Power Point Presentation for the Review of Literature on Bruxism

1. Effects of Bruxism on Dental
Hard Tissues and
Restorations
HUSNE DUYGU CARKCI, DDM

2. Definition – What is Bruxism
• Bruxism has explained as an oral parafunctional habit or activity that can
occur when a person is asleep or awake.
• It was first distinguished by Moritz Karolyi (1901) as a cause of periodontitis
and named “traumatic neuralgia”.
• Marie Pietkiewicz (1907) expand the definition as oral habit of clenching
and grinding of the teeth and called ‘la bruxomanie’
• The latest definition came from an international group of bruxism experts
(*) as “A repetitive jaw-muscle activity characterized by clenching or
grinding of the teeth and/or by bracing or thrusting the mandible. “ (2013)
* Bruxism defined and graded: an international consensus. Lobbezoo F1, Ahlberg J, Glaros AG, Kato T, Koyano K, Lavigne
GJ, de Leeuw R, Manfredini D, Svensson P, Winocur E. J Oral Rehabil. 2013 Jan;40(1):2-4. doi: 10.1111/joor.12011. Epub
2012 Nov 4.

3. Etiology of Bruxism
• There are many operative theories developed over the years
to define aetiology of bruxism
• F. Lobbezoo & M. Naeile ET al. indicated that bruxism
influenced by more central (psychological,
pathophysiological, genetic predisposition) factors than
peripheral (morphological) factors (*)
* Bruxism is mainly regulated centrally, not peripherally. Lobbezoo F1, Naeije M. J Oral Rehabil. 2001
Dec;28(12):1085-91.

4. The Etiological Factors of Bruxism
Morphological
Fators
• ‘Occlusal Theory’
hypothesis.
• Premature contact
points on the occlusal
side creates
mechanoreceptor
stimuli in periodontal
ligament thus clenching
or grinding action start.
• The deflecting tooth
contact theory got
interrogated by many
investigator.
Psychosocial
Factors
• Bruxist character
• Animal model
studies
correlates stress
and bruxing
activity on
masseter
muscles on
rodents.
Pathophysiological
factors
• Sleep
Disturbances, such
as parasomnias
• Some authors
highlights the
nocturnal sleep
architecture can
altered by sleep
bruxism
Neurological
Factors
Side Effects of
Drug or
Chemical Use
• Antidepressants,
alcohol, caffeine,
nicotine found
to have
triggering action
Central
Nervous
System
Disturbances
• Cerebral P.
Down S.
Epilepsy
Parkinson's D.
Genetic and
Familial
Predisposition
• Multiple genetic
factors/famillial learned
behaviour

5. Classification of bruxism
By when it occurs
By etiology
By motor
activity type
Awake Sleep Combined
Primary
or
idiopathic
Secondary
to diseases
Tonic
(clenching)
By presence
Phasic
(grindig)
Combined
Past Current

6. How Does Sleep Bruxism Manifest?
• Sleep bruxism is considered to be a parasomnia that occurs during sleep that is
characterized by either jaw clenching (tonic activity) and/or tooth grinding
(repetitive phasic jaw muscle activity).
• Several studies indicated the relation between RMMA and SB
• RMMA : can be defined as rhythmic masticatory muscle activity which is
characterized by pseudo-masticatory jaw movement which manifest once or
twice per hours in sleep
• This masticatory activity observed in % 60 of individuals with no bruxism history
and %80 of patients with SB *
• The presence of RMMA is also common in other sleep related disorders such as
obstructive sleep apnea, snoring and acid reflux during sleep.
* Sleep bruxism. Conceptual review and update.de la Hoz-Aizpurua JL1, Díaz-Alonso E,
LaTouche-Arbizu R, Mesa-Jiménez J. Med Oral Patol Oral Cir Bucal. 2011 Mar 1;16(2):e231-8.

