The junctional epithelium forms a cuff of attachment around the tooth and is therefore of key importance as a barrier to the entrance of bacteria down the tooth surface and into the periodontium. We have seen the value of rapid turnover in epithelia, which allows regular shedding of the surface cells, along with any organisms that have obtained a foothold. The junctional epithelium exploits this process and turns over in just 4 to 6 days (in marmosets). The cells are not shed against the tooth surface but migrate through the layers above and emerge at the junction of the tooth and gingival sulcus. The junctional epithelium exploits other features of its structure to control the microorganism of dental plaque. The individual cells are not held close together (fewer desmosomes), and this allows neutrophil leukocytes to patrol in between the cells. Lymphocytes and monocytes may also occasionally be seen in the junctional epithelium. They are seen in much greater numbers if the gingiva becomes inflamed. Lastly, to help sweep away and disable microorganisms invading the junctional epithelium, a fluid exudate flows between the cells of the junctional epithelium and emerges into the gingival crevice (see Chapter 4.2.4 Gingival Crevicular Fluid).
Fig. 3.12 A diagrammatic representation of the junctional epithelium. The basal cells are attached to the external basement lamina (EBL) by hemidesmosomes. The inner basement lamina (IBL) forms the epithelial attachment to enamel, also via hemidesmosomes. The central cells of the epithelium are loosely attached and allow gingival fluid to flow outward into the gingival sulcus. C, cementum; D, dentin; E, enamel; l-break/>LP, lamina propria.
If the junctional epithelium is surgically removed, a new junctional epithelium forms and attaches to the tooth. It is presumably derived from the epithelium of the sulcus.
3.7.1 Loss of Epithelial Attachment
If plaque accumulates on subgingival surfaces of the tooth, there is a shift in the balance of microorganisms toward more gram-negative organisms which are anaerobic and proteolytic. They are capable of penetrating into the gingival lamina propria and junctional epithelium where they break down collagen and other proteins. They produce endotoxins to which the immune system responds with an infiltration of neutrophils into the damaged epithelium and submucosa. The neutrophils engulf the bacteria which are then killed by enzymes inside lysosomes within the cell. The neutrophil may itself die and break up releasing the toxic content of lysosomes into the tissue which do further damage. A colorful metaphor describes this situation, as a battlefield littered with and polluted by the dead, both defending soldiers and enemy. The initial clinical manifestation of this shift in the dominance of some organisms is inflammation, redness, and swelling of the marginal gingiva. If a periodontal probe is inserted into the gingival sulcus, light bleeding occurs. This sign, bleeding on probing, is an important marker of gingivitis.
The breakdown of the junctional epithelium causes loss of its hemidesmosomal attachment to enamel. Loss of attachment is not readily recovered. It may allow progress of pathogenic bacteria into the periodontal ligament and damage the periodontal ligament and surrounding bone. The clinical manifestation of this progression is the presence of a pocket between the tooth and the periodontium (▶ Fig. 3.13). If the depth of the gingival sulcus is now measured, an increase beyond the normal 2 mm may be found. Deep pockets of over 4-mm depth indicate some loss of bone height and may lead to tooth mobility and eventual tooth loss.
Fig. 3.13 A diagrammatic representation of loss of epithelial attachment to the tooth and the development of a pocket with loss of periodontal ligament attachment to cementum. There has been bone loss from the crest of the alveolar bone. The junctional epithelium has grown down into the pocket preventing reattachment of periodontal fibers.
The oral bacteria associated with the development of inflammation in the periodontium are thought to be a consortium of organisms, which interact to cause periodontal disease together. They include Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia (see Chapter 4.3.6 From Symbiont to Pathobiont).
3.7.2 Influence of Female Hormones
At puberty, the ovaries begin a cyclic production of estrogen and progesterone in response to secretion of gonadotrophic hormones from the pituitary gland. The main functions of these hormones are the control of the menstrual cycle. However, they also affect many other parts of the body including the oral cavity. The early teens are associated with an increase in gingival bleeding. It can be demonstrated that this is the result of an increase in a number of bacteria known to cause gingivitis. These include gram-negative anaerobes such as members of the consortium already described and include Prevotella intermedia. The increase in these bacteria may be due to their ability to use estrogen and progesterone as substitutes for vitamin K, an essential growth factor.
During pregnancy, there is a sustained increase in both estrogen and progesterone levels, above even the cyclic peaks which occur just before the end of each menstrual cycle. The changes in the oral cavity during pregnancy are therefore more pronounced and common. In addition to the effect on bacteria already mentioned, there are vascular, cellular, and immune changes which are collectively responsible for the condition known as pregnancy gingivitis. The immune changes include a reduction in the migration of inflammatory cells. There is also an increase in a subset of CD4, cells which kill B lymphocytes, the cells responsible for producing antibodies to some of the very bacteria which are thriving in the high levels of the estrogen and progesterone. Progesterone causes increased vascular permeability and release of prostaglandins, both factors which support inflammation. Progesterone also reduces the production of collagenases, so the balance of collagen turnover between secretion and resorption is upset, allowing the collagen content of the gingival lamina propria to increase. These influences may lead to the development of a mass of healing (granulation) tissue in the gingiva. This mass is called a pregnancy epulis. It is quite harmless and regresses as does the gingivitis, after the birth of the child.
The onset of menopause is due to age changes in the ovaries, which fail to respond to pituitary hormones. The decrease in estrogen and progesterone contributes, along with other factors, to cause osteoporosis, a decrease in bone mass. There is no evidence that osteoporosis is linked with severe periodontal disease which also involves loss of bone around the teeth. Menopause is, however, associated with a decrease in mucosal secretions, including saliva. Dry mucosa is easily damaged and affects the comfort and retention of dentures.
Key Notes
The junctional epithelium must perform the functions of a barrier to infection and call up resources, if the barrier deteriorates into a battleground. In this thin layer of epithelium, all the defense mechanisms of the immune system may be recruited, including the special defenses of antibodies, neutrophils, macrophages, and complement. The conditions which initiate this deterioration, from