Fillingim R, Knott C, Ohrbach R, Greenspan JD, Diatchenko L, Maixner W, Dubner R, Bair E, Miller VE, Slade GD. (Sleep apnea symptoms and risk of temporomandibular disorder: OPPERA cohort. J Dent Res. Jul. 2013;92(7 Suppl):70S-7S. doi: 10.1177/0022034513488140. Epub May 20, 2013.

7 Zhou, Y., Gao, J., Luo, L. and Wang, Y. (2016), Does Bruxism Contribute to Dental Implant Failure?. Clinical Implant Dentistry and Related Research, 18: 410-420. doi:10.1111/cid.12300

8 Lobbezoo F, Brouwers JEIG, Cune MS, Naeije M. Dental implants in patients with bruxing habits. J Oral Rehabil. 2006; 32: 152-159. Ref.: https://goo.gl/56Lp4h

9 Chitumalla R, Halini Kumari KV, Mohapatra A, Parihar AS, Anand KS, Katragadda P. Assessment of Survival Rate of Dental Implants in Patients with Bruxism: A 5-year Retrospective Study. Contemp Clin Dent. 2018;9(Suppl 2):S278‐S282. doi:10.4103/ccd.ccd_258_18

10 Eduardo Anitua, Juan Saracho, Gabriela Zamora Almeida, Joaquin Duran-Cantolla, Mohammad Hamdan Alkhraisat; Frequency of Prosthetic Complications Related to Implant-Borne Prosthesis in a Sleep Disorder Unit. J Oral Implantol 1 February 2017; 43 (1): 19–23. doi: 10.1563/aaid-joi-D-16-00100

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