7. How Does Sleep Bruxism Manifest?
Sleep and
Waking
mechanism
Micro
arousals
RMMA
Cortical
and
Cardiac
Activation
Activation
of Motor
Neurons
Sleep Bruxism
1) Increase in masticatory muscle
contraction
2) Increase in clenching or grinding
action

8. Awake bruxism
• There is a strong psychosocial
component to awake bruxism
(tension or anxiety, family
responsibility, work stress*)
• Treatment strategy of awake
bruxism can be more of a challenge.
In a coercive use of a daytime
occlusal guard compliance can be a
major challenge.
* Winocur E1, Gavish A, Voikovitch M, Emodi-Perlman
A, Eli I. Drugs and bruxism: a critical review. J Orofac
Pain. 2003 Spring;17(2):99-111.

9. Assesment and Diagnosis of Bruxism
Questionnaires Clinical Findings
Intra Oral
Appliances
EMG / EEG /PSG
RecordingsBruxcore
Tooth wear indexes
Bitestrip

10. . Questionnaire/Survey method
• Questionnaires are quick and disclosing way of having
information about the parafunction on chair.
• Pintado et al. described individuals who respond positively
to 2 of the questions can be considered individuals with
bruxism

11. Survey questions used to assess bruxism (Pintado et al. *):
1) Has anyone heard you grinding your teeth at night?
2) Is your jaw ever fatigued or sore on awakening in the morning?
3) Are your teeth or gums ever sore on awakening in the morning?
4) Do you ever experience temporal headaches on awakening in the morning?
5) Are you ever aware of grinding your teeth during the day?
6) Are you ever aware of clenching your teeth during the day?
*Pintado MR, Anderson GC, DeLong R, Douglas WH. Variation in tooth wear in
young adults over a two-year period. J Prosthet Dent. 77:313–320, 1997.

12. Clinical observation
Most frequent signs and symptoms:
• Abnormal tooth wear and presence of bruxofacets
• Excessive tooth mobility
• Hypertrophy of the masseter muscle in voluntary contraction
• Pain in TMJ
• Headache
• Fatigue and discomfort in head-neck-jaw muscles in the morning
• Hypersensitivity in cold temperature
• Audible click sound on the TMJ
• Finding traces on the tounge and buccal region of the cheek

13. Intra-Oral Appliance
• Sleep bruxism activity can be assessed by using intraoral
appliances in two methods:
first observation of the abrasions within the appliance,
second measure of the bite strength on the appliance

14. EEG, EMG, PSG Recordings
• EMG monitoring devices were used to
measure sleep bruxism episodes in
patients' own home environments.
• Since there is no audio / video recording,
the EMG devices may exaggerate the
presence of the SB
• coughing, swallowing, sighing activities
can interfere with the recordings.

15. Polysomnography (PSG)
• Polysomnography has accepted as the golden standard for detecting
ongoing bruxism.
• A polysomnographic test uses EEG records to measure brain activity,
EKG records to measure heart activity, EMG records for masticatory
muscle activity.
• The system also uses the audio/video records to substrate non-
bruxing activities from the bruxing episodes.

16. POLİSOMNOGRAFİ İLE TEŞHİS EDİLEN UYKU BRUKSİZMLİ
HASTALARIN TEDAVİSİNDE İKİ FARKLI APAREYİN
ETKİNLİĞİNİN DEĞERLENDİRİLMESİ - Dt. YILDIZ KAVAKLI
HACETTEPE ÜNİVERSİTESİ SAĞLIK BİLİMLERİ ENSTİTÜSÜ
PROTEZ PROGRAMI DOKTORA TEZİ - ANKARA 2006

17. Effects of Bruxism on Soft Tissue
• The changes seen in soft tissues are usually occur on the edges of the tongue
and on the buccal mucosa
• tongue scallops seen in the edge regions happens against to the parafunction of
the teeth.
• It has suggested that protection reflex creates scallops by the force of reducing
contacts with pushing them away from the parafunctional edges.

