7 Periodontics
OVERVIEW
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.
1.0 DIAGNOSIS
A. Components of an accurate diagnosis of the extent and severity of periodontal disease
1. Medical history, including any serious familial conditions of parents or siblings such as diabetes or cardiovascular disease, and history of tobacco use.
5. Oral examination of the periodontal structures for the presence of plaque (an assessment of the patient’s level of home care); inflammation (redness, swelling, bleeding on probing); and destruction of the periodontal tissues (probing pocket depths, clinical attachment levels, tooth mobility, furcation involvement).
6. Notes should be made of areas of suppuration, abscess formation, minimal width of attached gingival (subtract pocket depth from width of gingiva), obvious recession, and areas of trauma from occlusion.
7. An examination of the teeth for dental caries, developmental defects, anomalies of tooth form, wasting, areas of hypersensitivity, and proximal contact relationships. This may include any of the following:
a. Erosion (sometimes called corrosion): usually in the cervical area of facial surface of tooth. May be caused by acid beverages or citrus fruits.
b. Abrasion: loss of tooth substance by mechanical wear. Horizontal toothbrushing (scrubbing) with an abrasive dentifrice is the most common cause.
c. Attrition: occlusal wear due to functional contacts with opposing teeth. Results in wear facets on the occlusal surfaces of teeth. May be due to functional or parafunctional habits.
B. The periodontal examination
1. Probing pocket depth (the distance from the gingival margin to the base of the pocket detected with the probe); clinical attachment loss (the distance from the cementoenamel junction [CEJ] to the base of the pocket detected with a periodontal probe); and bleeding on probing (a measure of inflammation in the periodontal tissues) are the most objective of periodontal measures and enable the clinician to differentiate between gingivitis and periodontitis.
2. Additional measures that can be made include gingival recession (exposure of the root surface due to an apical shift in the position of the gingival margin). Recession is measured from the CEJ to the crest of the marginal gingiva and is associated with attachment loss. This may be enhanced by trauma from toothbrushing, teeth that are positioned or have been moved buccally with orthodontics, or teeth that are large compared to the width of the periodontal supporting tissues.
3. Alveolar bone loss is frequently used as a measure of periodontal disease from examination of x-rays. This is not a reliable measure of periodontal disease because there is considerable variability in the normal height of the alveolar bone. Bone loss on x-rays should be evaluated in combination with probing pocket depth and attachment loss to provide an accurate measure of a patient’s periodontal status. Bone loss may be described as horizontal or vertical.
4. Suppuration is an important measure of the inflammatory response to periodontal infection because it is due to the presence of large numbers of neutrophils in the periodontal pocket. Suppuration from the pocket may be seen during periodontal probing or by palpation of the pocket wall. These areas should be aggressively treated to reduce the microbial challenge. Suppuration may be frequently seen in patients with severe disease or patients who have a systemic condition that alters the ability of the host to deal with infection.
C. Radiographic assessment
1. Bone loss on traditional x-rays. The average distance from the CEJ to the crest of the alveolar bone in health is approximately 2 mm. The normal angulation of the crest of the alveolar bone is parallel to a line joining the CEJs of adjacent teeth. A horizontal pattern of bone loss occurs parallel to this line. Angular bone loss is usually created when bone is lost on one tooth surface at a greater rate and greater extent than on an adjacent tooth surface. A full mouth series of periapical radiographs is recommended to visualize all proximal root surfaces and bone levels.
2. Digital and subtraction radiography. Digital radiography allows for computerized images to be stored and corrected for exposure. Digital radiography may reduce exposure to radiation compared to traditional x-rays. Using serial x-rays of teeth and bone taken at the same location and angulation, changes in bone density can be observed using a computerized technique known as subtraction radiography. Changes in bone density may be associated with disease progression.
E. Furcation assessment
The complex anatomy of the furcation makes this a difficult area to treat and maintain.
2. Factors involved. Factors that can predispose a tooth to furcation involvement include short root trunk length, short roots, and narrow inter-radicular dimension. The presence of cervical enamel projections into the furcation also can be a predisposing factor.
