Clinical Trial Details
— Status: Completed
Administrative data
| NCT number |
NCT05113030 |
| Other study ID # |
swati PCOS perio |
| Secondary ID |
|
| Status |
Completed |
| Phase |
|
| First received |
|
| Last updated |
|
| Start date |
November 1, 2021 |
| Est. completion date |
June 15, 2022 |
Study information
| Verified date |
April 2023 |
| Source |
Postgraduate Institute of Dental Sciences Rohtak |
| Contact |
n/a |
| Is FDA regulated |
No |
| Health authority |
|
| Study type |
Observational
|
Clinical Trial Summary
Polycystic ovary syndrome (PCOS) is the most common endocrinopathy in women, primarily
affecting the reproductive system, with substantial collateral negative health effects on
metabolic, psychological, and cardiovascular functions. Patients with this syndrome are at
higher risk of developing insulin resistance (IR), obesity, dyslipidemia, cardiovascular
disease (CVD), and endometrial carcinoma.IR and hyperinsulinemia are responsible for the
low-grade chronic systemic inflammation.
Periodontitis, an immuno-inflammatory disease, is a result of interaction between bacterial
attack and host inflammatory response, causing inflammation of supporting tissues of the
teeth leading to tissue destruction and tooth loss. Chronic low-grade inflammation is
emerging as a plausible etiologic mechanism linking periodontal disease and many systemic
diseases. Previous cross-sectional studies described a possible relationship between PCOS and
periodontitis and the impact of PCOS on gingival inflammation and vice-versa in terms of
increased inflammatory markers (hsCRP, IL-6, IL-17 and TNF-α). In PCOS females, there is an
alteration of various hormone levels in the body. Female sex steroid hormones play a key role
in periodontal disease progression and periodontal and implant wound healing. Human gingiva
has the capacity to metabolize hormones such as estrogen and progesterone. Moreover, gingival
tissue exhibits receptors for such hormones and it is considered as a target organ for their
direct action. These hormones might act on gingival cells by changing the effectiveness of
the epithelial barrier to bacterial injury or by affecting the collagen maintenance and
repair.
To avoid periodontal implications as these hormonal changes can worsen the vulnerability to
plaque-induced periodontal disease. So, present study is going to conduct in females with
PCOS and periodontitis at different age groups like adolescent and adult age groups. AIM -
Assessment of impact of polycystic ovary syndrome on periodontal status of women of
adolescent and adult age groups.
Description:
Polycystic ovary syndrome (PCOS) is the most common endocrinopathy in women, primarily
affecting the reproductive system, with substantial collateral negative health effects on
metabolic, psychologic, and cardiovascular functio ns.
It is a complex disease with characteristics of hyperandrogenism and chronic anovulation (CA)
with global prevalence ranging from 2.2% to 26% in Western countries, 2% to 7.5% in China,
6.3% in Sri Lanka,and 9.13% to 36% in India.Patients with this syndrome are at higher risk of
developing insulin resistance (IR), obesity, dyslipidemia, cardiovascular disease (CVD), and
endometrial carcinoma IR and hyperinsulinemia are responsible for the low-grade chronic
systemic inflammation. Periodontitis, an immunoinflammatory disease, is a result of
interaction between bacterial attack and host inflammatory response, causing inflammation of
supporting tissues of the teeth leading to tissue destruction and tooth loss. It has been
suggested as a risk factor for many systemic diseases such as diabetes mellitus,
dyslipidemia, obesity, CVDs, rheumatoid arthritis, and respiratory diseases. Chronic
low-grade inflammation is emerging as a plausible etiologic mechanism linking periodontal
disease and many systemic diseases. Increased concentrations of inflammatory biomarkers (CRP
and interleukin -6) have been reported in periodontitis and periodontal treatment helps in
decreasing these biomarkers. Timonen P et al. in their cross sectional study demonstrated
association of insulin sensitivity with the periodontal infection but they could not draw
definite conclusions about the role of reduced insulin sensitivity in the pathogenesis of
periodontal infection. Furthermore, Periodontal intervention may improve glycemic control,
insulin resistance and serum inflammatory cytokine levels in type II Diabetes patients having
chronic periodontitis. Both PCOS and periodontitis has been linked to elevated CRP levels,
therefore it is postulated that CRP might be a possible mediator of the association between
periodontitis and PCOS As, periodontitis and PCOS are associated with systemic inflammation
and insulin resistance, these two disorders may be linked through a common pathophysiologic
pathway. Previously conducted cross-sectional studies described a possible relationship
between PCOS and periodontitis and the impact of PCOS on gingival inflammation and vice-versa
in terms of increased inflammatory markers (hsCRP, IL-6, IL-17 and TNF-α). However, they have
not evaluated the effect of periodontal therapy on systemic inflammation and insulin
resistance in PCOS women suffering with periodontitis. It was hypothesized that periodontitis
and insulin resistance may add to the systemic inflammatory burden and may consequently
contribute to progression of PCOS and vice -versa. So, controlling systemic inflammatory
burden by scaling and root planing and medical treatment may have an effect in the management
of PCOS women ha ving periodontitis. Therefore, the study was attempted to evaluate the
effect of non-surgical periodontal therapy along with medical treatment on hsCRP, Homeostatic
Model Assessment (HOMA) and periodontal parameters in PCOS women having periodontitis.
