system towards the somatosensory cortex, there
occur various reflex activities, due to modifications of
muscle tone and onset of myogenous pain. However,
the correlations between reflex activity and pain
expression are not yet studied deeply.
According to several research projects, there are no
statistically significant differences in the EMG indices
in patients, which feel pain in the masticatory muscles
compared to those with no pain [12,29]. The authors
state that this phenomenon is due to central neuronal
adaptation mechanisms, modifications of the pain
modulation mechanisms and because of central
sensitization phenomena.
It should be taken into account that various poorly
expressed algic manifestations may be present for a
short term in healthy individuals as well.
It is to be noted that myogenous pain in younger
patients is more pronounced than in older patients. This
phenomenon was also observed by other researchers
[8,9,12,30,31], who explain it through the processes of
adaptation to chronic pain observed in older people.
The results demonstrate that the psychoemotional
factor (scale V), myogenous (scale II), circadian (scale
VI), and pain duration (scale VIII) are quite pronounced
in SB patients, that are either under or over 35. The pain
pattern in patients under 35 may be characterized as
a psycho-emotionalmyogenous circadian pain and for
the older patients as a psycho-emotional-myogenous-
arthrogenic circadian pain.
The data obtained confirm the results from the
scientific literature – consequent to aging (until 61
years); an increase of the masseter muscle thickness
can be observed [32].
There are several hypotheses regarding this problem:
the increase of the masseter muscle thickness may
occur as a result to muscle edema, fat accumulation,
deficiency of protein metabolism, effects of
psychoactive substances (alcohol, nicotine, etc.). Under
the influence of previous inflammatory processes, the
thickness of the muscle increases by approximately 4.3
mm [32].
Patients with SB show areas of muscle hypertonus
(trigger zones) in which ultrasonographic examination
shows changes in the echo-structure, left/right
asymmetry and modification of the masseter muscle
thickness.
In patients with SB under 35, the presence of local
pathological echogenics is more frequent, which
in most cases corresponds to the localization of
the algic areas during palpation of the masseter
muscles. In patients with SB over 35, besides the local
pathological echogenicity, quite frequently a diffuse
pathological echogenicity was observed. In the
scientific literature, these aspects are being debated – it
has been established that during the first stages of the
disorders of the masseter muscle activity, local hypo-
echogenic areas appear, which afterwards, due to the
aggravation of the disturbances, transform into diffuse
hyperechogenic zones [18].
An important dental index for SB is the presence of
dental abrasion. Surprisingly, there was no statistically
significant correlations observed between the EMG
activity of the muscles and the degree of dental
abrasion [33]. Some researchers consider that
Stomatology Edu Journal
currently, there is an overemphasis on SB as a causative
factor in tooth wear [4]. No valid correlations were
found between dental wear and the age of patients,
the occlusal factors and the degree of temporo-
mandibular joint dysfunction. These data demonstrate
that wear is associated with various factors, including
cerebral factors. Moreover, a specific study has not
revealed any statist ically significant differences in
the bioelectric activity of masticatory muscles during
sleep between patients with and without signs of
dental wear [31]. While assessing dental abrasion as a
diagnostic sign of SB, it is necessary to highlight other
etiopathogenic factors; dental abrasion is not the main
criterion in the diagnosis of SB, because it can occur
in other pathologies as well (acid reflux, long-term
consumption of acidic juices, etc.) [30,31].
In summary, the following SB manifestations occur
with a higher severity in patients under 35 years of
age (statistically significant), when compared to older
patients – p < 0.05):
• clinical signs of bruxism, assessed by means of the
clinical questionnaire (p < 0,05);
• dysfunction of the temporomandibular joint,
assessed by means of Fonseca questionnaire (p <
0.05),
• total number of clenches (TNC) (p < 0.001),
• total duration of clenches (TCT) (p < 0.001).
The following SB manifestations occur with a higher
severity in patients over 35 years of age (statistically
significant), when compared to younger patients – p <
0.05):
• pathological thickness of the masseter muscle
(MM), determined by ultrasound (p < 0.001),
• pathological echogenicity of the MM, determined
by ultrasound (p < 0.01),
• shorter sleep duration (p < 0.05), pathological
quality of sleep (p < 0.001).
The results obtained show that there are important
peculiarities of the clinical manifestations of primary
sleep bruxism according to the age of the patients,
which can be detected by the application of clinical
and paraclinical diagnostic methods, mainly by
using technologies able to continuously monitor the
bioelectric activity of the masticatory muscles and
the morpho-functional status of the stomatognathic
system through ultrasonography.
MANIFESTATION OF SLEEP BRUXISM ACCORDING TO THE AGE OF PATIENTS
5. Conclusions
1. The expression of primary sleep bruxism is
influenced by the age of the patients: the younger
patients (18-35 years of age) are characterized
by having more severe disorders regarding the
episodes of sleep bruxism, with more pronounced
myogenous-spastic manifestations; older patients
(35-50 years of age) are characterized by the
predominance of local and diffuse myogenic-
structural disturbances, with more pronounced
arthrogenic pains, with more severe quantitative
and qualitative disturbances of nighttime sleep.
2. The expression of the emotional stress and the
quantitative manifestations of dental abrasion are
not essentially different in patients with primary
sleep bruxism based on the age factor.
35