3. Probing. Furcations in mandibular molars are probed from the buccal/facial and from the lingual. Furcations in maxillary molars are probed from the mesial (mesial furcation between mesio-buccal and palatal roots), buccal (buccal furcation between the two buccal roots), and distal (distal furcation between disto-buccal and palatal roots).
F. Summarizing clinical findings
Using the information described previously, the clinician can now diagnose one of the following conditions (Box 7-1):
3. Periodontitis (periodontal inflammation that has extended into the periodontal ligament and alveolar bone, resulting in loss of clinical attachment and alveolar bone; usually accompanied by increased probing pocket depths, although deep pockets may not be present if recession of the gingival margin occurs at the same rate as attachment loss).
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.)
Developmental or Acquired Deformities and Conditions
Localized tooth-related factors that predispose to plaque-induced gingival diseases or periodontitis
Mucogingival deformities and conditions around teeth
Mucogingival deformities and conditions on edentulous ridges
* These diseases may occur on a periodontium with no attachment loss or on a periodontium with attachment loss that is stable and not progressing.
† Chronic periodontitis can be further classified based on extent and severity. As a general guide, extent can be characterized as localized (<30% of sites involved) or generalized (>30% of sites involved). Severity can be characterized based on the amount of clinical attachment loss (CAL) as follows: slight = 1 or 2 mm CAL; moderate = 3 or 4 mm CAL; and severe ≥ 5 mm CAL.
2. Plaque-induced gingivitis. The most common form of gingivitis is the result of an interaction between plaque bacteria and the tissues and inflammatory cells of the host. The severity and duration of the response can be altered by local and systemic factors that can affect plaque formation/retention and the host response.
a. Gingival diseases modified by systemic factors. Systemic factors that alter the magnitude or duration of the host response will impact the clinical appearance of gingivitis. Examples include endocrine changes during puberty, pregnancy, and diabetes. Blood dyscrasias (such as leukemia) may impact the immune response through their effects on white blood cells.
3. Non-plaque-induced gingival conditions. Gingival conditions, although not common, can occur in response to specific infections.
b. Gingival conditions may also be hereditary (hereditary gingival fibromatosis) or the result of allergies to common foods, restorative materials, toothpastes/mouth rinses, and chewing gum.
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.
1. The necrotizing periodontal diseases. The clinical appearance of the necrotizing diseases is unique among the periodontal diseases because of the characteristic ulceration and necrosis of the marginal gingival. This may be covered by a yellowish white or grayish slough or pseudomembrane and have blunting of the papillae, bleeding on provocation or spontaneous bleeding, pain, and fetid breath. The disease may present as necrotizing ulcerative gingivitis (NUG; no attachment loss) or necrotizing ulcerative periodontitis (NUP; with attachment and bone loss). Predisposing factors may be stress, smoking, and immunosuppression such as seen with human immunodeficiency virus (HIV) infection.
2. Abscesses of the periodontium. A localized purulent infection defined by its tissue of origin: gingival abscess or periodontal abscess. Frequent causes are impaction of food such as fish bones or popcorn into the periodontal tissues. An abscess may also be caused by suppuration from a periodontal pocket being unable to discharge through the pocket into the mouth and therefore draining into the periodontal supporting tissues, causing swelling and possible pain.
3. Periodontitis associated with endodontic lesions. These may be endodontic-periodontal lesions (pulpal necrosis leading to periodontal problems as pus drains through the periodontal ligament); periodontal-endodontic lesions (bacterial infection from a periodontal pocket spreads to the pulp causing pulpal necrosis); or a combined lesion (pulpal and periodontal necrosis occurring together). See Figure 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.)
