Pathophysiology of oral cavity diseases. Textbook. A. A. Bryk
passes into the tissues, excess fluid begins to accumulate in the connective tissue at the site. Excess fluid that is accumulated in the interstitial space is called edema which is manifested as localized swelling, another cardinal sign of inflammation.
In case of further damage, exudate may seep out of the tissue either as a clear, watery fluid (serous exudate) or as thick pus ranging from white to yellow in color, containing tissue debris and a large number of leukocytes (purulent exudate). The accumulation of purulent exudate in a limited cavity is defined as abscess. The formation of exudate can be so excessive that it hinders tissue repair. Excessive accumulation of exudate can lead to the formation of fistulas and sinus tracts. These drainage channels develop in the healthy, functioning tissue that replaces necrotic cells, allowing the excess exudate to drain out.
In some cases, the excessive exudate in the damaged tissues may require mechanical drainage, often by making an incision in the swollen area and placing a drainage tube in the incision site. This drainage procedure may be accompanied by the administration of antibiotics and anti-inflammatory drugs. The formation of exudate also leads to another clinical sign of inflammation – pain, as the exudate exerts compression of the sensory nerves in the area. Additionally, certain biochemical mediators that are present in the inflamed tissue can contribute to the sensation of pain. The edema and pain in tissues occurring as a result of the inflammatory process may then lead to a loss of normal tissue function, which is another cardinal sign of inflammation.
Leukocyte Chemotaxis
Chemotaxis is defined as directed movement of leukocytes along a concentration gradient of biochemical mediators (known as chemotactic factors or chemoattractants), which enhance this movement. The emigration and chemotaxis of leukocytes to the site of inflammation protect the tissue from further damage. Initially, leukocytes form the so called leukocyte barrier, effectively isolating the site of injury from the surrounding healthy tissue. Later, in the damaged tissue, leukocytes perform phagocytosis, which involves the capture and removal of foreign substances. These foreign substances may include pathogenic microorganisms or tissue remains. The presence of such substances interferes with the healing process, therefore they must be removed so that inflammation resolves and tissue regeneration begins.
THE ROLE OF OXYGEN METABOLISM DISORERS IN INFLAMMATION
In addition to the role of pathogenic factors and the activation of the immune response, as previously discussed, it is important to highlight some specific aspects of oxygen metabolism disturbances in the pathogenesis of periodontal inflammation.
In case of periodontitis, oxygen consumption increases, leading to a rise in the concentration of reactive oxygen species (ROS) and the development of oxidative stress (lipid peroxidation). Lipid peroxidation directly damages periodontal tissue, contributing to its degradation. It also has a significant indirect effect on the qualitative properties of saliva, against the background of functional changes in the salivary glands. Oxidative stress may also result from the dysfunction of antioxidant systems, such as insufficient glutathione regeneration or a deficiency of antioxidant enzymes. These processes often precede microcirculatory disorders, further exacerbating the inflammatory process.
THE ROLE OF MICROFLORA IN THE DEVELOPMENT OF ORAL DISEASES
Throughout a person’s life, the body is inhabited by a huge number of various bacteria. The roles of these bacteria can vary from beneficial to harmful, while some bacteria may have no noticeable effects. It is estimated that at least 700 species of microorganisms are present in the human oral cavity. Fortunately, the majority of these microorganisms maintain in the ecological balance and do not cause diseases. This is a normal part of the oral environment, playing a crucial role in protecting against the colonization of external bacteria that could affect systemic health. However, it is important to note that the most common oral diseases – dental caries, gingivitis, and periodontitis – are primarily caused by microorganisms. Nevertheless, bacteria are a necessary but not sufficient condition for the development of these diseases. Environmental conditions (particularly those related to the host) are generally considered to play a key role in the pathogenesis of these diseases. The same applies to infections by fungi of the genus Candida; most individuals carry this fungus, but oral candidiasis occurs relatively rarely.
The role of periodontal diseases as a risk factor in the development and/or progression of systemic conditions such as diabetes mellitus, rheumatoid arthritis, cardiovascular diseases, adverse pregnancy outcomes, and head and neck cancers has been the subject of extensive research in recent years.
Three primary mechanisms linking oral infections with systemic pathology have been revealed:
– The spread of infection from the oral cavity due to transient bacteremia,
– The circulation of microbial toxins,
– Systemic inflammation triggered by adverse immune responses to oral microorganisms.
CONCEPT OF BIOFILM
Periodontal diseases share many associative and cause-and-effect relationships with systemic diseases and may increase susceptibility to them through common risk factors, such as the presence of pathogenic Gram-negative anaerobic microorganisms in subgingival biofilms and the transformation of the periodontium into a reservoir for inflammatory mediators.
Under natural conditions, microorganisms can exist either as planktonic (free-floating) cultures or as biofilms. For the past 100 years, research activity has primarily focused on planktonic bacterial cultures; however, it is now widely recognized that microorganisms in the oral cavity are organized in the form of biofilms.
BIOFILM FORMATION
A biofilm is an accumulation of bacteria that exist as closely connected communities, adhering to various types of surfaces (both natural and artificial), typically in an aquatic environment containing sufficient concentrations of nutrients necessary to support the metabolic needs of the microbiota (Listgarten MA, 1999). Based on this definition, we can note that dental plaque has common characteristics with a biofilm. The oropharynx is an open ecosystem where bacteria are constantly present, seeking to colonize all favorable areas. Preferred targets for bacterial colonization include the hard and soft palate, subgingival and supragingival surfaces, teeth, lips, cheeks, and tonsils. Most bacteria can persist after biofilm formation on non-shedding surfaces, i.e., hard tissues (tooth and root surfaces, restorative materials, implants, dentures, etc.).
In conditions of healthy dental and gingival relationships, there is a balance between the additive and retention mechanisms of biofilms on the one hand, and the abrasive forces that tend to reduce biofilm formation (e.g., self-cleaning by the cheeks and tongue, dietary habits, and mechanical oral hygiene practices) on the other. Disruption of this ecosystem balance (due to its overload or weakening of immune mechanisms) may become a problem not only at the local level but also systemically. Therefore, the gold standard in the prevention of diseases associated with the pathogenic impact of microorganisms is the direct removal of biofilms from teeth, restorations, or dentures through regular tooth brushing.
Biofilm formation
Within minutes after thorough cleaning the tooth surface, a thin film (pellicle) forms. It is composed of proteins and glycoproteins found in saliva. The subsequent formation of the biofilm (dental plaque) occurs as follows:
– Association (Binding): Due to purely physical forces, bacteria freely bind to the thin pellicle.
– Adhesion (Sticking): Individual bacteria, having special surface molecules (adhesins), attach to receptors on the tooth surface. These bacteria are called «primary colonizers,» with examples including Streptococci and Actinomyces. Subsequently, other microorganisms join these primary colonizers.
– Bacterial Proliferation: Once attached, the bacteria begin to actively proliferate, increasing the bacterial population