7: Periodontics

7 Periodontics


Periodontal disease describes a group of inflammatory conditions that affect the supporting structures of the teeth or periodontium. The initiation, development, diagnosis, and subsequent treatment of the disease follow a well-documented sequence (Fig. 7-1). Microbial plaque is generally considered to be the initiating factor in periodontal disease. When plaque accumulates on tooth and gingival surfaces, it instigates the development of an inflammatory response in the periodontal tissues. The nature and duration of the inflammatory response is critical to the clinical outcome. If the inflammatory response is sufficient to control the challenge from plaque without destruction of periodontal ligament or alveolar bone, the clinical condition is termed gingivitis. If there is destruction of periodontal ligament and alveolar bone, the condition is termed periodontitis. The fundamental diagnosis of gingivitis or periodontitis impacts treatment. With gingivitis, there is no destruction of the periodontium and therefore treatment should be focused on removing plaque and controlling inflammation. In periodontitis, the removal of plaque and control of inflammation may be supplemented with attempts to repair or regenerate the lost periodontal tissues and correct any anatomical deformities that may have resulted from the disease process.

The following sections will help the reader review the process of diagnosis, treatment, and prevention while understanding the etiology and pathogenesis of the various periodontal conditions and how this may impact the ultimate prognosis for the patient.


A. Components of an accurate diagnosis of the extent and severity of periodontal disease

B. The periodontal examination

G. Clinical features of gingivitis

1. Overview. Gingivitis is frequently associated with changes in color, contour, and consistency that are due to changes in the levels of inflammation. Color changes are due to increases in blood flow; contour changes are due to increases in inflammatory exudates/edema within the gingival tissues; and the consistency changes are also due to levels of inflammation and/or fibrosis that frequently occurs when gingivitis is long-standing and chronic. Gingival bleeding is also a characteristic of gingivitis and can occur during mastication, tooth brushing, and/or periodontal probing.

Box 7-1 Classification of Periodontal Diseases and Conditions

Data from Armitage GC: Ann Periodontol 4:1, 1999. (From Newman MG, Takei HH, Klokkevold PR, Carranza FA: Carranza’s Clinical Periodontology, ed 10, St Louis, Elsevier, 2006.)

Gingivitis is usually characterized as gingival inflammation in the absence of clinical attachment loss. More recently, gingivitis also has been described in cases of gingival inflammation around teeth that have been successfully treated for periodontitis but have developed gingival inflammation with no additional attachment loss as a result of poor home care.

H. Clinical features of periodontitis

Periodontitis is defined as an inflammatory disease of the supporting tissues of the teeth caused by specific microorganisms or groups of specific microorganisms resulting in progressive destruction of the periodontal ligament and alveolar bone with pocket formation, recession or both. The clinical feature that distinguishes periodontitis from gingivitis is the presence of clinically detectable attachment loss. The most common forms of periodontitis and their distinguishing characteristics are listed in Box 7-2.

Box 7-2 Periodontitis

(From Newman MG, Takei HH, Klokkevold PR, Carranza FA: Carranza’s Clinical Periodontology, ed 10, St Louis, Elsevier, 2006.)

The disease periodontitis can be subclassified into the following three major types based on clinical, radiogra phic, historical, and laboratory characteristics.


G. Microbiology of specific periodontal diseases

H. Characteristics of specific periodontal pathogens

I. Local factors that may promote the accumulation and retention of plaque microorganisms and lead to periodontal disease

Although bacterial plaque is the primary etiologic factor for the initiation of periodontal disease, other factors that may contribute to gingival inflammation include calculus, malocclusion, faulty restorations, complications associated with orthodontic therapy, self-inflicted injuries, use of tobacco, and radiation therapy.

1. Calculus is mineralized bacterial plaque. It forms on natural teeth as well as on prosthetic devices. Precipitation of mineral salts into soft plaque usually starts within 1 to 14 days of plaque formation. The initiation of calcification and rate of calculus formation vary between individuals, within an individual, and for individual teeth. Calculus can be classified as supragingival and subgingival.


The pathogenesis (genesis of pathological change; the cellular events and reactions and other pathological mechanisms occurring in the development of disease) of the periodontal diseases is the result of a complex interaction between plaque microorganisms and the host response to the presence of those microorganisms on tooth and gingival tissues. As outlined in Figure 7-1 of the Overview to this review, microbial plaque is considered to be the initiator of the disease process because it serves as a challenge to the host and host tissues (periodontal tissues). How the host responds to the plaque challenge determines the severity and extent of the tissue damage associated with that response.

D. Characteristics of the host response in periodontal disease

1. Cells of the host response

b. Neutrophils (polymorphonuclear leukocytes; PMNs). These migrate from the blood vessels of the subepithelial vascular plexus into the periodontal pocket where they interact with plaque microorganisms (Fig. 7-3). The primary role of PMNs is to protect the body from infection. However, they are also considered to be an important cell in the destruction of the periodontal tissues. PMNs move from blood vessels toward sites of infection by a process of directed locomotion (chemotaxis) along a gradient of powerful chemotaxins such as C5a, IL-8, LtB4, and the bacterial protein N-fMLP (Table 7-1). PMNs are capable of internalizing microorganisms by a process of phagocytosis and, once internalized, they can kill and digest the microorganisms using a powerful mixture of oxygen radicals (H2O2, O2) and granule enzymes (myeloperoxidase) that form the biological equivalent of commercial bleach (see Fig. 7-3). Abnormalities in neutrophil function (neutropenia, agranulocytosis, Chédiak–Higashi syndrome, Papillon–Lefèvre syndrome, leukocyte adhesion deficiency) make the host more susceptible to infection (Table 7-2).

8. Environmental and systemic factors that may influence the progression of periodontal disease


Tumor necrosis factor (TNF) Macrophages/monocytes
Interleukin-8 (IL-8) Neutrophils (PMNs), endothelium
Platelet-activating factor Leukotriene B4 Many cells
C5a Serum/plasma
Neutrophil chemotactic factor Mast cells
Interleukin-1 (IL-1) B cells, macrophages
Interferon-γ (IFN-γ) Activated T cells
N-formyl-methionyl peptides Bacteria

PMNs, Polymorphonuclear leukocytes.

(From Newman MG, Takei HH, Klokkevold PR, Carranza FA: Carranza’s Clinical Periodontology, ed />

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Jan 5, 2015 | Posted by in General Dentistry | Comments Off on 7: Periodontics
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