7: General Pathology

General Pathology

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.


A host response to cellular injury that consists of vascular responses, migration and activation of leukocytes, and systemic reactions

Cellular injury may occur because of trauma, genetic defects, physical and chemical agents, tissue necrosis, foreign bodies, immune reactions, and infections

A protective response designed to rid the body of the initial cause of cell injury and the consequences of that injury

Inflammatory response consists of a vascular reaction and a cellular reaction

Cardinal signs of inflammation

Types of inflammation

Cells involved in inflammation (Figure 7-1)

Acute Inflammation

Vascular changes (Figure 7-2)

1. Transient vasoconstriction of arterioles lasting several seconds

2. Vasodilation

3. Increased permeability of microvasculature

a. An exudate of protein-rich fluid escapes into extravascular tissue, resulting in edema

b. Proposed mechanisms that explain the leakage of endothelium in inflammation to allow this response are:

4. Concentration of red cells in small vessels and increased viscosity of blood, known as stasis

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)



1. Recognition and attachment

2. Engulfment

3. Killing and degradation

4. Release of leukocyte products

5. Apoptosis-defined as programmed cell death used by the body to eliminate old cells

Chemical mediators (Table 7-1)


Actions of the Principal Mediators of Inflammation


(From Kumar V, Abbas AK, Fausto N Aster JC: Robbins and Cotran pathologic basis of disease, ed 8, Philadelphia, 2010, Saunders.)

1. General principles

2. Vasoactive amines

3. Plasma proteins

a. Complement system

(1) Consists of 20 component proteins found in greatest concentration in plasma

(2) Causes increased vascular permeability, chemotaxis, and opsonization (the process by which certain cells are made more susceptible to phagocytosis)

(3) C3 and C5 are the most important inflammatory mediators of the complement components

b. Kinin system

c. Clotting system

4. Other mediators

a. Arachidonic acid

(1) A lipid mediator that is a short-range hormone; is formed rapidly and acts locally

(2) Produces prostaglandins, leukotrienes, and lipoxins

(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

(b) Pathway initiating these prostaglandins occurs by two different enzymes, COX-1 and COX-2

(c) Leukotrienes cause intense vasoconstriction, bronchospasm, and increased vascular permeability

(d) Lipoxins inhibit leukocyte recruitment, neutrophil chemotaxis, and adhesion to the endothelium and may play a role in resolving inflammation

(e) Resolvins inhibit leukocyte recruitment and activation by inhibiting the production of cytokines

(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

(g) Tumor necrosis factor and interleukin 1

(h) Chemokines—small proteins that act as chemoattractants for leukocytes and control the normal migration of cells through various tissues

(i) Nitric oxide (NO)—released from endothelial cells; causes vasodilation by relaxing vascular smooth muscle; microbicidal; a mediator of host defense against infection

(j) Lysosomal components of leukocytes

(k) Oxygen-derived free radicals may be released from leukocytes following a phagocytic event and are potent mediators

b. Neuropeptides, such as substance P and neurokinin A, play a role in the initiation and propagation of inflammatory response

Outcomes of inflammation

Chronic Inflammation



Cells involved

Role of lymphatics

Systemic effects of inflammation—acute phase response or the systemic inflammatory response syndrome

1. Fever—produced in response to pyrogens that act by stimulating prostaglandin synthesis

2. Acute phase proteins, including C-reactive protein (CRP), fibrinogen, and serum amyloid A protein (SAA) increase during the inflammatory process

3. Leukocytosis

4. Sepsis

Systemic disease affected by chronic inflammation

Regeneration and Wound Healing2


General concepts

1. Involves a complex process that includes a number of steps

2. Repair process—a combination of regeneration and scar formation that is influenced by local and systemic factors that may inhibit or prolong the wound healing process

3. Generally, repair begins early in inflammation—formation of granulation tissue, which is a hallmark of healing


Scar formation—three processes occur (emigration and proliferation of fibroblasts in the site of injury, deposition of ECM, and tissue remodeling)

Jan 1, 2015 | Posted by in Dental Hygiene | Comments Off on 7: General Pathology
Premium Wordpress Themes by UFO Themes