The Effect of Non-Surgical Periodontal Therapy on Interleukin-34 in Stage I and II Periodontitis (A Controlled Clinical Trial With Biochemical Analysis)

Periodontal disease is a multifactorial infection induced by a complex of bacterial species that interact with host tissues and cause destruction of the periodontal structures, including the supporting tissues of the teeth, alveolar bone, and periodontal ligament.

The bacterial biofilm formation initiates gingival inflammation; however, periodontitis initiation and progression depend on dysbiotic ecological changes in the microbiome in response to nutrients from gingival inflammatory and tissue breakdown products that enrich some species and anti-bacterial mechanisms that attempt to contain the microbial challenge within the gingival sulcus area once the inflammation has initiated.

Current evidence supports multifactorial disease influences, such as smoking, diabetes mellitus, obesity, metabolic syndrome, osteoporosis, low dietary calcium and vitamin D and other immunoinflammatory responses that make the dysbiotic microbiome changes more likely for some patients than others and likely influence the severity of disease for such individuals.

During periodontitis, the pathogen triggers the white blood cells of the innate immune system to release proinflammatory mediators such as cytokines that play a vital role in the progression of the inflammation process of periodontitis. In addition, these pathogens can activate the acquired immune system contributing to the release of more cytokines and chemokines that cause permanent bone damage and irreversible periodontal attachment loss.

Cytokines are defined as soluble small proteins (~5-20 kDa) that bind to specific receptors on certain cells, stimulate some internal cellular changes, and cause multiple genetic and chemical regulations.