18. Effects of Bruxism on Soft Tissue
• The marks (linea alba) on the buccal mucosa are caused by negative pressure in the oral cavity
during the breathing of individuals with the interaction of the maxillary and mandibular teeth.
• This line-like formation in the cheek mucosa, usually found in the area of the buccinator muscle
and it seems lighter than normal mucosa appearance
• In the study conducted by *Kampe et al., 58.6% of patients with bruxism showed tooth marks on
the buccal area in 41.4% respectively.
* Kampe T, Tagdae T, Bader G, Edman G, Karlsson S. Reported symptoms and clinical findings in a group of subjects with
longstanding bruxing behaviour. J Oral Rehabil, 24: 581–587, 1997

19. • The possible consequences of Bruxism are listed in table above.
• Of interest to restorative dentists is the effect of bruxism on prosthodontic
rehabilitation. Some of the literature suggests that bruxism is associated with
increased mechanical and/or technical complications of tooth and implant-
supported prostheses.
Yap AU, Chua AP. Sleep bruxism: Current knowledge and contemporary management. J Conserv Dent 2016;19:383-9

20. Tooth Wear
• It has been reported that the most common pathological
dental hard tissue condition arise from bruxism is excessive
tooth abrasion (tooth wear).
• Knight DJ et al. used an index that only asses the occlusal
and incisal abrasion

21. • The tooth abrasions were classified as 0-3 and accordingly 0-was
indicating no wear,
• 1- presence of certain facets of enamel containing occlusal-incisal
structure change,
• 2- occlusal-incisal structure change with the presence of dentin
abrasion,
A guide to managing tooth wear:the Radboud philosophy
B. Loomans1 and N. Opdam1

22. • 3- dentin abrasion (2 mm below the occlusal and the structure has
completely disappeared) that indicates excessive wear.

23. Tooth Wear Types (NCCLs)
• The etiology includes the effect of external and internal acids,
mechanical abrasive movements and can be associated with many
factors, such as the flexion of teeth under the name of masticatory
forces.

24. Abrasion:
• Abrasion is a term derived from the Latin words "abradere, abrasi,
abrasum" meaning "excavation"
• It can be explained as Friction between a tooth and a threaded
mechanical agent (such as faulty in brushing)
• Oral hygiene habits ,personal habits (putting foreign objects in the
mouth), demastication (wear from chewing food)
• clinical image:
horizontal wear area on the cervical region.

25. Attrition:
• Derived from the Latin words atter, attrivi, attritum, which means
'friction on the surface of anything'
• Physiological abrasion of teeth as a consequence of tooth to tooth
contact in a life time without any foreign material involved
• The grade of attrition is basically related to age
• If there is more than normal wear compared to the age of the
patient, the pathological attrition can be discussed.

26. Erosion:
• Derived from the Latin words "erosi, erodere, erosum" which means to
rot, decay.
• Loss of tooth surface by a chemical process that does not involve bacterial
action.
• Extrinsic acids (food, beverages - granolas, nuts, acid juices - , medicine)
• Intrinsic acids (acid reflux disease - GERD, bulumia)
• Clinical signs : Increased incisal translucency, smooth silky-shining, silky-
glazed appearance, sometimes dull surface.
• studies show that, the presence of erosive environment enhance the
bruxism related wear rates compare to the non-erosive oral
environment*.
OCCLUSAL WEAR OF TEETH AND RESTORATIVE MATERIALS - A REVIEW OF CLASSIFICATION, ETIOLOGY,
MECHANISMS OF WEAR, AND SOME ASPECTS OF RESTORATIVE PROCEDURES, ACTA ODONTOLOGICA
SCANDINAVICA; OCT 1993, 51 5, p299-p311, 13p.

27. Abfraction:
• Abfraction is a term defined by the Grippo in 1991, derived
from the Latin words “frangere-fractum”, which means
'breaking-rupture‘
• Pathological dental hard tissue loss caused by
biomechanical occlusal forces applied outside of the centric
• Clinical signs: V-shaped lesion appearance formed at the
gingival-enamel border.

