Pathophysiology of oral cavity diseases. Textbook

Pathophysiology of oral cavity diseases. Textbook
A. Yu. Ryabinina

M. L. Blagonravov

A. A. Bryk

This textbook is intended for students of medical universities specializing in «Dentistry», as well as for residents and postgraduate students. It has been prepared by authors from the Medical Institute of the Federal State Autonomous Educational Institution of Higher Education «Peoples’ Friendship University of Russia named after Patrice Lumumba». The textbook presents relevant educational material on the pathogenesis of dental diseases.

Pathophysiology of oral cavity diseases

Textbook

A. A. Bryk

A. Yu. Ryabinina

M. L. Blagonravov

© A. A. Bryk, 2024

© A. Yu. Ryabinina, 2024

© M. L. Blagonravov, 2024

ISBN 978-5-0064-8007-0

Created with Ridero smart publishing system

INTRODUCTION

The textbook comprehensively addresses pathophysiology of dental diseases, covering the pathogenetic basis of inflammatory processes, the role of microflora, mechanisms of immunity, characteristics of dystrophic changes, as well as microcirculatory and functional disorders of the oral cavity. Special attention is given to the pathogenesis of inflammatory diseases such as pulpitis, periodontitis, gingivitis, and others. Additionally, the influence of systemic diseases on the condition of oral cavity tissues is discussed.

The purpose of this textbook is to provide students with contemporary educational material on the pathogenesis of various dental diseases in an accessible format, as well as to assist in the development of professional skills necessary for successful practical activity.

FEATURES OF NON-SPECIFIC PATHOLOGICAL REACTIONS IN THE ORAL CAVITY

Despite the variety of pathological conditions in the oral cavity, several key pathogenetic mechanisms that underlie the development of dental diseases of various etiologies can be identified. The typical (non-specific) pathological reactions affecting oral tissues include:

– Inflammation

– Dystrophy (including against the background of microcirculatory disturbances)

– Functional (hyperfunction) and mechanical trauma

– Functional insufficiency (hypofunction)

– Tumor growth (neoplasia)

These typical processes have several key characteristics. The pathogenesis of inflammation in the oral cavity is primarily influenced by microflora. In case of dystrophic changes in the periodontium, degenerative alterations predominate with no signs of the inflammatory process. Functional disorders are caused by prolonged hypo- or hyperfunction of periodontal tissues. Mechanical damage to tooth tissues can include, for example, improper use of hygiene products – horizontal movements with a toothbrush that contribute to the formation of non-carious lesions, and the use of hard-bristled toothbrushes leading to gingival recession, including the loss of marginal gingiva and exposure of the tooth root, as well as iatrogenic factors that exert a traumatic impact on periodontal tissues (such as overhanging edges of fillings and crowns, or poor-quality filling of the contact surfaces of teeth leading to trauma to marginal areas of the periodontium). The development of neoplastic processes is associated primarily with disruptions in the growth and differentiation of cells within oral tissues.

INFLAMMATION

Inflammation is a non-specific response to injury and it occurs stereotypically, regardless of the nature of the damage. However, it is characterized by a number of features.

CHARACTERISTICS OF THE INFLAMMATORY RESPONSE

– Regardless of the etiological factor, the inflammatory process has three essential components: alteration (tissue damage), exudation (release of fluid and blood cells from vessels into tissues and organs), and proliferation (multiplication of cellular elements).

– The extent and duration of the injury determine the degree and duration of the inflammatory response. The inflammatory response can be localized – and limited to the area of injury, or systemic (generalized) if the damage is extensive.

– The inflammatory response is classified as acute or chronic based on the speed of the process. Microscopic changes occur in the damaged tissues in both acute and chronic inflammation. These changes cause symptoms which can be observable in clinical practice.

– Local clinical changes in the site of inflammation are known as cardinal signs of inflammation: redness, heat, swelling, pain, and loss of normal tissue function. In more extensive responses, systemic signs of inflammation may also be present (such as fever, intoxication, leukocytosis, etc.).

– Vascular response. Microscopic manifestations of inflammation involve small blood vessels, (or the microcirculatory bed). It includes arterioles, capillaries, and venules in the area of injury, as well as red blood cells, white blood cells, and chemical substances known as biochemical mediators. Under normal conditions, blood and its cellular components flow through the microcirculatory bed. Oxygen and nutrient exchange necessary for the health of surrounding tissues occurs as plasma fluid passes between the endothelium lining the walls of arterioles and capillaries. Plasma is the liquid component of blood, consisting mainly of water and proteins, in which blood cells are suspended. Normally, most of the plasma that passes out of the microcirculatory bed returns to the bloodstream through venules. Lymphatic vessels, in turn, remove excess plasma that does not reenter the blood vessel. These processes are disordered resulting the development of inflammation.

– Ischemia. Initially, a brief reflex constriction of blood vessels occurs in the area of injury.

– Arteriovenous hyperemia. Dilation of the same small blood vessels is then observed for several seconds. Dilation is an increase in the diameter of vessels, caused by biochemical mediators released at the moment of injury. The expansion of the microcirculatory bed vessels leads to an enhancement of blood flow through them. The enhanced blood flow filling the capillary bed in the damaged tissue is known as hyperemia. Hyperemia contributes to the appearance of two clinical signs of inflammation: erythema and heat. Erythema, or redness, is easily noticeable in most inflamed tissues of the oral and facial area, while localized temperature changes are more difficult to detect.

Exudation: the release of fluid and blood cells from vessels into tissues and organs.

Key Mechanisms of Development:

– Increased Permeability: During hyperemia, the permeability of the vessels in the microcirculatory bed increases, making blood vessels «leaky.» Endothelial cells contract, creating gaps between them. As a result, plasma fluid with low protein content, devoid of cells, passes between the endothelial cells and enters the tissues. This fluid is called transudate and is similar to the type of fluid that typically moves from the microcirculatory bed into tissues to supply oxygen and nutrients. The loss of fluid from the microcirculatory bed leads to an increase in blood viscosity. The blood becomes thicker and cannot flow as easily, ultimately resulting in a reduced flow through the microcirculatory bed.

– Leukocyte Emigration: As blood flow slows down, red blood cells begin to accumulate in the center of the blood vessels, while leukocytes migrate to the periphery of the vessels. This movement of leukocytes to the periphery is called margination. Leukocytes are now able to adhere to the inner walls of the damaged blood vessels, which have become «sticky» due to specific factors on the cell surfaces. This process is known as leukocyte pavementing. Subsequently, leukocytes begin to exit the vessels into the damaged tissues, accompanied by a significant amount of fluid. The emigration of leukocytes into the damaged tissues is facilitated by the opening of intercellular junctions between the endothelial cells lining the blood vessels; these cells contract in response to biochemical mediators. As leukocytes (primarily neutrophils) migrate through the walls of blood vessels and the surrounding basement membrane, they further increase the permeability of the microcirculatory bed, allowing larger molecules and other cells to exit.

Formation of Exudate

The fluid that now passes into the damaged tissues is called exudate. This fluid contains cells and a higher concentration of protein molecules than transudate. The presence of both transudate and exudate in the damaged tissue promotes the dissolution of harmful agents that may be present and facilitates the transport of these agents through the lymphatic vessels to lymph nodes, which stimulates an immune response. As transudate 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.