Available evidence suggests that oxidative stress may be a common link for the association
between periodontitis and components of the metabolic syndrome, diabetes, and CVD. Both
nitrites and nitrates, which appear in nitric oxide (NO) metabolism, and myeloperoxidase
(MPO) are considered to reflect the strength of oxidative stress.
AIM - assessment of impact of polycystic ovary syndrome on periodontal status of women of
adolescent and adult age groups. A cross-sectional study PRIMARY OBJECTIVES Comparative
evaluation of periodontal parameters like Bleeding on probing(BOP), probing pocket
depth(PPD), clinical attachment level(CAL)in both groups. Comparative evaluation of serum
hsCRP levels( high sensitivity C reactive proteins) in both the groups. SECONDARY OBJECTIVES
Assessment of Plaque index, Gingival index, Gingival phenotype, Gingival recession, Education
status, Socio-economic status, Anthropometric parameters. Objectives Outcome Method of
measurement of outcome Comparative evaluation of periodontal parameters( BOP, PD, CAL,PI, GI)
in both the groups.
The present cross-sectional study will be conducted in the Department of periodontology, Post
Graduate Institute of Dental Sciences, Rohtak in collaboration with Department of Obstetrics
and Gynaecology Post Graduate Institute of Medical Sciences, Rohtak
1.PLAQUE INDEX(PI)- Plaque index by Silness and Loe 43(1964) will be used for assessment of
plaque. For the scoring, a mouth mirror, an explorer and a light source will be used on air
dried teeth and gingiva. GINGIVAL INDEX (GI) : Lӧe and Silness-Gingival Index by Loe and
Silness (1963) will be used. 3.BLEEDING ON PROBING (BOP):BOP will be recorded as 1 (present)
if it occurred within 15 sec of probing and 0 (absent) if no bleeding occurred. It will be
calculated in %.
After adding all the scores, total score will be divided by the total no. of surfaces
accessed and multiplied by 100. It will be designed as % sites with bleeding on probing.
4.PROBING POCKET DEPTH (PPD):Probing pocket depth will be measured as the distance from the
gingival margin to the base of the clinical pocket. The probing depth measurements will be
assessed using a calibrated manual periodontal probe (PCP-UNC 15Hu-Friedy, Chicago, IL, USA).
5. CLINICAL ATTACHMENT LEVEL (CAL): Clinical Attachment Level will be measured as the
distance between the base of the clinical pocket and the cemento-enamel
junction(CEJ).Measurements will be made at 6 sites of involved tooth- mesio-buccal,
mid-buccal, disto-buccal, mesio-lingual, mid-lingual, disto-lingual using UNC-15 probe.
Measurements will be rounded to the nearest whole millimetre. Distance of base of the pocket
from gingival margin, distance of free gingival margin from CEJ. 6. Gingival health
(According to AAP,2017 classification) 7. Gingivitis (Dental plaque induced)-According to
AAP,2017 classification
8.SURVEILLANCE OF PERIODONTITIS( According to AAP,2017 classification) Radiographs (if
needed) for evaluation of staging and grading of periodontitis. (According to AAP, 2017
classification) 9. Gingival phenotype Thin scalloped biotype in which there is a greater
association with slender triangular crown, subtle cervical convexity, interproximal contacts
close to the incisal edge and a narrow zone of KT, clear thin delicate gingiva, and a
relatively thin alveolar bone.
Thick flat biotype showing more square-shaped tooth crowns, pronounced cervical convexity,
large interproximal contact located more apically, a broad zone of KT, thick, fibrotic
gingiva, and a comparatively thick alveolar bone. Thick scalloped biotype showing a thick
fibrotic gingiva, slender teeth, narrow zone of KT, and a pronounced gingival scalloping. 10.
Gingival recession It is defined as the apical shift of the gingival margin with respect to
the cemento-enamel junction (CEJ); it is associated with attachment loss and with exposure of
the root surface to the oral environment
Cairo, 2011:
According to American Academy of Periodontology and European Federation of
Periodontology,2017 classification. 11. Analyses of Anthropometric Parameters,Waist
circumference (WC) will be measured in centimetres, at the midpoint between the lower margin
of the lowest palpable rib and the top of the iliac crest. For waist-to-hip ratio (WHR), hip
circumference will be measured around the widest portion of the buttocks. BMI(Kg/m²) will be
recorded as weight in kilograms divided by height in meters squared. 12.Blood Sampling- Blood
samples for the investigation of serum hsCRP will be collected after overnight fasting.
Venous blood from the antecubital vein will be collected after applying a tourniquet in plain
tubes without additive. Serum hsCRP levels will be assessed using a kit‡ with high
sensitivity methodology in an auto-analyzer§ according to the manufacturer's instructions.
The test principle will be particle-enhanced immune-turbidimetric assay, in which human CRP
agglutinates with latex particles coated with monoclonal anti-CRP antibodies. The turbidity
induced by the formation of immune complexes will be measured at 546 nm.
The lower detection limit for the assay was 0.15 mg/L. Serum Testosterone levels (if
required) 13. PCOSQ (Polycystic ovary syndrome questionnaire)- Given by Cronin et al. for
psychological status and quality of life. 14. Phenotype of PCOS- According to Rotterdam
criteria and AE-PCOS Society criteria.
