Docstoc

Occlusal Parafunction – its causes and management

Document Sample
Occlusal Parafunction – its causes and management Powered By Docstoc
					                 OHD III
     Fixed Prosthodontics Assignment


         Convenor: Dr Tim WH Yuen




Title: Occlusal Parafunction – its cause and

management


Name: Jimmy Yang 0037127

Length: 3000 words

Due date: 7th October 2002




                             1
Occlusal Parafunction – its causes and management
Occlusal parafunction is the term given to oral behaviours that have no
functional purposes. These include bruxism (grinding or clenching of
teeth), lip-biting, nail-biting, pencil chewing, thumb-sucking, and abnormal
posturing of the jaw1. These parafunctional activities are common and
usually do not have an adverse effect on the structures of the mouth.
However, in some patients, it does present as a major problem. Occlusal
parafunctional activities may result in excessive tooth wear, muscular pain,
severe malocclusion, degenerative joint conditions, temporomandibular
joint (TMJ) disk derangements, muscular hypertrophy, headache, and
periodontal tissue injury. A heavy bruxist in a matter of 6 to 9 months can
destroy expensive fixed prostheses. It is therefore important that the
dentist have an understanding of the aetiology, diagnosis and management
of oral parafunctional behaviours.
The main form of occlusal parafunctions that causes major problems is
bruxism; hence this review will mainly focus on bruxism particularly,
nocturnal (sleep) bruxism.           Other occlusal parafunctions will be
mentioned briefly.

Sleep bruxism
Sleep bruxism is considered an involuntary oromandibular movement with
tooth grinding or clenching occurring during sleep, regardless of cause2.
The most common consequence of sleep bruxism is abnormal wear of teeth.
Tooth wear may be observed on a single tooth or the entire arch. During
grinding of teeth, forces are directed in both axially and horizontally. The
horizontal forces will increase the likelihood of cusp fracture and tooth
mobility. The occlusal surfaces of posterior teeth can be worn to such a
level below contact area creating spacing problems and food impaction.
Sharp edges of the flattened teeth may also irritate the cheeks1. The
excessive wear of teeth, despite being accompanied by some compensation
eruption of teeth, will decrease the vertical dimension of occlusion and
result in reduced facial height. During the natural wearing of teeth, the
pulp will recede gradually, laying down secondary dentine to protect itself.
In the case of heavy bruxism however, the wear rate is greater than the rate
of deposition of secondary dentine. This may result in pain, tooth
hypersensitivity to temperature changes, pain on percussion. In severe
cases, there may even be pulpal exposure resulting in pulpitis and pulpal

                                     2
death3.
Other than tooth wear, other consequences of bruxism includes muscular
pain of the masticatory system. This is not easily identified clinically, but
patients present with pain and can have long-term serious effects. Sleep
bruxism is considered an important aetiological factor in several muscular
and TMJ conditions. These include muscular pain, tightness and fatigue
upon rising, muscular incoordination, osteoarthritis, crepitus, limitations of
jaw movements, and possibly, TMJ clicking and locking of the jaw. Sleep
bruxism may also be an important aetiological factor in certain types of
muscle contraction headaches1.
Muscular hypertrophy is a likely result of chronic bruxism. The enlarged
and overdeveloped muscle is the most noticeable in the masseter muscles
on both sides of the face. The hypertrophy of the muscle is not painful,
however it can be an aesthetic problem for some patients4.
Previously it was believed that bruxism also causes periodontal disease.
The heavy forces of bruxism increase bone loss and causes tooth mobility.
However, there has been no further support to this theory, hence it is now
believed that bruxism does not cause periodontal disease1.

The nature of sleep bruxism
Bruxism often involves an intense rhythmic grinding pattern and periods of
forceful clenching. These bruxism events occur throughout the night but
usually occur in 90 minute intervals. The episodes of bruxism can last up
to as long as 5 minutes, and in one case report, the total tooth contacting
time during sleep is 162 minutes5.
The forces of sleep bruxism are more harmful than normal masticatory
forces because the contractions are often isometric, the intervals are longer
and the teeth contact is in an eccentric, unstable jaw position. Bruxism
episodes are most commonly found during stage 2 sleep, although it can
occur at any stage. It can sometimes be found during rapid eye movement
(REM) stage, but occurs most often when the patient goes from a deeper
stage of sleep to a lighter stage6.
Bruxism occurrences are highly variable throughout life. The episodes of
bruxism fluctuate from night to night, from month to month and from year
to year. It seems that the episodes are related to the stressful events that
happens during the patient’s life that are physically and emotionally
difficult1. This will be discussed later in more detail.


