Chapter 33 Microbiology of periodontal disease
Periodontal diseases can be defined as disorders of supporting structures of the teeth, including the gingivae, periodontal ligament and supporting alveolar bone. Everyone suffers from various degrees of periodontal disease at some point, and it is one of the major diseases afflicting humankind. However, in most people, the common chronic inflammatory diseases involving the periodontal tissues can be controlled, using mechanical cleansing techniques and good oral hygiene. A minority experience rapid progressive disease that requires assessment and management by periodontists.
Periodontal disease can be broadly categorized into gingivitis and periodontitis. These are yet again subdivided into numerous categories; a recent classification of periodontal diseases is given in Table 33.1. It should be noted that there is no universally acknowledged classification of periodontal disease and the clinical descriptors used relate to:
A Dental plaque-induced gingival diseases
2 Gingival disease modified by systemic factors (e.g. puberty-associated gingivitis, pregnancy-associated gingivitis)
B Non-plaque-induced gingival lesions
The healthy gingival crevice is a unique environment created by a mineralized structure, the tooth, that is part embedded in the connective tissue and part exposed to the oral environment. The gingival crevice is more anaerobic than most locales of the mouth and is constantly bathed by the gingival crevicular fluid (GCF) and its humoural and cellular defence factors, including polymorphs. Dramatic changes ensue during the transition of the crevice into a periodontal pocket. The oxygen tension or Eh falls further and becomes highly anaerobic and the flow of GCF increases. The mostly proteolytic bacteria living in the periodontal pocket raise the pH to alkaline levels (pH 7.4–7.8; compared with neutral values in health), which in turn promotes the growth of bacteria such as Porphyromonas gingivalis.
The exposed cemental surface of the tooth is first colonized mainly by pioneer dwellers, including streptococci and Actinomyces spp. Secondary colonizers such as Prevotella and Porphyromonas spp. can adhere to this layer of cells by coaggregation. Others, such as Peptostreptococcus micros, can adhere to the crevicular epithelium. Thus, the inhabitants and the ecology of a deep periodontal pocket are markedly different from that of the gingival crevice.
The periodontium comprises the gingivae, periodontal ligament, cementum and alveolar bone (Fig. 33.1). Although the dentogingival junction is perhaps the most vulnerable site for microbial attack, it is not breached as long as oral hygiene is satisfactory. However, when plaque accumulates close to the gingival margin, the host defences are overcome, and gingival inflammation (gingivitis) and subsequent periodontal inflammation with loss of attachment ensue (periodontitis).
Fig. 33.1 The progression of a marginal periodontium from health to disease. (1) A healthy gingival sulcus with minimal supragingival plaque. (2) Established chronic gingivitis with minor inflammatory enlargement. (3) Long-standing chronic gingivitis with subgingival plaque extension into the pocket. (4) Chronic periodontitis with destruction of the periodontal membrane, alveolar bone loss and apical migration of the epithelial attachment.
Both the specific and non-specific immune responses of the host to subgingival plaque are considered to play critical roles in the initiation, progression and recovery from periodontal diseases. One of the most important components of the host response is the GCF, which contains both specific and non-specific defence factors (Table 33.2).
|B and T lymphocytes||Polymorphs|
|Antibodies: IgG, IgA, IgM||Complement system|
IgG, immunoglobulin G.
Clinically healthy gingiva contain small numbers of polymorphonuclear leukocytes (PMNLs). Their numbers increase markedly during the onset of gingivitis and periodontitis. The PMNLs migrate from venules and enter the gingival sulcus through the junctional epithelial cells. When PMNLs encounter bacteria, phagocytosis ensues, and the ingested organisms are then killed with a combination of proteolytic and hydrolytic enzymes, and other cell-derived killing agents such as hydrogen peroxide and lactic acid. Although phagocytosis can occur in the absence of antibody, the presence of immunoglobulins and complement enhances the process. The interaction between PMNLs and plaque bacteria may result in:
Thus, PMNLs may have both a protective and a damaging effect on host tissues. Phagocytosis, which may occur within the host tissues and possibly at the interface with subgingival plaque, is important in preventing the microbial ingress into the tissues.
The presence of antibody implies that the T cell (helper and suppressor) and B cell interactions occur in periodontal tissues. Cells required for a wide range of immune reactions, present in gingival tissues of periodontitis patients, possess antigen specificity for plaque bacteria. When stimulated, either antibodies (from B lymphocytes) or lymphokines (from T lymphocytes) are produced.
Antibodies and complement present in the periodontal tissues interact to produce hypersensitivity reactions, which may damage host tissues and also contribute to periodontal disease. There is evidence that all four types of hypersensitivity may be involved in the pathogenesis of periodontal disease.
As most of the periodontal plaque flora is anaerobic, special care must be taken to preserve the viability of these organisms during sampling, dispersion and cultivation of plaque samples. Ideally, the sample should be taken from the advancing front of the lesion at the base of the pocket, although in practice, this is difficult because of contaminants from the superficial plaque at the top of the pocket. The techniques involved in microbiological studies of pocket flora include:
Although bacteria are definitive agents of periodontal diseases, there are conflicting views as to whether a single or a limited number of species are involved in the disease process – the specific plaque hypothesis – or disease is caused by any combination of a wider range of non-specific bacteria – the non-specific plaque hypothesis.
In certain disease states such as necrotizing ulcerative gingivitis, the key aetiological agents are fusobacteria and spirochaetes. Furthermore, this disease can be resolved by appropriate antibiotics active against anaerobes (e.g. metronidazole). Other studies have convincingly shown the direct involvement of Aggregatibacter actinomycetemcomitans in aggressive (juvenile) periodontitis, and disease resolution after therapy with tetracycline, which is active against this organism. These observations led to the theory of specific plaque hypothesis.
This hypothesis proposes that collective groups or consortia of different bacteria have the total complement of virulence factors required for periodontal tissue destruction and that some bacteria can substitute for others absent from the pathogenic consortium. This hypothesis implies that plaque will cause disease irrespective of its composition, and it is supported by the clinical findings of numerous bacterial species in diseased periodontal pockets.
This simple yet elegant hypothesis implies that periodontal disease is an endogenous or an opportunistic infection, caused by an imbalance in the composition of the resident microflora at a site, owing to an alteration in the ecology of the local habitat (Fig. 33.2).
The non-specific plaque hypothesis and the ecology hypothesis imply that periodontal disease may be treated by reducing the plaque to an acceptable level and the maintenance of healthy plaque, or by achievement of total plaque control. In contrast, the specific plaque hypothesis implies that therapy should be directed at elimination of specific pathogens, for instance, by appropriate antibiotic therapy.
Healthy gingival sulcus has a scant flora dominated by almost equal proportions of Gram-positive and facultative anaerobic organisms; spirochaetes and motile rods make up less than 5% of the organisms (Table 33.3). With increasing severity of disease, the proportions of strict anaerobic, Gram-negative and motile organisms increase significantly (Fig. 33.3).
|Health||Streptococcus sanguinis (previously Streptococcus sanguis)||Mainly Gram-positive cocci with few spirochaetes or motile rods|