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African Journal of Biomedical Research
Ibadan Biomedical Communications Group
ISSN: 1119-5096
Vol. 5, Num. 3, 2002, pp. 141-143
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African Journal of Biomedical
Research, Vol. 5, No. 3, Sept, 2002, pp. 141-143
Short communication
HEMATOLOGICAL VALUES
IN JUVIENILE
PERIODONTITIS PATIENTS IN IBADAN, NIGERIA
DOSUMU
E.B1*, AROWOJOLU
M. O2., AKANDE O. O3. AND AKINGBOLA T.S4.
1,
2 Department of Preventive Dentistry, College of Medicine,
University of lbadan,
3Departments
of Physiology/Oral Pathology College of Medicine, University of lbadan.
4Department
of Haematology, College of Medicine, University of lbadan.
*Author
for correspondence
Received: January 2002
Accepted
in final form: September 2002
Code Number: md02029
In
this study, clinical and hematological examinations of forty adolescent patients
in the
group (15-22) years with established clinical features of chronic periodontitis
but without any diagnosable medical disease were done. The patients were
divided into two
Groups (A &B). Group A were diagnosed as having juvenile periodontitis (JP)
while group B had the plaque-induced chronic periodontitis i.e. non- JP and were
used as control. We then compared the following hematological features between
these two groups and the expected normal values here in the tropics; White Blood
Cell (\VBC)-total and differential, Packed Cell Volume (PCV) and the blood film
appearance. According to the general blood examination of both groups, almost
all the numerical values were within the normal range as compared to the documental
normal value in Nigeria. It was therefore concluded that low lymphocyte
responsiveness, lymphocyte dysfunction and a deficiency of neutrophil chemotaxis
as earlier reported may
be involved in the pathogenesis of JP rather than the numerical value
of these cells. The relationship of periodontal disease to other neutrophil functions
such as phargocytosis and bactericidal activity requires further
investigation.
Key Words: Hematological
values, juvenile periodontitis
INTRODUCTION
Periodontitis is an infectious
disease caused by periodontopatic bacteria. The initiation and progression
of periodontitis do not always occur in the same manner, because the host defensive
mechanism varies among patients and race (Page et al 1985; Genco et al 1986,
Genco, 1992); hence this study was designed to evaluate the numerical value
of the defense cells in juvenile and non- juvenile periodontitis patients compare
with the expected normal values in Nigeria.
MATERIALS
AND METHODS
The study was carried out at the
periodontology unit of the Dental School, and
Haematology Department, College of Medicine, University of lbadan, lbadan. Ethical
clearance was obtained from University College Hospital/College of Medicine Ethical
Committee. The data were collected at the first visit, that is, before any form
of periodontal therapy was begun. Forty patients of the same age range (15-22)
years were selected for participation in this study and they were divided into
two equal groups. The first group of 20 patients was diagnosed as having Juvenile
Periodontitis while the remaining 20 patients had chronic periodontitis sequel
to heavy accumulation of plaque and calculus. The second group was used as the
control group.
Clinical Examination: Clinical
examination was performed on the remaining teeth excluding the third molar
and the following criteria were used to describe the conditions (1) the number
of teeth missing, that is not sequel to decay (2) probing depth, which was
expressed as the mean value of distances from the gingival margin to the base
of the gingival crevice measured as four points around each tooth, the mean
found and expressed as the value for that tooth.(3) Number of teeth in which
the alveolar bone showed resorption of more than half of the root length, which
was measured from cementoenamel junction to root apex at an arbitrary point
on a radiography by the method described by Schei et al (1959).
We diagnosed the first group
with Juvenile Periodontitis due to the age of onset and their clinical findings
according to the criteria of Page and Schroder (1982). The graduations of the
peripheral whole blood cell, Packed Cell Volume (PCV) and the white blood cell
(WBC) were examined for both groups.
Laboratory Tests: Approximately
3.Oml peripheral blood was drawn from each of the participating patients in
both groups for hematological WBC (total and differential) and the film appearance.
The parameters were determined in
hematology unit laboratory of the University College using standard methods.
RESULTS
Clinical Examination: The
clinical findings at the first visit are as shown in Table 1. All the patients
showed severe bone resorption with relatively deep mean pockets probing depth
and a corresponding mean degree of mobility. The oral hygiene status of the
chronic periodontitis patients was poor considering the high value of the mean
OM-S index as compared to the JP patients which was fair.