Chronic Periodontitis
The following characteristics are common to patients with chronic periodontitis:
Aggressive Periodontitis
The following characteristics are common to patients with aggressive periodontitis:
Localized form:
2.0 ETIOLOGY
A. Periodontal microbiology
c. The major organic constituents of the plaque biofilm are polysaccharides, proteins, glycoproteins, and lipids. The major inorganic constituents are calcium and phosphorous with trace amounts of sodium, potassium, and fluoride. Saliva is the main source of inorganic components in supragingival plaque, whereas those in subgingival plaque are derived primarily from the gingival crevicular fluid.
B. Dental plaque formation
Plaque formation can be divided into three phases:
1. The first phase is formation of the pellicle, which occurs within seconds after the tooth surface is cleaned. The pellicle consists of glycoproteins (mucins), proline-rich proteins, phosphoproteins (e.g., statherin), histidine-rich proteins, enzymes (e.g., amylase), and other molecules that serve as attachment sites for bacteria.
2. The second phase is the initial adhesion and attachment of bacteria. The initial adhesion is reversible and is mediated through van der Waals and electrostatic forces. After initial adhesion, a firm attachment is established that is dependent upon specific adhesion–receptor interactions.
3. The third phase is colonization and plaque maturation. This occurs when the firmly attached bacteria start growing, resulting in the formation of microcolonies.
C. Dental plaque as a complex bacterial biofilm
1. Overview. Dental plaque is a biofilm composed of microcolonies encased in a polysaccharide matrix. Fluid-filled channels run through the plaque mass, permitting the passage of nutrients. Bacteria growing in a biofilm are more resistant to antimicrobials than those grown in a planktonic, or free-swimming form. Bacteria grown in biofilms communicate with each other through quorum sensing. Quorum sensing is important in the regulation of expression of specific genes.
2. Maturation. As the biofilm matures, there is a shift from a predominance of facultative, gram-positive microorganisms to gram-negative, anaerobic microorganisms.
3. Complexes. Results of DNA-DNA hybridization studies (“checkerboard” analyses) have led to the identification of complexes of periodontal micro-organisms that were given color designations.
a. The so-called red complex (P. gingivalis, Tannerella forsythia, and Treponema denticola) is associated with bleeding on probing and deeper pockets.
F. Plaque hypotheses in the initiation of periodontal disease
1. The nonspecific plaque hypothesis states that periodontal disease results from the elaboration of noxious products by the plaque biomass, indicating that the quantity of plaque is of most importance in the initiation of disease. This hypothesis is contradicted by the finding that some patients with little plaque have severe periodontitis.
G. Microbiology of specific periodontal diseases
1. Periodontal health. The microflora associated with periodontal health is primarily composed of gram-positive facultative cocci and rods. These microorganisms are primarily of the genera Streptococcus and Actinomyces.
2. Gingivitis. The microflora associated with gingivitis was assessed in a classic model system referred to as experimental gingivitis. In this model, periodontal health is established by professional cleaning and personal oral hygiene measures. This is followed by a 21-day period of abstinence from all oral hygiene measures. The initial microbiota is composed of gram-positive rods and cocci and gram-negative cocci. In the transition to gingivitis, gram-negative rods and filaments appear, followed by spirochetal and motile microorganisms.
3. Chronic periodontitis. The microflora of chronic periodontitis is composed predominantly of gram-negative, anaerobic species. The species most often includes P. gingivalis, T. forsythia, P. intermedia, Campylobacter rectus, Eikenella corrodens, F. nucleatum, Actinobacillus actinomycetemcomitans, Peptostreptococcus micros, and Treponema and Eubacterium species. There also is recent evidence that the herpes virus microorganisms, Epstein–Barr virus 1, and human cytomegalovirus, are associated with chronic periodontitis and the presence of P. gingivalis, T. forsythia, P. intermedia, and Treponema denticola.
4. Aggressive periodontitis. A. actinomycetemcomitans is generally accepted as the primary etiological agent of localized aggressive periodontitis. Other associated microorganisms include P. gingivalis, E. corrodens, C. rectus, F. nucleatum, B. capillus, Eubacterium brachy, Capnocytophaga species, and spirochetes.
5. Necrotizing diseases. High levels of P. intermedia, spirochetes, and Fusobacterium species are found in the necrotizing periodontal diseases.
