Microbiology of periodontal diseases
Periodontal diseases occur in all parts of the world and few individuals live out their natural life span without becoming affected. However, in the majority of individuals, the common chronic inflammatory diseases which involve the gingival and periodontal tissues can be controlled, if not cured, using mechanical cleansing techniques and encouraging good oral hygiene. A small but significant number of patients experience rapidly progressive disease which requires assessment and treatment by periodontologists.While there is no doubt that microorganisms play an important role in the aetiology of most forms of periodontal disease, there is dispute as to whether their involvement is of a specific or non-specific nature. At present, clinical and radiological examination are unable to diagnose active disease or to predict which patients are likely to experience severe progressive periodontitis. Tissue destruction can be recorded with certainty only in a retrospective manner. Therefore, much of the current research in periodontology is directed towards developing laboratory tests which will allow high-risk patients and active disease to be identified early and ensure that subsequent specialized treatment is effective. An area of current interest is AIDS-related periodontal disease which is described in Chapter 16.
The main types of periodontal disease which are believed to have a microbial aetiology are shown in Table 5.1. However, as detailed knowledge about the aetiology of some of these conditions, e.g. chronic periodontitis, becomes available, it is likely that periodontal infections with apparently the same clinical signs and symptoms will turn out to be due to a number of different host–parasite interactions.
|: rapidly progressive|
|Acute herpetic stomatitis|
The term periodontium refers to the anatomical structures involved in resisting forces applied to the teeth, especially the gingivae, periodontal ligament, cementum and alveolar bone. The part of the periodontium which supports the coronal portion of the root is known as the marginal periodontium (Figure 5.1). A detailed description of these tissues and the changes which occur with the onset of disease is outside the scope of this book and students should consult standard periodontology textbooks. While the dentogingival junction is a site of potential weakness, the host defences are able to function effectively as long as oral hygiene is satisfactory (Table 5.2). However, when plaque is allowed to accumulate undisturbed and close to the gingival margin, the host defences become stressed.
|B and T lymphocytes||Polymorphonuclear and mononuclear phagocytes|
|Antibodies: IgG, IgM and IgA||Complement components|
|Enzymes from host|
It is not known why some individuals are more susceptible to periodontal disease than others. One explanation may be related to genetic variations in the biochemical composition or anatomical arrangement of the periodontal tissues among individuals.
Both the specific and non-specific immune responses of the host to subgingival plaque are believed to play important roles in the development, progression and recovery from periodontal diseases. Although specific immune reactions may occur either in the gingival crevice/periodontal pocket, or within the periodontal tissues themselves, non-specific factors usually act in the former sites only.
One of the important components of the host response is the gingival crevicular fluid (GCF) which contains both specific and non-specific factors (Table 5.2). Although it is convenient to describe these factors separately, it is important to remember that in vivo they interact closely, e.g. antibodies can act as opsonins thereby potentiating phagocytic activity. The nature of the non-specific host factors are shown in Table 5.3.
|Host cells||Gingival crevicular fluid|
|Anatomical epithelial seal in the base of the gingival sulcus||Mechanical washing action; tendency to cleanse crevice|
|Rapid repair of junctional epithelium following injury||Antimicrobial factors, e.g. lysozyme|
|Shedding of surface cells with attached bacteria from sulcular epithelium into crevice|
|Phagocytosis together with migration of polymorphonuclear and mononuclear phagocytes through the junctional epithelium|
Although small numbers of polymorphonuclear leucocytes (PMNLs) are present in clinically healthy gingivae, there is a marked increase in numbers during the onset of gingivitis which persists during periodontitis. The PMNLs migrate from venules and enter the gingival sulcus through the junctional epithelial cells. The increased number found in periodontal disease is probably related to the chemotactic activity of complement, low molecular weight peptides and other plaque products.
