Management of gingival inflammation in pregnant women appears to be an important therapy in preventing incidence of premature, low birth-weight babies
Perry A. Ratcliff, DDS, and
Trisha O?Hehir, RDH
News releases in October 1996 informed the public that a pregnant woman with periodontal disease is at higher risk for a premature, low birth-weight baby (PLBWB). In Spring 1995, four related research papers were presented at the American Association for Dental Research meeting showing the correlation between a Porphyromonas gingivalis infection and PLBWB. Subsequently, a full research paper was published in the October 1996 Journal of Periodontology.
Studies by Dr. Offenbacher and co-workers in North Carolina have documented that an oral P. gingivalis infection in pregnant women will increase the probability of having a PLBWB by seven times. Alcohol increases the probability by only 11/2 times. Smoking increases the probability by only one time. The use of smoking and alcohol in combination increases the probability of having a PLBWB by 21/2 times.
This knowledge creates a new responsibility in dentistry. The dentist, the hygienist, and the physician must cooperate in the care of the mother and the baby in utero.
Blood supply during natural labor
Why does a P. gingivalis oral infection and PLBWB relationship occur? To answer that question, one must consider the events that occur in the uterine cell wall, the amniotic fluid, and the cord, as well as gingival epithelium, connective tissue, and the oral infection.
To understand premature partuition, one must understand the mechanisms of when and how partuition occurs. The level of prostaglandin (PGE2) is the critical factor in the induction of labor. Some women are given an injection of PGE2 to induce labor. The natural source of PGE2 is from the epithelial cells of the placenta and the cord. The cord, which has a high blood supply, is a major producer of PGE2 and has a bi-directional delivery of PGE2 into the amniotic fluid and into the mother`s blood stream.
The level of PGE2 in the amniotic fluid of a pregnant woman at eight months is one-half of that at nine months when normal partuition begins. The amount of PGE2, which stimulates labor, is sufficiently higher at the end of the ninth month and causes contractions to be induced.
All PGE2, whether from the placenta, cord, or inflamed gingiva, that goes into venous blood is neutralized in the lungs, liver, and spleen. Neutralization of PGE2 as it moves from venous blood to arterial blood is probably 90 percent, according to reports. Presumably, this still leaves a higher level of PGE2 in the arterial blood stream than would normally exist without the pregnancy.
Since the placenta and the cord are major producers of PGE2, and since these organs are eliminated as "after birth" when the baby is born, then the production of PGE2 in the mother is significantly reduced after delivery. Thus, labor stops.
The passage of gingival antigens
A sequence of events occur in the development of a periodontal pocket or lesion. It has been established that gingival inflammation will lead to PGE2 production.
But how does gingival inflammation start? The work of Dr. Rizzo showed that bacterial antigen or endotoxin by itself would not pass through gingival epithelium unless it had a facilitating permeation agent. When he added hydrogen sulfide to the endotoxin solution, there was an immune response. This suggests that hydrogen sulfide will act as a facilitating permeation agent to allow antigen to pass through healthy epithelium into healthy connective tissue. The same has been shown for antigen in combination with methyl mercaptan. Antigen must have a facilitating permeation agent to penetrate into healthy gingiva.
Dr. Gaffar repeated the work by Dr. Rizzo, except hyaluronidase was used as a facilitating permeation agent. Again, when the hyaluronidase was added to the antigen, it penetrated through the epithelial barrier into the underlying tissues. This is understandable since the intercellular space between epithelial cells is filled with chondroitin sulphate and hyaluronic acid. The hyaluronidase would lyse hyaluronic acid facilitating intercellular penetration.
P. gingivalis is an organism that makes both hyaluronidase and the enzyme gingivain. Electron microscopic photographs of this bacteria show gingivain vesicles attached to the external surface of the cell wall and some vesicles are free-floating in the surrounding medium. These gingivain vesicles will break the cell wall of a desquamated epithelial cell and, in the process, form hydrogen sulfide and methyl mercaptan. These become the facilitating permeation agents that allow antigen to cross the epithelial barrier.