                                      3
Prevalence and risk factors of sleep bruxism
Sleep bruxism and tooth grinding is reported in 5% to 8% of the general
adult population and in 14% to 20% of children under 11 years of age 7.
The prevalence decreases linearly with age. There is no difference
between genders.       The occurrence of sleep bruxism is probably
underestimated, because it is generally based on either a bed partner’s or
family member’s report of grinding sounds. It is even more difficult to
assess people who sleep alone, denture wearers who sleep without their
dentures or patients who predominantly clenches their teeth during sleep2.
There are several risk factors for sleep bruxism reported. It is 1.9 times
more prevalent in smokers, although it remains uncertain whether this
increased prevalence is directly related to higher blood nicotine
concentrations8. Other reported risk factors include obstructive sleep
apnea syndrome, caffeine or alcohol intake, stressful life events and
anxiety2. Some antidepressant drugs, particularly the selective serotonin
reuptake inhibitors (SSRI), are reported to induce iatrogenic bruxism
during sleep and wakefulness9.

Aetiology of sleep bruxism
Many aetiological theories to explain bruxism have been formulated over
the years. Although these theories are hard to confirm or refute because
of the controversial character of the disorder, most suggest a multifactorial
aetiology.      Basically, three groups of aetiological factors can be
distinguished; morphological, pathophysiological, and psychological
factors10.
Morphological factors: Within this group, anomalies in dental occlusion
and articulation as well as in the anatomy of the oro-facial region can be
distinguished. These factors were formerly considered the most important
initiating and perpetuating aetiological factors for bruxism. More recently
however, the role of occlusal-anatomical factors is believed to be much
smaller, if at all present10.
In the study done by Ramford11, he held certain occlusal characteristics
mainly responsible for the initiation of the disorder. Bruxism is an
instrument with which an individual tries to eliminate occlusal
interferences. Despite in Ramfjord’s study, no controls were included,
and the use of indirect measures for bruxism, the conclusion of this study
have had a major impact on clinical dentistry for many decades. Today,
the outcomes of better controlled studies have shown otherwise. For

                                      4
example, Rugh et al.12 studied the influences of artificial occlusal
interferences, incorporated in crowns in the molar region, on masticatory
muscles activity (MMA) during sleep. In contrast with the findings of
Ramfjord, artificial interferences caused a significant decrease of
sleep-related MMA in 90% of the cases.
In other better controlled studies, the elimination of interferences in
occlusion and articulation was shown to have no influence on bruxism
activities13. Moreover, not every bruxer has occlusal interferences and not
every person with such interferences is a bruxer14.
Two recent studies have examined the possible relationship between
bruxism and the anatomy of the oro-facial region. Both authors found no
differences in the dentofacial morphology between bruxers and
non-bruxers15.

Pathophysiological factors: More and more, pathophysiological factors
are suggested to be involved in the precipitation of bruxism. Although the
exact pathophysiologic mechanisms remain to be elucidated, studies
suggest that sleep bruxism is influenced by central and autonomic-cardiac
nervous system processes related to oromotor functions and sleep-waking
regulation. Influence of genetic factors will also be mentioned2.
Sleep bruxism patients exhibit rhythmic masticatory muscle activity
(RMMA), with or without tooth grinding sounds, in 80% to 95% of sleep
bruxism episodes16. RMMA activities also exhibit in normal controls, but
is threes times more often in sleep bruxism patients16. It is also found that
RMMA in sleep bruxism patients is preceded by a sequence of
microarousals2. Therefore it is believed that sleep bruxism may represent
an extreme physiologic oromotor activity occurring during sleep associated
with sleep microarousals.
It has been suggested that catecholaminergic drugs, such as levodopa and
propranolol affects sleep bruxism. Levodopa in particular is reported to
have a mildly suppressive effect while Propranolol reduces sleep bruxism
in patients2. Recently, monoaminergic SSRI drugs have been found to
induce movement disorders17, and bruxism during sleep or wakefulness is
becoming widely reported following SSRI therapy9. It seems that
medications that act on the neurotransmitter system may be responsible for
the development of iatrogenic bruxism.
Twenty percent to 50% of sleep bruxism patients may have a family
member who reports tooth grinding18. Although genetic factors may

                                      5
predispose a person to bruxism, environmental factors are also probably
involved. To clarify, studies over several generations and chromosomal
identification are required2.

