Calculus is calcified plaque. The calcification is less significant than the bacterial content which induces inflammation and, later, tissue destruction. However, calculus distorts the gingival crevice and, by extending the stagnation area, probably promotes even greater bacterial proliferation (Fig. 5.5). Supragingival calculus mainly forms opposite the orifices of the major salivary glands in the lower incisor and upper first molar areas. It cannot be removed by the patient and provides a rough, plaque-retentive surface.

Several compounds, such as pyrophosphates, added to dentifrices have been shown to reduce calculus formation to variable degrees. However, any clinical benefit has not been unequivocally established.

Bacterial plaque, a dense mat of bacteria (Box 5.8), extends from the gingival margins into pockets.

Extension and calcification of plaque leads to formation of subgingival calculus within periodontal pockets. The deposits are thin, more widely distributed, harder, darker and more firmly attached than supragingival calculus. Calculus appears laminated histologically, with altered staining, probably due to breakdown products from blood cells oozing into the pockets. Subgingival calculus helps to perpetuate chronic periodontitis. It forms a reservoir of bacteria, helping to sustain inflammation, and acts as a barrier to healing.

Plasma cells typically predominate but are accompanied by lymphocytes and neutrophils which migrate into pockets. Inflammatory cells infiltrate the connective tissue and spread between the principal fibres (Figs 5.9 and 5.10). Dense masses of these cells accumulate, especially under the epithelium in the connective tissue apposed to plaque and calculus.

Pocketing, a characteristic feature of chronic periodontitis, is due to the slower destruction of gingival soft tissues than of periodontal ligament and bone (Fig. 5.11). Less frequently, where gingival tissue is thin, it may be lost at the same rate as the supporting tissues and gingival recession results. Pockets round the teeth provide a protected environment in which bacteria grow more freely. There is no effective drainage and the wall of the pocket presents a large area where bacteria or their products can irritate the tissues. Pockets also favour the growth of anaerobes which probably contribute greatly to tissue destruction.

Pockets surround the teeth. One wall is formed by cementum, the other soft tissue replacing the destroyed bone and periodontal fibres. The outer wall consists of connective tissue infiltrated by chronic inflammatory cells and lined by epithelium continuous with the gingival epithelium at the pocket mouth. The epithelial attachment forms the deep boundary. The epithelium is often hyperplastic, but blood vessels may extend through it almost to its surface.

‘Ulceration’ of the lining is often described but rarely seen histologically.

The epithelial attachment migrates from enamel on to cementum, forming the floor of the pocket (Figs 5.12 and 5.13). The attachment to cementum is strong and a clear refractile cuticle (see Fig. 5.2) can sometimes be seen joining the epithelium to the root surface. The length of the epithelial attachment is variable but may extend several millimetres.

Periodontal fibres are destroyed progressively from the gingival margin down to the level of the floor of the pocket. More deeply, the fibres retain their normal appearance.

Bone destruction starts at the alveolar crest. The usual level of the remaining bone is just deep to the floor of the pocket where the superficial fibres of the periodontal ligament are attached. The zone of inflammation is separated from the underlying bone by a zone of fibrous tissue. This so-called fibrous walling-off is typical of chronic periodontitis and invariably present (see Fig. 5.12). It has been suggested that the inflammatory lesion may extend beyond this to affect the alveolar bone and remaining periodontal ligament during periods of active disease, but histological evidence of this is lacking. Osteoclasts are rarely seen, probably because their action is intermittent and the rate of bone destruction extremely slow.

Confirmation that osteoporosis may be related to premature alveolar bone loss has been handicapped by the difficulties in measuring bone mineral density (BMD) accurately. However, it has been confirmed that diminished bone mineral density, measured by dual X-ray absorptiometry in several parts of the skeleton, showed a highly significant correlation with the thickness of the mandibular alveolar process in the first premolar region.

Other studies have also shown that age-related bone loss is greater in women than men after the age of 50 years. There is also a significant increase in mandibular cortical porosity and concomittant decline in bone mass, with an estimated loss of bone mineral content of 1.5% per year in women, but only 0.9% in men.

With formation of pockets and subgingival plaque there is enormous proliferation of bacteria of all kinds. Subgingival plaque appears to have a dense zone attached to the tooth surface where the bacteria are mainly Gram-positive. By contrast, plaque related to the pocket wall is less densely packed but involves many Gram-negative bacteria, including anaerobes and spirochaetes. Bacteria particularly associated with destructive disease include Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans, B. intermedius, Wolinella recta, spirochaetes with axial filaments, or in other cases Eikenella corrodens, and other corroding bacteria. The latter’s colonies cause pitting (‘corrosion’) of the surface of culture media.

Also present are Fusobacterium nucleatum and as yet unidentified anaerobic vibrios and spirochaetes. Where there is severe and relatively acute bone loss associated with severe inflammation, in young adults, for example, Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis appear to be particularly important. Where inflammation is minimal in spite of extensive bone loss there may be greater numbers of Prevotella melaninogenica and Eikenella corrodens. Many of the bacteria implicated in destructive periodontitis are dangerous pathogens and in other body sites can cause severe or lethal systemic infections. For example, Capnocytophaga ochraceus, Selenomonas sputigena and Eikenella corrodens have been implicated in life-threatening infections, particularly in patients with granulocytopenia.

In human periodontal disease, it remains unclear which particular types of bacteria are responsible for tissue destruction. However, inoculation of specific bacteria into the mouths of germ-free animals has yielded somewhat unexpected results. Thus, various Gram-positive bacteria typically produce large amounts of plaque, but Gram-negative bacteria do not. Certain bacteria of either group can induce or accelerate periodontal tissue damage, but there is typically little inflammation or lymphocytic infiltration of the tissues. In Gram-positive infections also, few osteoclasts are seen. However, A. viscosus in particular produces a bone-resorbing factor. Gram-negative bacteria also stimulate osteoclastic activity and numerous osteoclasts are seen at the sites of tissue destruction.

That individual species of bacteria may be responsible for periodontal tissue destruction is also suggested by the finding in monkeys that the severity of periodontal damage correlates well with the numbers of Porphyromonas gingivalis which can be isolated. Further, antimicrobial treatment that suppressed P. gingivalis led to healing and bone regeneration. Greater numbers of P. gingivalis also appear to be associated with enhanced periodontal disease activity in humans.

Periodontal destruction may result from the actions of bacterial products or indirectly from immunologically mediated processes or both in varying degree. Bacterial products (virulence factors) that may contribute to tissue damage include enzymes, toxins and bone-resorbing factors.

Other virulence factors act by interfering with host defences. Substances cytotoxic for human leucocytes (leukotoxins) are produced by A. actinomycetemcomitans in particular. This bacterium is involved in juvenile periodontitis and can also cause osteomyelitis and infective endocarditis in humans. Other bacterial factors potentially capable of damaging host defences are immunoglobulin proteases. Neisseria gonorrhoeae can produce IgA proteases which help it overcome mucosal defences and contribut/>