28. Effects on dental hard tissues:
• Abfraction denominates stress-induced noncarious lesions and often
refers the parafunctional activity (bruxism) with the action of the
severity (low, medium, and high), the direction (horizontal and
vertical) and the amount of force applied.
• Abfraction mostly seen in single tooth
• They are less common in
the mobile teeth.
İnsical attrition
indicating the
great occlusal
force due to the
malposition and
bruxism
J Am Dent Assoc. 2004 Aug;135(8):1109-18; quiz 1163-5. Attrition, abrasion, corrosion
and abfraction revisited: a new perspective on tooth surface lesions.
Grippo JO1, Simring M, Schreiner S.

30. • Materials and methods: Two intact human mandibular teeth, a non-
carious right second premolar and a right central incisor, extracted for
orthodontic and prosthodontic reasons, respectively, were selected
based on the presence of regular crown and root morphology and lack
of wear.
• The 3-D geometry of the incisor was reconstructed from 25 transverse
sections
• Material properties of enamel and dentin (Young’s modulus, Poisson’s
ratio) were as follows:
• enamel 46.9 GPa, 0.30; dentin: 15.4 GPa, 0.31

31. • The incisor model (Model II) was assigned two different supports:
• (1) at 1.6 mm apical to the cementoenamel junction and fixed zero-
displacement in X, Y, and Z directions (Model IIA).
• (2) the same as Model IIA, except extra supports at the area of tooth
contact with fixed zero-displacement in Y and Z directions (Model IIB)
to simulate tooth crowding.

32. • Concentrated loads of 100 N were applied to the Model I premolar;
at the buccal cusp tip, parallel or 45° to the long axis of the tooth
• Model IIA incisor; at the mid labial point on the incisal edge, parallel
or 45° to the long axis of the tooth
• Model IIB incisor, at the mid- proximal point on the incisal edge,
parallel or45° to the long axis of the tooth

33. • The directions and sites of applications were selected to
simulate physiological patterns of contact during inter-
cuspal position, laterotrusive and retrusive movements.
• Outputs were presented in the form of strain contours of
tension and principal maximum (E1, tensile strains) and
minimum (E3, compressive strains) strain vector plots.
• The location of the stress concentration highlighted by the
model was correlated to clinical observations of NCCLs

34. • Results: Strains were high at the point of loading and rapidly decreased in the occluso-
gingival direction and increased on both buccal and lingual surfaces, regardless of the load
direction.
• Non-axial load (b) generated larger surface tensile strains than axial load (a) and strains
increased and became concentrated near the CEJ close to the area around the fulcrum,
both buccally and lingually.

35. • Vector plots on approximal of the CEJ on the enamel surface (a) revealed that tensile
strains on the buccal side of the proximal view were predominantly horizontal while the
higher compressive strains were vertical
• Vector plots (b) showed that tensile strains on the buccal side of the approximal view
were predominantly vertical, while the smaller compressive strains were horizontal

36. • Model IIA lower central incisor:
• Generally, this model showed the same trends of strain distribution as Model I
premolar. That is, strains were high at the point of loading and concentrated near
the CEJ both labially and lingually.

37. • Tensile strain values were greater at the lingual concavity than those at the highly curved
(convex) lingual cingulum, and increased again toward the pivot area, regardless of the load
direction.
• Vector plots of the strain showed that tensile strains were concentrated around the CEJ,
while those under oblique load were predominantly on the labial or lingual sides

38. • Model IIB lower central incisor: Oblique loading created higher tensile strains
than vertical loading, and the strains increased towards the ‘constrained’ area at
the approximal contact area and the CEJ.

39. • Under vertical loading, tensile strains on the labial (a) and lingual sides (b) also
increased toward the constrained areas.
• Tensile strains at the CEJ on the labial surface tended to concentrate at the line
angle opposite to the loading side.