6. Periodontal abscesses. Microorganisms associated with abscesses of the periodontium include F. nucleatum, P. intermedia, P. gingivalis, P. micros, and T. forsythia.
7. Dental implants. Healthy sulci around dental implants are characterized by a predominance of coccoid, aerobic species with a low number of gram-negative anaerobic species. In contrast, the pockets associated with peri-implantitis are colonized by high proportions of anaerobic, gram-negative rods, motile microorganisms, and spirochetes. They also may be colonized by other species such as Pseudomonas aeruginosa, Candida albicans, and Staphylococci.
H. Characteristics of specific periodontal pathogens
1. Actinobacillus actinomycetemcomitans is a nonmotile, gram-negative straight or curved rod. There are five serotypes based on polysaccharide composition. It grows as smooth, white, nonhemolytic colonies on blood agar plates. It is capnophilic, meaning it grows well in a CO2 environment (5%–10%). It is most closely associated with localized aggressive periodontitis. Specific virulence factors include:
2. Tannerella forsythia is a nonmotile, gram-negative pleomorphic rod. It grows slowly only under anaerobic conditions and requires specific growth factors such as N-acetylmuramic acid. Specific virulence factors include proteolytic enzymes that cleave immunoglobulins and complement components. It is a member of the red complex of bacteria.
3. Porphyromonas gingivalis is a nonmotile, gram-negative pleomorphic rod. It grows anaerobically and becomes darkly pigmented on blood agar plates. It also can invade epithelial and endothelial cells. It is most closely associated with chronic periodontitis and is a member of the red complex of bacteria.
4. Prevotella intermedia and Prevotella nigrescens are both nonmotile, gram-negative, rods. They grow anaerobically and become darkly pigmented when grown on blood agar plates. P. intermedia is most closely associated with pregnancy gingivitis and necrotizing periodontal diseases.
5. Campylobacter rectus is a motile, gram-negative rod that has a polar flagellum. It grows anaerobically and grows as a pigmented colony when sulfide is added to the medium.
6. Fusobacterium nucleatum is a nonmotile, gram-negative bacillus that has pointed ends. It grows anaerobically. Specific virulence properties include induction of apoptotic cell death in mononuclear and polymorphonuclear cells, and release of tissue-damaging substances from leukocytes. F. nucleatum can be found in both healthy and diseased patients. F. nucleatum is considered to be an important bridging microorganism between early and late colonizers of dental plaque.
7. Spirochetes are motile, gram-negative spiral micro-organism. Those most often associated with periodontal diseases include Treponema denticola, T. vincentii, and T. socranskii. They are difficult to grow and require strict anaerobic conditions. Specific pathogenic properties include penetration of epithelium and connective tissue and production of proteolytic enzymes that can degrade collagen and destroy immunoglobulins and complement factors. Oral treponemes are closely associated with necrotizing periodontal diseases. T. denticola is a red complex bacterium.
I. Local factors that may promote the accumulation and retention of plaque microorganisms and lead to periodontal disease
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.
a. Supragingival calculus is often white in color, unless stained by food and tobacco products. Between 70% and 90% of supragingival calculus is composed of the inorganic components, calcium phosphate (75%), calcium carbonate (3%), and traces of magnesium phosphate and other metals. The majority of the inorganic component of calculus is crystalline in structure. The main crystal forms are hydroxyapatite (58%), magnesium whitlockite (21%), octacalcium phosphate (12%), and brushite (9%). Saliva is the primary source of substances important in the mineralization of supragingival calculus. Due to the proximity of Wharton’s and Bartholin’s ducts, and Stensen’s duct, supragingival calculus commonly forms on the lingual surfaces of mandibular anterior teeth and buccal surfaces of maxillary molars.
b. Subgingival calculus is often dark due to exposure to gingival crevicular fluid. The composition is similar to supragingival calculus. However, the components important in mineralization are derived from the gingival crevicular fluid rather than saliva.
c. The organic component of calculus is composed of a mixture of protein-polysaccharide complexes, desquamated epithelial cells, leukocytes, and microorganisms.
e. The two proposed mechanisms by which plaque becomes mineralized are:
(1) A local rise in the degree of saturation of calcium and phosphate ions, potentially due to an increase in pH of saliva and binding of calcium and phosphate ions into colloidal proteins in saliva, which ultimately leads to a precipitation of calcium phosphate salts.
