*3.1.2 Metalloproteinases*

*Periodontal Disease - Diagnostic and Adjunctive Non-surgical Considerations*

established periodontal injury are known [6].

**2. Biomarkers**

or a therapeutic intervention [7].

must be compared with other variables [8].

**3. Biomarkers for the diagnosis of periodontitis**

In the pathology of periodontitis, the clinical, radiographic, and histological characteristics of the gingival groove and pouch epithelium, the underlying connective tissue and the types of resident and infiltrating blood cells in the initial, early,

Currently, the diagnosis requires rapidity, sensitivity, and specificity since determining the stage in which the patient is located is fundamental for a good treatment; for this reason molecules are currently being sought that vary when the person is healthy and when the person has the disease. However, despite all the researches that exist regarding chronic inflammation, the diagnosis of periodontitis is based on clinical measurements; these not only show low sensitivity and specificity as diagnostic tests but are also subjective and laborious. The objective of this chapter is to try to describe what a biomarker is, the types of biomarkers evaluated in periodontitis, the sources to obtain these biomarkers, and their usefulness.

The definition of biomarkers as established by the National Institute of Health (NIH) is as follows: biomarkers are the biological, biochemical, anthropometric, physiological, etc. characteristics, which are objectively measurable, capable of identifying physiological or pathological processes, or a pharmacological response

There are different types of biomarkers; the ideal biomarker must be specific,

Before a biological marker is used in human health studies, its validation is fundamental; therefore, the selection and approval process requires careful consideration of specificity and sensitivity, establishing accuracy, precision, quality assurance, analytical procedure, and interpretation of measurement data, which

**3.1 Importance of the different biomarkers used for the diagnosis of periodontitis**

Because there are certain molecules, like trace elements, proteins (cytokines), and proteolytic enzymes, these have been considered as possible biomarkers of periodontal disease, we will try to discuss the relevance of these groups below.

Inflammation has evolved as a protective response to an injury, is a primordial response that eliminates or neutralizes foreign organisms or materials, in general; the innate inflammatory response starts in minutes and, if all is well, resolves in a matter of hours. In contrast, chronic inflammation persists for weeks, months, or even years [9]. The inflammatory response that occurs in periodontal disease is mediated mainly by B and T lymphocytes, neutrophils, and monocytes/macrophages. These are activated to produce inflammatory mediators, including cytokines and chemokines [10]. Several pro-inflammatory cytokines including interleukins like IL-1, IL-6, IL-12, IL-17, IL-18, and IL-21; tumor necrosis factor alpha (TNFα); and interferon (IFN-γ) have been demonstrated to be involved in the pathogenesis of periodontitis [2].

*3.1.1 Proteins (cytokines) involved in the inflammatory process of periodontitis*

sensitive, predictive, rapid, economical, noninvasive, and stable in vivo and in vitro. Additionally, it must have enough preclinical and clinical relevance to modify decisions regarding the pathological process in which applies [7].

**20**

There is significant evidence showing that collagenases, along with other matrix metalloproteinases, play an important role in periodontal tissue destruction. The main group of enzymes responsible for the collagen and other protein degradation in extracellular matrix (ECM) is matrix metalloproteinases (MMPs) [11]. Several works have shown that matrix metalloproteinases are upregulated in periodontal inflammation; transcription of matrix metalloproteinase genes is very low in healthy periodontal tissue. In periodontal disease, secretion of specific matrix metalloproteinases is stimulated or downregulated by various cytokines [12].