Psychophysiologic Aspects: There is a common belief that psychologic
stress contributes to sleep bruxism. Based on subjective reports, a number
of studies have suggested that tooth-grinding patients are more anxious,
aggressive, and hyperactive2.       Several of these studies associated
psychosocial factors with bruxism. A controlled questionnaire study by
Olkinuora in 1972 demonstrated that bruxers can be considered
emotionally out of balance and that they tend to develop more
psychosomatic disorders19. Their personalities would be characterized by
perfectionism and an increased tendency towards anger and aggression.
Kampe et al., who also demonstrated more anxiety in a group of bruxers,
later confirmed these findings20. However, the role of psychological
factors in the aetiology of bruxism is still far from clear. It appears that
this role differs between individuals and is probably smaller than
previously assumed.

Based on the evidence reviewed above, it seems that bruxism has a
multifactorial aetiology indeed. There is strong evidence that the role of
occlusal characteristics and other morphological factors is small if at all
present. There is convincing evidence, however, that sleep bruxism is part
of an arousal response and can be influenced by drugs that affect the central
dopaminergic system. There is also a role for factors like heredity and
stress10.

Diagnosis
For dentists, recognition of sleep bruxism is based mainly on the clinical
observations, but chairside diagnosis has limitations.
A history of tooth grinding sounds is a primary feature of sleep bruxism
and is often reported by a patient’s bed partner. A current history of this
sound suggests ongoing sleep bruxism. The occurrence of tooth grinding
sounds, however, is highly variable over nights and cannot always be
detected reliably, e.g. in patients who sleep alone. Clicking or locking of
TMJ may be reported by the patient. The patient may also report
masticatory muscle pain upon morning awakenings.              This usually
                                                            2
suggests the occurrence of sleep bruxism the previous night . Tooth wear

                                      6
is a secondary feature of sleep bruxism and can be identified by clinical
examination. Tooth wear can be seen on the incisal edges of the anterior
teeth or the occlusal surfaces of the posterior and can be either localized or
generalised. The patient may complain of tooth pain or tooth sensitivity
to heat and cold due to exposed dentine caused by bruxism21. However, a
definitive diagnosis of sleep bruxism cannot be made by tooth wear alone,
it may only indicate a history of bruxism rather than ongoing disorder 22.
Masseter muscle hypertrophy is another secondary sign used for sleep
bruxism but needs to be differentiated from inflammatory swellings,
tumours, etc2. Bruxcore Plates is an intraoral appliance used to evaluate
bruxism activity by counting the number of abraded microdots on its
surface and by scoring the volumetric magnitude of abrasion. However,
the reliability of this device is low because masticatory EMG activity
recorded during sleep does not correlate with the data scored on this plate23.
To provide a more definitive diagnosis, electrophysiologic monitoring
using the ambulatory system or sleep laboratory recordings is needed2.
The presence of wear on a splint will also help in determine the diagnosis
of sleep bruxism. However, the inserting of a splint will reduce sleep
bruxism in about half of the patients, so the absence of marks on the splint
is not indicative of an absence of pre-existing bruxism1.

Management of sleep bruxism
Currently, there are no specific strategies for the management of sleep
bruxism. The dentist’s main role is to reduce the patient’s complaints (e.g.
pain, tooth sounds) and prevent further damage of the orofacial structures
such as tooth wear, fracture of dental restorations. There are three
categories of approaches in the management of sleep bruxism. They are
dental appliances such as the use of hard acrylic mandibular or maxillary
splints, cognitive or behavioural therapy and pharmacologic approaches.
With the current level of knowledge, oral splints and cognitive and
behavioural strategies are most appropriate for the long-term care of these
patients.


Dental approaches:
Hard acrylic occlusal appliances and soft vinyl mouth guards are most
commonly used for managing specific orofacial pains and protecting the
teeth. Soft mouth guards, however, are contraindicated for long-term

                                      7
usage, as they are not durable enough2. Hard acrylic occlusal splints are
more suitable for long-term use, but the influence of this appliance on sleep
bruxism is not clear. Some studies shows a decrease in masticatory
activity during sleep, others indicated an increase or no change 24. At
present, hard acrylic occlusal splint appliances may be indicated in patients
who require protection of their teeth from further damage, to reduce
tooth-grinding sounds during sleep, or to manage muscular pain 24. There
is another approach that is to irreversibly adjust the patient’s occlusion,
however since the occlusal factors to sleep bruxism genesis have not been
clearly demonstrated, this treatment is not considered a first-line approach
in the management of sleep bruxism25.