(2) The induction of small foci of calcification due to the presence of seeding agents such as the intercellular matrix of plaque. This second mechanism is known as the epitactic concept or heterogeneous nucleation. Mineralization starts extracellularly around both gram-positive and gram-negative microorganisms, although Bacterionema and Veillonella species can form intracellular hydroxyapatite crystals.
2. Materia alba is a concentration of microorganisms, salivary proteins and lipids, desquamated epithelial cells, and leukocytes that is less adherent than dental plaque. The presence of bacteria may lead to materia alba serving as an irritant to gingival tissues.
3. Stains on the teeth are primarily an aesthetic concern as they do not contribute to gingival inflammation.
4. Malocclusion, manifest as irregular alignment of the teeth, may create plaque retentive areas and make plaque removal more difficult. Roots of teeth that are prominent in the arch or that are associated with frenum attachments often exhibit gingival recession. Mesial drift and/or extrusion associated with failure to replace missing teeth may result in occlusal problems that contribute to food impaction and plaque retention.
5. Faulty restorations, manifest by overhanging margins, rough surfaces, open margins, open contacts, and overcontoured crowns may create an environment conducive to plaque retention. This is especially detrimental when the faulty restoration is located subgingivally, where a niche is created for the growth of disease-associated microorganisms and plaque removal is difficult.
6. Subgingival margins, even when not faulty, are associated with plaque accumulation, gingival inflammation, and deeper pockets. Well-contoured supragingival margins have little detrimental effect on the periodontium.
7. Removable partial dentures may result in increased mobility of abutment teeth and increased plaque accumulation.
8. Orthodontic therapy has been shown to increase plaque retention and to result in increases in the numbers of Prevotella melaninogenica, P. intermedia, and Actinomyces odontolyticus. It also can lead to direct damage of gingival tissues and the creation of excessive forces on the periodontium. These factors may be of most importance in adult patients undergoing orthodontic therapy. In all cases, periodontal health should be established prior to initiating orthodontic therapy.
9. Self-inflicted injuries, such as improper tooth brushing, improper use of toothpicks, application of fingernail pressure against gingival tissues, and application of caustic agents against the gingival tissues (e.g., aspirin) can damage gingival tissues.
3.0 PATHOGENESIS
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.
A. Periodontal health. In periodontal health there is insufficient plaque challenge to elicit an inflammatory response that is clinically visible as a change in color, contour, or consistency of the gingival tissues. When clinically healthy periodontal tissues are viewed by histology, there is usually some degree of gingival inflammation present. Perfect periodontal health is nearly impossible to achieve due to our inability to completely remove plaque from tooth and gingival surfaces. The lack of plaque challenge can be due to:
B. Gingivitis. The pathological changes observed in gingivitis are characterized by changes in color, contour, and consistency of the gingival tissues that are frequently associated with increased redness, swelling, and bleeding on probing. These clinical and histological changes are due to the presence of an increased inflammatory response that extends into and destroys cells and matrices of the gingival tissues but does not result in destruction of periodontal ligament and bone. The pathology associated with gingivitis is completely reversible with the removal of plaque and the resolution of the inflammation.
C. Periodontitis. The pathological changes in periodontitis are the same as those that occur in gingivitis except that the inflammation and tissue destruction extend from the gingival tissues into the periodontal ligament and alveolar bone, resulting in an irreversible destruction of periodontal tissues. The extent and severity of periodontal destruction reflects the extent and severity of the inflammatory process.
