Pathophysiology of oral cavity diseases. Textbook. A. A. Bryk

physiology 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