Behavioural and Cognitive approaches:
Biofeedback has been reported to reduce sleep bruxism, but the effect does
not persist after withdrawal of the treatment26. In this approach, loud
auditory tones are used to wake the patients up every time the masticatory
EMG activity exceeds a threshold pre-determined. This is classic
conditioning where the contingent arousals act as a punishment. However,
the effect of the arousals and the resultant consequences during
wakefulness remains to be assessed27.
Another behavioural approach is a combination of arousal and
overcorrection procedures (operant conditioning). This is where after the
patients are awakened during sleep bruxism episodes; they are required to
perform positive behaviours e.g. brushing teeth as an overcorrection. This
method is suggested to be more effective than just simple arousal of the
patient28.
Cognitive approaches, such as suggestive hypnotherapy, in which patients
are instructed to relax their jaw muscles, have been reported to reduce
masseter EMG activity during sleep29. Stress management or changing a
life style has been suggested if patients are experiencing stress or anxiety.
Either a dentist or an appropriate health professional can educate patients
the possible links between sleep bruxism and life stress and instruct them in
managing oromotor reactions to life events by relaxation strategies such as
respiratory exercise30. Other methods include relaxation techniques,
avoiding intense mental or physical activity in the evening, refraining from
the use of alcohol, caffeine and tobacco close to bedtime, etc. However,
the efficacy of these approaches remains to be proved2.


                                      8
Pharmacologic approaches:
Generally, there are no effective pharmacologic treatments for SB.
Although several drugs have been suggested as useful, their effects are not
fully convincing, and they are not recommended for long-term use. Some
of these medications are benzodiazepines, tricyclic anti-depressants,
L-dopa, propranolol, etc., only few controlled studies have identified any
specific action on sleep bruxism and evaluated efficacy and safety in sleep
bruxism management2.

There have been no recent major breakthroughs in sleep bruxism
management. Cognitive and behavioural managements, which includes
stress management and lifestyle changes may be beneficial. Oral splint
appliances are useful to protect teeth from damage. A few medications
may be helpful for a short-term period, particularly when there is secondary
pain, but controlled studies are needed to assess their efficacy, safety and
patient acceptance and tolerance.


Diurnal parafunction
Daytime parafunction includes a wide range of activities. They are
grinding and clenching of teeth, thumb- or finger-sucking, lip- or
cheek-biting, nail biting, postural habits, unilateral chewing, and
movements associated with musical instruments and other foreign objects.
Oral parafunctional habits during waking hours may result in problems
similar to sleep bruxism.          Diurnal parafunction can affect the
periodontium, masticatory muscles, dentition and the temporomandibular
joint31.
There are several causes thought to have contributed to diurnal
parafunctional habits. Some are learned and maintained by internal or
external reinforcements. For example, the patient may develop into the
habit of unilateral chewing to avoid pain from a cracked molar on one side
of the mouth. Another example may be when a patient protrudes his or
her mandible forward to compensate for a retrognathic jaw, and this action
is positively reinforced by the improved physical appearance.
The aetiology of diurnal parafunction is quite difficult to identify clinically;
the best way would be to take a thorough history and to interview the
patient. After the cause is identified, the patient is made aware of the
problem and would take note when he performs the habit again.

                                       9
Occlusal parafunction includes sleep bruxism and other daytime habits of
the oral cavity that have no functional purposes. In most of the cases,
these parafunctional activities do not cause potential problems. However,
in some cases, it may result in serious destruction of the oral structures.
Sleep bruxism is thought to be mainly caused by pathophysiological factors
while diurnal parafunction is a learned behaviour. Management of
occlusal parafunctions includes the use of occlusal splints to prevent further
damage, behavioural and cognitive approaches.