40. • Conclusion:
• The results of this study show that tooth morphology and locations of loading
may have an influence on the initial location of non-carious cervical lesions
• Some non-carious lesions are narrow and angular at the cemento-enamel
junction, and some extend broadly into the root region. However, the wedge
shaped lesion may be representative of the effect of tooth flexure, abrasion, or
both.
• It may not be possible to define a typical abfaction shape and dimension.
• If the process of abfraction were to begin above the support in dentine, it
could quickly spread to involve the adjacent tooth substance, producing
the sub-gingival lesions that are sometimes seen clinically.

41. • İn a study conducted by Frida A. Xhonga progress of tooth wear and
the change in structural morphology on teeth evaluated on bruxist
subjects, compared to non-bruxers.

42. • According to the SEM results of the study, examination of an intact enamel
specimen(5a) appeared relatively smooth when compared to inactive dull lookin
wear facet(5b) in enamel of the same specimen.
• Well defined grooves and striations from the depth of various degrees could be
easily identified in enamel (6a). A similar pattern of scratches was observed in
dentine of the worn teeth(6b).

43. • The junction of intact
enamel and an active
wear-facet on the
occlusal surface were
revealed (arrow).
• Further evidence of
breaking up of the
enamel could also be
seen.

44. • The study also revealed statistically significant results on the
amount of tooth wear, presence of dental erosion and incidance
of dental erosion in comparison of bruxers and non-bruxers.

45. • Conclusion of the study:
• tooth wear progressed faster in bruxers than in non-bruxers.
• The frequency of wear-facets, occured three times more in bruxers.
• Bruxing forces could also be related to erosion of natural teeth and
other hard tissues.
• SEM results revealed that enamel prisms were damaged and fractured
off.
• The clinical appearance of wear-facets can be seen shiny and glazed
because the pulverized enamel particles are capable of serve as a
polishing or abrasive media in bruxism.

46. Restorative Challenges
• NCCL restorations are a very common occurrence in clinical practice,
they also represent one of the less durable types of restorations and
have a high index of loss of retention, marginal excess, and
secondary caries.
• Some intrinsic characteristics of the NCCL create unique challenges
to dental adhesion.
• Recent studies demonstrate important histological differences
between prepared dentin and the affected dentin from NCCLs.

47. • Work based on Raman analysis showed that the compositional and structural
alterations in mineral and matrix components of NCCLs affected dentin.
• A heterogeneous hypermineralized layer, with characteristic features such as high
phosphate/low carbonate content, high degree of crystallinity, and partially
denatured collagen, was revealed in the affected dentin substrate of NCCLs.

48. • In total-etch systems, the failure of 40% phosphoric acid to dissolve
intertubular dentin of NCCL-affected teeth and the more acid-resistant
sclerotic mineral deposits present in the tubules may be responsible for
the absence of resin tags in dentin.
• The bond strength between the resin and the dentin substrate is also
affected due to the alteration in the dentin substrate and a reduction in
bond strength by up to 26% has been reported in the study*.
• Some authors agree that restorations placed in teeth whose
dentin/enamel had been prepared, or roughened, showed a statistically
significant higher retention rate than those placed in teeth with
unprepared dentin. Kwong SM, Tay FR, Yip HK, Kei LH, Pashley DH. An ultrastructural study of the application of
dentine adhesives to acid-conditioned sclerotic dentine. J Dent 2000;28(7):515–28.

49. • In this study, elementary mercury vapour (Hg0) that relased from dental amalgam
fillings due to bruxism has been investigated.
• At least 4 occlusal amalgam fillings in contact with antagonists in intercuspal position
were examined with Bruxocore bruxism monitoring device to measure the level of
ongoing sleep bruxism.
• Mercury exposure was assesed from the Hg concentration in plasma and urine.
• Mechanical wear on amalgams from SB showed a little increase the Hg uptake, but the
magnitude of this effect seem to be less than the use of chewing gum.

50. Thank you for you attention..