Investigation of Lipoxin A4, Annexin A1 and Interleukin-1 Beta Levels in Individuals With Periodontitis.

Eda Cetin Ozdemir

Status: Completed

Conditions: Peridontal Disease

Treatments: Other: Obtaining CGF from patients

Study type: Observational

Funder types: Other

Identifiers

NCT06700161

2024/4-13 M (Other Grant/Funding Number)

09.05.2024-117

Details and patient eligibility

About

Since the researchers thought that Annexin A1, Lipoxin A4 and IL-1 Beta parameters, which have been found to be related to inflammatory conditions, may increase in periodontitis, a common inflammatory gum disease, we wanted to evaluate the changes in Annexin A1, Lipoxin A4 and IL-1 Beta levels in the Gingival Crevicular Fluid of participants with periodontitis.

Full description

Periodontitis is a chronic, multifactorial inflammatory disease characterized by microbial-mediated, host-mediated inflammation, resulting in periodontal attachment loss and eventual tooth loss. Given the high prevalence and systemic effects of periodontitis, research into the pathogenesis and treatment of periodontal disease is crucial to improving oral health and overall health outcomes.

In recent years, there has been great interest in determining the role of lipid mediators in pro- and anti-inflammatory events, which are of great importance in the pathogenesis of periodontitis. LIPOXIN A4 (LXA4), which serves as an inflammatory shutdown signal, is produced from arachidonic acid via interactions between individual lipoxygenases. Preclinical models have demonstrated the potential and efficacy of LXA4 in preventing the onset of periodontitis and treating periodontal disease by regenerating lost periodontium. LXA4 is produced by the dual oxygenation of arachidonic acid by 5-lipoxygenase and 12-lipoxygenase and mediates inflammatory suppression signals in vivo. LXA4 is biosynthesized by leukocytes, endothelial cells, and platelets via transcellular pathways and has potent inhibitory effects on various inflammatory mechanisms.

Annexins (ANXA) belong to the calcium (Ca+2) binding protein family that plays a role in inflammatory host defense. ANXA1, also known as lipocortin 1, is an anti-phospholipase protein that binds to cell membranes via a calcium-dependent pathway. ANXA1 inhibits the production of proinflammatory lipid mediators by inhibiting the activity of phospholipase A2. In addition, ANXA1 can modify many different steps and various cells involved in the inflammatory process. ANXA1 has long been classified as an anti-inflammatory protein due to its control over leukocyte-mediated immune responses. An ex vivo study has shown that the induction and translocation of ANXA1 protein to the cell membrane is stimulated by IL-6 . It has also been reported to be a critical negative regulator of proinflammatory mediators including IL-1, IL-6 and cyclooxygenase-2, while it has also been reported to stimulate the release of the anti-inflammatory cytokine IL-10 .

Since the researchers thought that Annexin A1, Lipoxin A4 and IL-1 Beta parameters, which have been found to be related to inflammatory conditions, may increase in periodontitis, a common inflammatory gum disease, we wanted to evaluate the changes in Annexin A1, Lipoxin A4 and IL-1 Beta levels in the Gingival Crevicular Fluid of participants with periodontitis.

Enrollment: 60 patients

Sex: All

Ages: 18 to 85 years old

Volunteers: No Healthy Volunteers

Inclusion criteria

• The patient must be a volunteer
• He/she must be over 18 years old
• He/she must not have any systemic disease

Exclusion criteria

• Smoking, drinking alcohol
• Being pregnant or breastfeeding
• Not volunteering
• Having had periodontal treatment in the last 6 months
• Having used antibiotics or anti-inflammatory drugs in the last 6 months.

Trial design

60 participants in 2 patient groups

Control group

Description:

Healthy group

Treatment:

Other: Obtaining CGF from patients

Test group

Description:

Stage III Grade C Periodontitis

Treatment:

Other: Obtaining CGF from patients