Document Details
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Document Type |
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Article In Journal |
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Document Title |
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SALIVARY PAP LEVELS IN EARLY ONSET AND ADULT PERIODONTITIS PATIENTS THROUGH our INITIAL PERIODONTAL THERAPY SALIVARY PAP LEVELS IN EARLY ONSET AND ADULT PERIODONTITIS PATIENTS THROUGH our INITIAL PERIODONTAL THERAPY |
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Document Language |
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Arabic |
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Abstract |
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Periodontal diseases reflect a
constellation of inflammatory mediators
which act individually or synergistically
to promte disease progression. (1)
Bacteria or their products and
components are the driving force
behind the observed tissue destruction.
Substances from periodontopathic
bacteria initiate and drive the inflammatory
response and their continued
presence is essential for maintenance
of the inflammation. Nevertheless,
endogenous molecules mediate the
inflammatory process and playa major
role in its ampification and perpetruation
and in the ensuing tissue
destruction. (2)
Cellular response to inflammation
involves the formation and accumulation
of bioactive mediators. Platelet
activting factor (PAF)is among the most
potent of these mediators, as it leads to
cell damage through several
mechanisms. (3)
PAF is a family of structurally
related, acetylated phospholopids
capable of inducing marked proinflammatory
responses. (4.5) Although
originally named for its ability to cause
aggregation and histamine release from
rabbit platelet (6) PAF has since been
documented to promote a wide range of
phlogistic processes which are initiated
via specific PAF receptors on various
cells and tissues. These processes
include the stimulation of diverse
targets and effects, such as polymorphonuclear
leukocyte (PMN) activation
(e.g. chemotaxis, aggregation, lysosomal
enzyme release,. arachidonic acid
metabolism, and superoxide production),
monocyte macrophage aggregation and
phagocytosis, eosinophil activation,
increased ,vascular permeability, vasoconstriction,
and smooth muscle
contraction. (4.5. 7)
PAF is rapidly synthesized by
various inflammatory cells after
activation by either immunologically or
nonimmunologically triggered signals. (8)
Interestingly, PAF is produced by a
variety of activated inflammatory
cells including many of the same
cells which it targets, such as PMN,
vascular endothelial cells, monocytes,
eosinophils, basopils, platelets and
lymphocytes. Thus the pleiotropic
effects of these acetylated phospholipids
develop as a result of paracrine and autocrine stimulation of the
inflammatory process. (1)
The presence of PM in nonnal human
mixed saliva was first reported in 1981
by Cox et al.(9) Pure parotid saliva
apparently has no detectable PM activity,
which suggests that PM in mixed saliva
originates from a 5'Ourceother than this
salivary gland. (9)Moreover, edentulous,
healthy subjects have undetectable or
significantly decreased levels of salivary
PMYO) In combination these results
suggest that PM in mixed saliva may be
derived from periodontal tissues. (8)
Subsequent investigations indicate
that the gingival crevice appears to be the
source of PM in nonnal human mixed
saliva. (10) Consistent with these
observations, the presence of PM in
gingival tissues and crevicular fluid has
been associated with clinical signs of
periodontal inflammation. (11.12.13)
Salivary PM levels in periodontitis
patients have been correlated with the
extent of periodontal disease. (8)Similarly,
the levels of PM in saliva from patients
with refractory periodontitis were
elevated in comparison to patients who
had responded to conventional
periodontal therapy and maintenance.(14)
Thus a number of separate studies
provide the basis for suggestion that PM
a proinflammatory phospholipid autacoid
may be involved 'in periodontal tissue
injury and disease.
The crosssectional studies outlined
above indicate that the levels of PM is
saliva are correlated with the extent of
periodontal disease. However, longitudinal
studies to assess the effect of
periodontal treatment on salivary p,
periodontitis patients have
insufficient. The purpose of this stu ".
thus to evaluate salivary PM Ie
throughout initial peiodontal treatm..
in patients with early onset and ad!
periodontitis in relation to CUnil
parameters of the diseases.
MATERIALSArID MEfDODS
Duman subjects:
The subjects of this study were divid
into two groups, as follows:
Group I (subdivided into):
Study Group I: Ten early onsetl
periodontitis patients with radiographic'
evidence of alveolar bone loss, of ages
ranging from 19 to 29 years.
Control Group I: Ten healthy control
subjects matching their study group in
age and sex, enjoying clinically healthy
gingiva and no radiographic evidence of
bone loss.
Group II (subdivided into):
Study Group II: Ten chronic adult
periodontitis patients diagnosed :
through clinical and radiographic
examinations of ages ranging from 35
to 50 years.
Control Group II: Ten healthy control
subjects with clinically healthy gingiva
and no radiographic evidence of bone
loss, matching their study group in age
and sex.
The medical and dental history of each
subject were reviewed to exclude those
suffering from systemic illness. Patients
having been subjected to antibiotics or
2 |
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ISSN |
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1110-015X |
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Journal Name |
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Alexandria Dental JOUrnal |
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Volume |
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24 |
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Issue Number |
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4 |
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Publishing Year |
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1418 AH
1998 AD |
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Article Type |
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Article |
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Added Date |
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Monday, April 16, 2012 |
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Researchers
| فريد بدريه | A. Badria, Farid | Researcher | | |
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