Periodontal disease: Wikis


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From Wikipedia, the free encyclopedia

Periodontal diseases are those diseases that affect one or more of the periodontal tissues:

  1. alveolar bone
  2. periodontal ligament
  3. cementum
  4. gingiva

While many different diseases affect the tooth-supporting structures, plaque-induced inflammatory lesions make up the vast majority of periodontal diseases[1] and have traditionally been divided into two categories:[2]

  1. gingivitis or
  2. periodontitis.

While in some sites or individuals, gingivitis never progresses to periodontitis,[3] data indicates that gingivitis always precedes periodontitis.[1]


Historical methods of disease analysis and classification

Investigation into the causes and characteristics of periodontal diseases began in the 18th century with pure clinical observation, and this remained the primary form of investigation well into the 19th century.[4] During this time, the signs and symptoms of periodontal diseases were firmly established:[1]

  1. Rather than a single disease entity, periodontal disease is a combination of multiple disease processes that share a common clinical manifestation.
  2. The etiology (cause) includes both local and systemic factors.
  3. The disease consists of a chronic inflammation associated with loss of alveolar bone.
  4. Advanced disease features include pus and exudates.
  5. Essential aspects of successful treatment of periodontal disease include initial debridement and maintenance of proper oral hygiene.

The advent of microscopy allowed later studies performed at the turn of the 19th century to report the histological structures and features of periodontal lesions, but most were limited to advanced stages of the disease. Progress in microscopy in the 1960's, such as advances in histopathology and stereology, allowed researchers to focus on earlier stages of inflammatory processes while the innovation of experimentally-induced periodontal disease in both human and animal models allowed for more detailed research into the temporal progression of the pathogenesis of plaque-induced periodontal disease.[5]

Historically, chronic plaque-induced periodontal diseases were divided into three categories:[6]

  1. subclinical gingivitis
  2. clinical gingivitis
  3. periodontal breakdown

Modern methods of disease analysis and classification

In 1976, Page & Schroeder introduced an innovative new analysis of periodontal disease based on histopathologic and ultrastructural features of the diseased gingival tissue. Although this new classification does not correlate with clinical signs and symptoms and is admittedly "somewhat arbitrary," it permits a focus of attention on important pathologic aspects of the disease that were, until recently, not well understood.[1] This new classification divided plaque-induced periodontal lesions into four stages:

  1. initial lesion
  2. early lesion
  3. established lesion
  4. advanced lesion

Initial lesion

Unlike most regions of the body, the oral cavity is perpetually populated by pathogenic microorganisms; because there is a constant challenge to the mucosa in the form of these microorganisms and their harmful products, it is difficult to truly characterize the boundary between health and disease activity in the periodontal tissues. As such, the initial lesion is said to merely reflect "enhanced levels of activity" of host response mechanisms "normally operative within the gingival tissues."[1][5][7]

Healthy gingiva are characterized by small numbers of leukocytes migrating towards the gingival sulcus and residing in the junctional epithelium.[5][7] Sparse lymphocytes, and plasma cells in particular, may exist just after exiting small blood vessels deep within the underlying connective tissue of the soft tissue between teeth.[5][7] There is, however, no tissue damage, and the presence of such cells is not considered to be an indication of a pathologic change.

On the contrary, the initial lesion shows increased capillary permeability with "very large numbers" of neutrophils migrating from the dilated gingival plexus into the junctional epithlieum and underlying connective tissue (yet remaining within the confines of the region of the sulcus) and macrophages and lymphocytes may also appear. Loss of perivascular collagen occurs; it is thought that this is due to the degradative enzymes released by extravasating leukocytes, such that the collagen and other connective tissue fibers surrounding blood vessels in the area dissolve.[1][7]

The initial lesion appears within two to four days of gingival tissue being subjected to plaque accumulation. When not generated through clinical experimentation, the initial lesion may not appear at all, and instead, a detectable infiltrate similar to that of the early lesion, explained below, appears.[8]

Features of the Initial Lesion:[1]

Early lesion

While the early lesion is not entirely distinct from the initial lesion, it is said to encompass the inflammatory changes that occur from days four to seven after plaque accumulation has commenced.[7] It is characterized by a matured leukocytic infiltrate that features mainly lymphocytes. Immunoblasts are quite common in the area of infiltration, while plasma cells, if present, are only at the edges of the area.[1] The early lesion can occupy up to 15% of the connective tissue of the marginal gingiva and up to 60-70% of collagen may be dissolved.[9]

Fibroblasts appear altered, exhibiting electron-lucent nuclei, swollen mitochondria, vacuolization of the rough endoplasmic reticulum and rupture of their cell membranes, appearing up to three times the size of normal fibroblasts and found in association with moderately-sized lymphocytes.[9]

The early lesion displays acute exudative inflammation; exudative components and crevicular lymphocytes reach their maximum levels between days 6-12 after plaque accumulates and gingival inflammation commences[6] with the quantity of crevicular fluid being proportional to the size of the reaction site within the underlying connective tissue. The junctional epithelium may even become infiltrated with enough leukocytes so that it resembles a microabscess.[10]

Features of the Early Lesion:[1]