                                      10
Bibliography
1. Mohl, A textbook of occlusion, Chicago, Illinois, Quintessence
    Publishing Co., Chapter 18, 1991
2. Kato et al. Bruxism and orofacial movements during sleep, dental
    clinics of North America, Vol. 45, No.4, p. 657-684
3. Ingle, J.LI. Alveolar osteoporosis and pulpal death associated with
    compulsive bruxism. Oral sur. Oral med. Oral Patho. 13:1371~1381,
    1960
4. Oppenheim, H., and Wing, M. Benign hypertrophy of masseter muscle.
    Arch. Otolaryngol. 70:207~210, 1959.
5. Trenouth, M.J. The relationship between bruxism and
    temporomandibular joint dysfunction as shown by computer analysis of
    nocturnal tooth contact patterns. J. Oral Rehabil. 6:81~87, 1979
6. Reding et. Al. Nocturnal teeth-grinding: all night psychophysiologic
    studies. J. Dent. Res. 47:786~797, 1968
7. Glaros AG: Incidence of diurnal and nocturnal bruxism. J Prosthet Dent.
    45:546~549, 1981
8. Lavigne GJ et al. Cigarette smoking as a risk factor or an exacerbating
    factor for restless legs syndrome and sleep bruxism. Sleep 20:290~293,
    1997
9. Brown ES, Hong SC, Antidepressant-induced bruxism: Successfully
    treated with gabapentin. J Am Dent Assoc 130:1467~1469, 1999
10. Lobbezoo F, Bruxism is mainly regulated centrally not peripherally, J
    Oral Rehab 28:1085~1091, 2001
11. Ramjford, SP, Bruxism, a clinical and electromyographic study. J Am
    Dent Assoc 62:21, 1961
12. Rugh, JD et al., Experimental occlusal discrepancies and nocturnal
    bruxism. J Pros Dent 51:548, 1984
13. Kardachi, B, A comparison of biofeedback and occlusal adjustment on
    bruxism, J perio, 49:367, 1978
14. Greene CS, Marbach JJ, Epidemiologic studies of mandibular
    dysfunction: a critical review. J pros dent 48:184
15. Miller VJ, et al. The effect of parafunction on condylar asymmetry in
    patients with temporomandibular disorders. J oral Rehab, 25:721, 1998
16. Sjoholm T, et al. Masseter muscle activity in diagnosed sleep bruxists
    compared with non-symptomatic controls. J Sleep Res 4:48~55, 1995
17. Gerber PE, Lynd LD: Selective serotonin-reuptake inhibitor-induced
    movement disorders. Ann Pharmacother 32:692~698, 1998

                                   11
18. Abe K, Shimakawa M: Genetic and developmental aspects of sleep
    talking and teeth grinding. Acta Paedopsychiartr 33:339~344, 1966
19. Olkinuora M, Psychosocial aspects in a series of bruxists compared
    with a group of non-bruxists. Preceedings of the Finnish Dental Society,
    68, 200, 1972
20. Kampe T, et al., Personality traits in a group of subjects with long
    standing bruxing behaviour. J Oral Rehab, 24:388, 1997
21. Rugh JD, Harlan J, Nocturnal bruxism and temporomandibular
    disorders. Adv Neurol 49:329~341, 1988
22. Lavigne GJ, et al., Principles and practices of sleep medicine, ed 3.
    Philadelphia, WB Saunders, pp 773~785, 2000
23. Pierce Cj, Gale EN, Methodological consideration concerning the use
    of Bruxcore plates to evaluate nocturnal bruxism. J Dent Res
    68:1110~1114, 1989
24. Clark GT, et al., Nocturnal electromyographic evaluation of myofascial
    pain dysfunction in patients undergoing occlusal splint therapy. J Am
    Dent Assoc 99:607~611, 1979
25. Clark GT, et al., A critical evaluation of occlusal therapy: Occlusal
    adjustment procedures. J Am Dent Assoc 110:743~750, 1985
26. Pierce Cj, Gale EN: A comparison of different treatments for nocturnal
    bruxism. J Dent Res, 67:597~601, 1988
27. Cherasia M, Parks L, Suggestions for use of behavioural measures in
    treating bruxism. Psychol Rep 58:719~722, 1986
28. Clark GT, et al., The treatment of nocturnal bruxism using contingent
    EMG feedback with an arousal task. Behav Res Ther 19:451~455, 1981
29. Clark JH, Reynolds PJ, Suggestive hypnotherapy for nocturnal bruxism:
    apilot study. Am J Clin Hyphnosis 33:248~253, 1991
30. Attanasio R, An overview of bruxism and its management. Dent Clin
    North Am, 41:229~241, 1997
31. Glaros AG, Effects of bruxism: a review of the literature. J Pros Dent,
    38:149~157, 1977




                                    12