September 21, 2011

The cyclic nature of the female sex hormones is often reflected in gingival tissue changes. Fluctuating levels of progesterone and estrogen may have an adverse effect on gingival response to bacterial plaque. During puberty, the female experiences an increase in the production of estrogen and progesterone resulting in an increase in the prevalence of gingivitis without an increase of plaque. However, in areas where food debris, plaque, and calculus are deposited, clinically there may be a nodular hyperplastic reaction of the gingiva. Milder gingivitis cases respond well to scaling and root planing with frequent oral hygiene instructions. Severe cases may require microbial culturing, antimicrobial mouth rinses, and slow-release subgingival antimicrobial therapy. Whenever possible, involvement of a parental figure with home care procedures is recommended.


Adolescent girls are susceptible to the eating disorders bulimia nervosa and anorexia nervosa. Signs and symptoms of chronic regurgitation of gastric contents on intraoral hard and soft tissues consist of smooth erosion of the tooth, usually on the tongue surfaces of the upper front teeth. In addition there can be an enlargement of the salivary glands, which can decrease salivary flow resulting in increased oral mucous membrane sensitivity and gingival redness.


Gingival inflammation is often aggravated by an imbalance and/or increase in estrogen and progesterone. In certain individuals they are more inflamed and red preceding the onset of menses. At times during the menstrual period there may be minor increase in tooth mobility. Intraoral apthous ulcers, herpetic lesions, and candida (yeast) infections occur in some women during the phase of the cycle when progesterone is the highest. Frequent supportive periodontal therapy appointments with particular emphasis on oral hygiene are recommended for those women who are clinically symptomatic with their menstrual cycle.


The net effect of gestational changes is twofold: increased gingival swelling, redness, and bleeding occurring as a physiologic change during pregnancy; and alterations in host response and tissue physiology serving to increase the gingival inflammatory response to bacterial plaque. Increased signs of gingival inflammation become evident after the first trimester and peak during the latter part of the third trimester, regressing after parturition. The most common site of gingivitis is usually seen in the anterior regions of the mouth, but can be more generalized and may cause false pocketing with increased probing depths but minimal changes in attachment levels. Pyogenic granulomas, “pregnancy tumors,” may develop, which generally will regress postpartum. Increased tooth mobility unrelated to attachment loss has also been noted but usually requires no treatment. Expectant mothers should be provided with a comprehensive plaque control program to minimize the exaggerated inflammatory response to the gingival tissues.


Oral contraceptives may produce the gingival changes seen during pregnancy. Certain brands of oral contraceptives may cause more significant changes than others. In recent years, the quantity of synthetic hormones contained in most oral contraceptive agents has decreased and it appears that current oral contraceptive agents no longer affect the gingiva to the same degree as previously reported. While the increased gingival inflammation associated with pregnancy regresses after parturition, many women take oral contraceptives for extended periods of time, emphasizing the need for long-term periodic office visits to monitor periodontal health. While the effects of progesterone and estrogen on the gingiva cannot be avoided, thorough plaque control reduces the incidence and severity of adverse gingival changes.


Some patients report experiencing burning sensations in the oral cavity and altered taste sensations. For many years menopause-related desquamate gingivitis have been described among postmenopausal women and are thought to be related to the hormonal changes of menopause. Ongoing studies are examining the association of postmenopausal primary osteoporosis with upper and lower jawbone mineral density, tooth loss, bony ridge atrophy, and periodontal attachment loss. Most recent evidence points to a probable cause between osteoporosis and tooth loss as well as alveolar bone loss.

SEE ALSO: Menarche, Menopause, Oral contraception, Oral health

Suggested Reading

  • Mahn, L. K., & Escott-Stump, S. (2000). Krause’sfood, nutrition, and diet therapy (10th ed., pp. 516—533). Philadelphia: W. B. Saunders.
  • Newman, M. G., Takei, H. H., & Carranza, F. A. (2000). Carranza’s clinical periodontology (9th ed., pp. 513—526). Philadelphia: W. B. Saunders.
  • Rose, L. F., Genco, R. J., Cohen, D. W., & Mealey, B. (2000). Periodontal Medicine, 252—253.
  • Wilson, W. G., & Kornman, K. S. (1996). Fundamental of Periodontics, 151—163. Chicago: Quintessence Publishing Co.
  • World Workshop in Periodontics. (1996). Annals of Periodontology, 1(1), 290-292.


Category: P