Established lesion

The hallmark of the established lesion if the overwhelming presence of plasma cells in relation to the prior stages of inflammation. Beginning two to three weeks after first plaque formation, the established lesion is widespread in both human and animals populations[11] and can be seen commonly associated with the placement of orthodontic bands on molars.[12]

Similar to the initial and early lesions, the established lesion features an inflammatory reaction confined to the area near the base of the gingival sulcus, but unlike prior stages, displays plasma cells clustered around blood vessels and between collagen fibers outside the immediate area of the reaction site.[1] While most of the plasma cells produce IgG, a significant number do produce IgA (and rarely, some produce IgM).[13] The presence of complement and antigen-antibody complexes is evident throughout the connective and epithelial tissue.[13]

It is in the established lesion that epithelial proliferation and apical migration begin. In health, the junctional epithelium creates the most coronal attachment of the gum tissue to the tooth at or near the cementoenamel junction. In the established lesion of periodontal disease, the connective tissue lying subjacent to the junctional epithelium is nearly destroyed, failing to properly support the epithelium and buttress it against the tooth surface. In response to this, the junctional epithelium proliferates and grows into the vacant underlying spaces, effectively causing the level of its attachment to migrate towards apically, revealing more tooth structure than is normally evident supragingivally (above the level of the gumline) in health.

While many established lesions continue to the advanced lesion (below), most either remain as established lesions for decades or indefinitely; the mechanisms behind this phenomenon are not well understood.

Features of the Established Lesion:[1]

Advanced lesion

Many of the features of the advanced lesion are described clinically rather than histologically:[4]

Because bone loss makes its first appearance in the advanced lesion, it is equated with periodontitis, while the first three lesions are classified as gingivitis in levels of increasing severity.[1]

The advanced lesion is no longer localized to the area around the gingival sulcus but spreads apically as well as laterally around a tooth and perhaps even deep into the gum tissue papilla. There is a dense infiltrate of plasma cells, other lymphocytes and macrophages. The clusters of perivascular plasma cells still appears from the established lesion. Bone is resorbed, producing scarring and fibrous change.[1]

Features of the Advanced Lesion:[1]

Treatment of Periodontal Disease

The treatment of periodontal disease begins with the removal of sub-gingival calculus (tartar). This is commonly addressed by the surgical procedures known as root planing and scaling. These procedures debride calculus by mechanically scraping it from tooth surfaces.

Dental calculus, commonly known as tartar, is comprised almost entirely of calcium phosphate salt, the ionic derivative of calcium phosphate (the primary composition of teeth and bone). As an ion, calculus has lost two electrons and is electrically unstable. Clinically, calculus stuck to teeth appears to be hardened to the point requiring mechanical scraping for removal – it is, however, highly susceptible to micro-dissolving compositions that adhere additionally elections to its matrix and subsequently release calculus components from their electrostatic bonds.

One such product is Periogen, which employs Tetrapotasium Polyphosphate and Sodium Tripolyphosphate in the presence of Sodium Fluoride, which dissolves dental calculus in several weeks of home use.


  1. ^ a b c d e f g h i j k l m n Page, RC; Schroeder, HE. "Pathogenesis of Inflammatory Periodontal Disease: A Summary of Current Work." Lab Invest 1976;34(3):235-249
  2. ^ Armitage, GC. "Periodontal diagnoses and classification of periodontal diseases," Periodontology 2000 2004;34:9-21.
  3. ^ Ammons, WF; Schectma, LR; Page, RC. "Host tissue response in chronic periodontal disease I: The normal periodontium and clinical and anatomic manifestations of periodontal disease in the marmoset." J Perio Res 1972;7:131
  4. ^ a b Riggs, J. "Suppurative inflammation of the gums and absorption of the gums and alveolar process." Penn J Dent Sci 1876;3:99
  5. ^ a b c d Attström, R; Graf-de Beer M; Schroeder, HE. "Clinical and stereologic characteristics of normal gingiva." J Perio Res 1975;10:115
  6. ^ a b Lindhe, J; Hamp, SE; Löe, H. "Experimental periodontitis in the beagle dog." J Perio Res 1973;8:1
  7. ^ a b c d e Payne, WA; Page, RC; Ogilvie, AL; Hall, WB. "Histopathologic features of the initial and early stages of experimental gingivitis in man." J Perio Res 1975;10:51
  8. ^ Listgarten, MA; Ellegaard, B. "Experimental gingivitis in the monkey." J Perio Res 1973;8:199
  9. ^ a b Schroder, HE; Page, RC. "Lymphocyte-fibroblast interaction in the pathogenesis of inflammatory gingival disease." Experientia 1972;28:1228
  10. ^ Schroder, HE. "The structure and relationship of plaque to the hard and soft tissues: electron microscopic interpretation." Int Dent J 1970;20:353
  11. ^ Avery, BE; Simpson, DM. "The baboon as a model for the study of periodontal disease I: Clinical and light microscopic observations." J Perio 1973;44:675
  12. ^ Zachrisson, BW. "Gingival conditions associated with orthodontic treatment II: Histologic findings." Angle Orthod 1972;42:352
  13. ^ a b Genco, RJ; Mashimo, PA; Krygier, G; Ellison, SA. "Antibody-mediated effects on the periodontium." J Perio 1974;45:330


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