General Blood Examination: The
results are shown in Tables 1 and 2. According to their general blood counts
all of the values were within normal limits when compared with the accepted
normal in the tropics
DISCUSSION
Early-Onset periodontitis (EOP) may serve as models in which
certain pathogenic features are amplified, thus permitting insights into basic
mechanisms underlying all forms of
periodontitis. (Fenesy, 1998). Epidemiological evidence indicates the existence
of high risk groups and suggests that a variety of disease markets (risk factors)
may predispose individuals to periodontitis Johnson et al (1988) Some forms of
increased disease susceptibility or intrinsic defects may be involved in patients
with EOP; for example, neutrophil dysfunction Van Dyke et
al (1985), abnormal lymphocyte subsets Kinane et al 1989), and aberrant cytokine
production Page et al (1985). Furthermore, a high prevalence of EOP patients
in certain families and linkage with specific human leukocyte antigen (HLA) phenotypes
have suggested that genetic factors may be involved in some
cases and "Common risk factors" have been pointed out in these families. However,
studies reported to date have not shown much consistency in the association of
HIL.A phenotype with periodontal disease. Nishimura et al (1990) reported that
the association between HLA antigens and periodontal disease differs from race
to race.
Table 1: Clinical findings
at first clinic visit
Oral examination
|
JP Patients
|
Non JP patients
|
Mean Probing Depth
|
5.70 ±1.05
|
5.38 ±0
|
Bone Loss (%)
|
46.18 ± 1.02
|
44.03 ±1.01
|
Mean Degree of Mobility
|
2.081± 0.53
|
2.080 ±0.46
|
Mean OHI-S Index Value
|
1.18 ± 0.47
|
2.68 ± 0.86
|
Mean ± S.E.; P < 0.05
Suzuki et al (1985)
reported that depressed neutrophil functions is not restored after periodontal
therapy and suggested that such neutrophil
dysfunction is congenital. Van Dyke et al (1985) reported the same result
from family studies.
In this study, we report the clinical and hematological
profiles of chronic periodontitis (JP and non- JP) patients in the SouthWestern
zone of Nigeria. We have demonstrated that the hematological range of values
(including the neutrophil and lymphocyte) for these patients falls within the
accepted normal range of values
in the Tropics Ezeillo (1981) Ukaejiofor (1979).
When these values were compared
between the two different groups (JP and non JP) it was also observed that
there was no significant difference, suggesting that the quantitative values
of haematological indices are not associated with chronic
periodontal diseases.
Table 2: Mean haematological
values of JP and Non JP patients
Subject
|
Age
|
Mean PCV
|
Total WBC X 109/L
|
Differential counts
(%)
|
Platelets
|
Film appearance
|
N
|
L
|
M
|
B
|
E
|
N
|
A
|
M
|
JP
Patients
|
18.3
|
0.41 ±0.04
|
5.34 ±1.65
|
42.9 ±6.29
|
51.9± 5.32
|
0.65
±0.75
|
0
|
4.5 ± 1.5
|
199.75
±14.46
|
16
|
2
|
2
|
Non-JP Patients
|
19.3
|
0.39 ±0.01
|
6.09 ±1.48
|
48.9 ± 4.8
|
49.6 ±4.56
|
0.63 ±0.76
|
0.4
±0.6
|
0.8 ± 0.8
|
183.06
±9.97
|
18
|
1
|
1
|
Normal Patients
|
|
0.40 ±.05
|
4- 10
|
60
|
35
|
2
|
1
|
2
|
250
|
-
|
-
|
-
|
Key: N = Normal; A
= Anisotosis; M = Microcytosis
Neutrophil being the principal
cell type involved in host defenses against extrinsic bacteria attack, its
function must be evaluated by assessing the entire process from chemotactic
response to digestion of antigens. The relationship of periodontal disease
to other neutrophil functions such as phagoytosis and bactericidal activity
requires further investigation.
Further Studies need to be
conducted comparing different races as well as investigating a large number
of families with multiple members affected to help identifying the linkage
of periodontal disease with specific human leukocyte antigen (HLA)
phenotypes.
In conclusion, rather than
the quantitative values of these cells (neutrophil and lymphocyte) which we
found to be within the accepted normal range of values in the tropics, their
defective functions (qualitative value) as reported previously may explain
the pathogenesis of EOP of which JP is one.
ACKNOWLEDCEMENT: The
authors acknowledge the immense contribution of Mr. S.A. Olomu of the Haematology
research Laboratory, College of Medicine, University of lbadan, lbadan for
the laboratory processing of the
blood samples.
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