The extent and severity of the inflammatory response can be influenced by:
1. The failure to remove plaque from tooth and gingival surfaces, resulting in a chronic challenge to the host.
D. Characteristics of the host response in periodontal disease
1. Cells of the host response
a. Overview. Neutrophils, monocytes/macrophages, mast cells, and dendritic cells are considered to be cells of the innate immune response that is with us and protects us from birth.
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).
c. Monocytes/macrophages. Monocytes are also part of the leukocyte family but live much longer in the tissues than neutrophils. They are responsible for ingesting antigens (such as bacteria) and presenting them to the cells of the specific immune response. They are also very important in regulating the immune response through the release of chemical signals called cytokines.
d. Mast cells are important in immediate inflammation and are responsible for creating vascular permeability and dilation. They are important cells in anaphylaxis and allergic responses.
e. Dendritic cells are distributed throughout the tissues and are important in antigen processing and presentation to cells of the specific immune response.
f. Lymphocytes. The predominant lymphocytes are B cells and T cells. B cells differentiate into plasma cells and are responsible for the production of antibodies. T cells (derived from the thymus) fall into two major groups: T-helper cells (CD4 cells), which help in the production of antigen specific antibodies by B cells and plasma cells, and T-cytotoxic cells (CD8 cells), which are important in controlling intracellular antigens such as bacteria, fungi, and viruses. Natural killer (NK) cells are T cells that can recognize and kill tumor and virally infected cells.
2. Controlling the bacterial challenge. Neutrophils (PMNs) are the most important cells involved in controlling the bacterial challenge. They migrate from blood vessels under the gingival epithelium (subepithelial vascular plexus), into the periodontal pocket, where they form a barrier to protect the body from periodontal bacteria. They phagocytose and kill bacteria and also release large quantities of oxygen radicals and enzymes (myeloperoxidase, lysozyme, collagenase) into the extracellular environment.
3. Tissue destruction in periodontal disease. Periodontal cells and tissues are destroyed by cells and proteins of the immune response. Matrix metalloproteinases (MMPs) are considered the most important proteinases involved in the destruction of periodontal tissues. They are produced by most cells of the periodontal tissues, but PMNs produce large quantities of MMP-8 (collagenase) that is responsible for destroying collagen of the periodontal connective tissues and periodontal ligament. Oxygen radicals (superoxide and hydrogen peroxide) produced by inflammatory cells (PMNs and macrophages) are also toxic to cells of the periodontium having a direct effect on cell functions and DNA.
4. Cytokines are important signaling molecules released from cells. The cytokine IL-1 is important in bone resorption; IL-8 is important in attracting inflammatory cells (chemotactic); and tumor necrosis factor (TNF) is important in activating macrophages.
5. Prostaglandins are produced from arachidonic acid of cells membranes in response to cyclo-oxygenases (COX-1 and COX-2). They have widespread proinflammatory effects but can be inhibited by nonsteroidal anti-inflammatory drugs (aspirin and other NSAIDs).
6. Pathogenesis of gingivitis. The development of gingivitis from healthy tissues is characterized in three stages (Table 7-3):
a. Stage 1. Initial lesion: 2 to 4 days with vascular dilation, infiltration of PMNs, perivascular collagen loss, and increased gingival crevicular fluid flow.
b. Stage 2. Early lesion: 4 to 7 days with increase in vasculature, lymphocyte infiltration, increased collagen loss, and redness and bleeding on probing.
7. Pathogenesis of periodontitis. There are few differences between Stage 3 of gingivitis and the destructive lesion of periodontitis, except that the inflammatory lesion becomes bigger and moves into the periodontal ligament and bone. The severity and extent of periodontal destruction is determined by the magnitude and duration of the inflammatory response. With increased severity of the response, there is an increase in the release of the tissue destructive MMPs and proinflammatory cytokines listed above. Risk factors such as smoking, diabetes, and genetic susceptibility to an enhanced or diminished host response may impact the extent and severity of the host response (Fig. 7-4).
8. Environmental and systemic factors that may influence the progression of periodontal disease
| CHEMOTAXIN | SOURCE |
|---|---|
| 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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