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 what is normally a commensal relationship, into a full-scale defense against pathogens, are vital to uncover.
Review Questions
1. What causes the extraction of molar teeth to be more difficult than incisor teeth?
2. Does the periodontal ligament support the tooth like a hammock (under tension) or like a cushion (under compression)?
3. What are the functions of the periodontium?
4. Why is it important to place an avulsed tooth back in its socket as soon as possible?
5. What similarities and differences are there between cementum, dentin, and bone?
6. What features of the junctional epithelium provide a barrier to the progress of plaque microorganism into the periodontal ligament?
7. What is the nerve and blood supply of the periodontium?
8. How is the periodontium affected by changes in the level of female hormones?
9. What evidence suggests that cementum formation may be induced by cells of epithelial origin?
10. What are the functions of cementum?
11. What role do epithelial cell rests have in preventing ankylosis?
12. Why is the formation of new cementum essential during healing of the periodontal ligament?
References
[1] Lindskog S, Blomlöf L, Hammarström L. Evidence for a role of odontogenic epithelium in maintaining the periodontal space. J Clin Periodontol 1988; 15(6):371–373
[2] Fujiyama K, Yamashiro T, Fukunaga T, Balam TA, Zheng L, Takano-Yamamoto T. Denervation resulting in dento-alveolar ankylosis associated with decreased Malassez epithelium. J Dent Res 2004; 83(8):625–629
[3] Xiong J, Mrozik K, Gronthos S, Bartold P. Epithelial cell rests of Malassez contain unique stem cell populations capable of undergoing epithelial mesenchymal transition. Stem Cells Dev. 2012; 21 (11):2012–25
[4] Luan X, Ito Y, Diekwisch T. Evolution and development of Hertwig’s epithelial root sheath. Dev Dyn 2006 May; 235(5): 1167–1180
[5] Harahashi H, Odajima T, Yamamoto T, Kawanami M. Immunohistochemical