During the inflammatory response, there is a failure to maintain an oxygenated blood supply to the supporting connective tissue and covering epithelium. The osmotic gradient changes with the accumulation of debris from dead cells. Edema fills the intercellular spaces stopping active transport and reducing nutrient supply to local cells. The reduction of oxygenated blood brings a change from aerobic glycolysis to anaerobic glycolysis. This reduces the adenosinetriphosphate (ATP) energy source from 36 to two. Cellular nutrition is virtually discontinued. Epithelial ulcerations occur. The ulceration then is seen clinically as gingival bleeding.
The ulcer is a portal of entry for bacteria into the gingiva. It is possible that P. gingivalis organisms in gingival tissue may move elsewhere in the body. In the presence of gingival infection, there will be a transitory bacteremia that follows either brushing or eating.
The dental profession has viewed this transitory bacteremia with the general feeling that it is of no clinical significance. In earlier historical periods, physicians have recommended the extraction of teeth to reduce the amount of infection that the host was getting from the mouth. A P. gingivalis bacteremia of oral origin could be the source for developing a nidus of infection in the area of the vagina, placenta, or cord. This could increase the rate of PGE2 production in the pregnant female. It could play a role as "the straw that broke the camel`s back" to precipitate labor and reduce the normal development of the fetus.
It should be noted that, because a study was done on P. gingivalis, this does not mean that P. gingivalis is the only exciting factor in the development of a PLBWB. P. gingivalis elaborates a relatively strong gram negative lipopolysaccharide antigen. Other organisms can produce antigenic stimulus at least equal to that of P. gingivalis. To protect the fetus, we must assume that bacteria other than P. gingivalis may induce the PLBWB syndrome. Perhaps P. gingivalis should be considered more as a marker in Dr. Offenbacher?s research rather than a sole cause/effect factor.
The high incidence of premature, low birth-weight babies associated with periodontal infection must be considered. Local treatment to prevent this event should consist of thorough debridement together with careful, at-home disease control. Some products in the marketplace offer the chemical advantage of removing cysteine, methionine, hydrogen sulfide, and methyl mercaptan.
Perry A. Ratcliff, DDS, is a board certified periodontist, past president of the American Academy of Periodontology, professor emeritus at the University of California, San Francisco, and a research consultant for Ropar Pharmaceutical Co. Trisha O?Hehir, RDH, is the senior consulting editor of RDH. She also is editor of Perio Reports, a newsletter for dental professionals that addresses periodontics.
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- Ratcliff PA. Chlorine dioxide products reduce bleeding on probing and probe scores. Accepted for presentation IADR, 1997.
Watch disease in pregnant patients
Management of gingival disease in a pregnant patient has not been taken as a serious matter in many dental offices. This attitude could be summed up by the belief that delivery of the baby will solve the increase in inflammation found in the mouth. Treatment should instead consider the seriousness of the infection and its relationship to the development of the fetus.
Antigen has been understood for many years, and the bacteria residing in dental plaque is well understood. We know that by removing plaque, or keeping it to a minimum, inflammation in the gingiva will be reduced. Likewise, the irritation of calculus can be controlled by the hygienist through scaling, root planing, and polishing in conjunction with oral hygiene participation.
It is important to prevent penetration of lipopolysaccharide (LPS) antigen into the gingiva by neutralizing the permeation agents. These thiol compounds can be destroyed by oxidative consumption as shown by Dr. Lynch through the use of RetarDEX oral rinse.
Since bleeding on probing is the clinical sign of an open portal of entry for bacteria into the deeper tissues, it becomes critical for the clinician to recognize this and to understand how to arrest it. Certainly, improved plaque removal and calculus removal has a major impact on the reduction of bleeding on probing.