When PMNLs come in contact with bacteria, phagocytosis begins. The polymorphs attach to and ingest the microbial cell, which becomes bound within the phagosome. The latter then fuses with a proteolytic and hydrolytic enzyme-rich lysosome to form a digestion vacuole, in which microbial killing occurs. In addition, other host-cell-derived killing agents may be involved, e.g. hydrogen peroxide and lactic acid. Although phagocytosis can occur in the absence of antibody, the presence of immunoglobulins and complement enhance the process.
The outcome of the interaction between PMNLs and plaque bacteria may result in either death of the microorganism, death of the leucocytes, or both. After neutrophil autolysis, lysosomal enzymes (e.g. collagenase, hyaluronidase, chondroitin sulphatase, elastase and acid hydrolases) are released around the surrounding host cells and may cause damage to the periodontal tissues.
Therefore, PMNLs may have both a protective and perhaps a damaging effect on host tissues. Patients who have compromised PMNL function due, for example, to agranulocytosis or cyclic neutropenia, usually develop aggressive periodontitis, which tends to support the concept that overall neutrophils are protective. Claims that patients with juvenile periodontitis and rapidly progressive periodontitis have defects in PMNL function should be accepted with caution, due to difficulties in the interpretation of assay results and failure to take into account the variation in values which can occur in the same individual from day to day.
Phagocytosis is probably important in preventing the microbial invasion of the gingival and periodontal connective tissues. However, some microbial antigens have been demonstrated within the periodontal tissues (e.g. Treponema spp, A. actinomycetemcomitans and B. gingivalis), and therefore it is likely that phagocytosis will take place within the host tissues and perhaps also at their interface with subgingival plaque.
Specific IgM, IgG and IgA antibodies to subgingival plaque microorgainsims and some of their metabolites have been demonstrated in GCF. and serum. These antibodies are derived both from serum and from plasma cells in the gingival connective tissues (local antibody formation). The significance of an elevated titre of specific antibody to a periodontopathogen is uncertain at present. Various possibilities have been suggested, for example, that antibodies (1) are protective, (2) are involved in damaging hypersensitivity reactions to the host tissues, and (3) are non-specific and unrelated (i.e. epiphenomena). The presence of antibody suggests that the required T-helper and T-suppressor interactions with B lymphocytes occur satisfactorily in the periodontal tissues. In addition, all the cells required for a wide range of immune reactions have been demonstrated in the gingival tissues of chronic periodontitis patients and are known to possess antigen specificity for plaque bacteria. When stimulated either antibodies (from B lymphocytes) or lymphokines (from T lymphocytes) are produced.
Since antibodies and complement are present in the periodontal tissues, hypersensitivity reactions which could result in damage to host tissues may contribute to periodontal disease. While there is evidence that all four types of hypersensitivity may be involved under certain circumstances, their precise role in pathogenesis or in recovery remains uncertain (Table 5.4).
|Type 1 (anaphylactic)||Type 2 (cytotoxic)||Type 3 (immune complex)||Type 4 (cell-mediated)|
|Antibody-mediated (B lymphocyte)||+a||+b||+b||—|
|Main effector mechanisms||Histamine from mast cell degranulation. Vascular permeability increased||Components from complement activation produce increased vascular permeability, chemotaxis, phagocytosis and cell lysis||Antigen-antibody complexes deposited in tissues, especially blood vessel walls. Components of complement activation produce acute inflammation with possible necrosis||Lymphokines and killer T cells. Accumulation and activation of macrophages, inflammation and possibly bone resorption|
|Possible role in periodontitis||Uncertain||Uncertain||Uncertain||Uncertain|
2. Clinical studies in patients with a healthy periodontium have shown that, if oral hygiene is discontinued, the accumulation of dental plaque which occurs is paralleled by the onset of gingivitis. If plaque is then removed and normal oral hygiene reintroduced, the tissues are restored to health.
The microbial composition of the gingival crevice area in health and disease is shown in Table 5.5. The flora associated with health consists mainly of streptococci and Actinomyces spp. This changes both quantitatively and qualitatively during the development of disease, and differences can be demonstrated in plaque samples from healthy and diseased sites, as well as between different types of periodontal diseases (for details, see below under specific diseases).