Concepts of general pathology relate to multiple facets of dental hygiene care. Inflammatory diseases significantly affect the oral cavity, and research continues to focus on the linkages among inflammatory processes, systemic diseases, and oral diseases.
Advances in genomics contribute to our understanding of the genetic basis of oral health conditions and their treatments. Individuals vary in their genetic makeup and hence their response to microbial challenges, injury, risk factors, and treatments. Dental hygienists use genomic information to assess clients for periodontal and other disease risks and will use genetics in planning effective care and evaluating therapeutic outcomes in the not-too-distant future.
This chapter reviews major concepts related to inflammation, wound healing, and repair; genetics; and the differential diagnostic process that enables dental hygienists to integrate the biologic basis of health and disease into client care and acquire skills in diagnostic decision making.
FIGURE 7-1 Components of acute and chronic inflammatory responses: circulating cells and proteins, cells of blood vessels, and cells and proteins of the extracellular matrix. (From Kumar V, Abbas AK, Fausto N, Aster JC: Robbins and Cotran pathologic basis of disease, ed 8, Philadelphia, 2010, Saunders.)
FIGURE 7-2 Major local manifestations of acute inflammation, compared with normal. 1, Vascular dilation and increased blood flow (causing erythema and warmth). 2, Extravasation and deposition of plasma fluid and proteins (edema). 3, Leukocyte emigration and accumulation at the site of injury. (From Kumar V, Abbas AK, Fausto N, Aster JC: Robbins and Cotran pathologic basis of disease, ed 8, Philadelphia, 2010, Saunders.)
5. Leukocytes, mainly neutrophils, accumulate along the vascular endothelium (margination); the endothelium becomes lined by leukocytes (pavementing); leukocytes adhere to the endothelium and, soon after, migrate through the vascular wall into interstitial tissue (diapedesis or emigration)
b. Phagocytosis is greatly enhanced by opsonins, specific proteins such as immunoglobulin G (IgG) antibodies, fragments of the complement protein C3, and plasma lectins that are recognized by specific receptors on leukocytes
(From Kumar V, Abbas AK, Fausto N Aster JC: Robbins and Cotran pathologic basis of disease, ed 8, Philadelphia, 2010, Saunders.)
(a) Vascular phenomenon created by C3a, C5a, and to a lesser extent, C4a; stimulate histamine release from mast cells; called anaphylatoxins because they have similar effects in the reaction of anaphylaxis
(3) Prevents the spread of infection and inflammation; localizes microorganisms at the site of phagocytosis; helps clot formation to stop bleeding and for repair, chemotaxis of neutrophils, and increased permeability of vessels
(a) Prostaglandins, including PGE2, PGD2, PGF2a, PGI2, and TxA2, are most important in inflammation, causing increased permeability, the chemotactic effects of other mediators, and vasodilation resulting in edema as well as pain and fever in inflammation
(f) Platelet-activating factor (PAF) causes platelet stimulation, vasoconstriction, bronchoconstriction, vasodilation, and increased venular permeability; far more potent than histamine; increased leukocyte adhesion to endothelium; chemotaxis, degranulation, and oxidative burst; also boosts synthesis of other mediators
 Responsible for endothelial activation, which induces the synthesis of endothelial adhesion molecules and chemical mediators; producing enzymes associated with matrix remodeling; and increasing the surface thrombogenicity of endothelium
FIGURE 7-3 Repair responses after injury and inflammation. Repair after acute injury has several outcomes, including normal tissue restitution and healing with scar formation. Healing in chronic injury involves scar formation and fibrosis. (From Kumar V, Abbas AK, Fausto N, Aster JC: Robbins and Cotran pathologic basis of disease, ed 8, Philadelphia, 2010, Saunders.)
2. Angiogenesis from adjacent blood vessels occurs through the vasodilation and increased permeability of existing vessels, degradation of ECM, migration of endothelial cells, maturation of endothelial cells and remodeling into capillary tubes, and recruitment of periendothelial cells to support endothelial tubes and to form the mature vessel