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Dr. Paul Keyes
"One's dental health depends, almost entirely, on how well the things that get into one's mouth get out..."

Dr. Paul Keyes
ANTI-INFECTIVE PERIODONTAL THERAPY
EXPERIENCES AND RECOLLECTIONS


    "If your readers, while watching what they do in a mirror, brush their teeth and gums carefully once day with pure baking soda, they will kill many periodontal-
disease associated microorganisms. I have never seen and I know of no clinician who has ever seen serious periodontal disease in a person who has regularly brushed with salt and soda, alone or in combination."

-Dr. Paul Keyes
My serious interest in periodontal diseases started in the 1960s with findings in hamsters that were under study for dental caries.  Animals not infected with the cariesogenic streptococcus, Streptococcus mutans, often developed periodontal lesions (Keyes, 1962).


A filament-forming catalase-positive bacterium, which was named Actinomyces viscosus, was isolated from these animals. When this bacterium was inoculated into non-infected animals, it induced periodontal lesions and root caries (Jordan and Keyes, 1964).


Socransky and coworkers also induced periodontal lesions in gnotobiotic rats they infected with a human strain of Actinomyces naeslundi  (Socransky, Hubersak, and Propas, 1970).  Steven Bellack and Harold Jordan isolated  A. viscosus from periodontopathic plaques in children with Down’s syndrome. When one of these isolates was used to infect rats that had been maintained in germ-free equipment, it induced severe periodontal lesions and root caries (Jordan, Keyes, and Bellack, 1972).


In 1974 I started to treat periodontal infections in patients who had been sent to the NIH dental clinic. A number of these patients were so-called “refractory” cases, because they had not responded well to surgery, traditional maintenance therapy, and the self-care measures they had used.  Since some strains of actinomyces have a periodontopathic potential, I originally intended to use therapy that would control strains of actinomyces in these patients.  However, the loss of all laboratory support precluded my following the prevalence of these microorganisms.  In retrospect, this was not a serious loss.


As an alternative method for assessing bacteria associated with periodontal lesions I used a method similar to one used for many years by Arnim (1964), namely microscopic examinations of subgingival plaques with a phase-contrast microscope.  A TV camera, monitor, and tape recorder attached to this microscope made it possible to see and record microorganisms that were recovered from infected pockets and to follow their prevalence during treatment. It soon became apparent that between health and disease there were striking differences in the prevalence of white blood cells, the types of microorganisms, their patterns of organization, their activity and behavior (Keyes et al 1982). Although microorganisms could only be identified morphologically, I decided that all disease-associated bacteria would be considered risk factors and therapeutic targets.

 
The therapeutic measures I used were similar in principle to the germ-life-control measures that Thomas B. Hartzell had advocated many times between 1916 and 1941 (Hartzell, Henrici and Gray, 1916; Hartzell, 1925, 1927, 1930, 1932, 1939, 1941).  The following questions then arose with regard to the various therapeutic measures that I used: 1) Can I find a combination of therapeutic measures that will bring under control high counts of WBCs and disease associated microorganisms (DAMs)?  If long-term control can be attained, what will happen clinically? Will lesions stay the same, get worse, or get better?

 

 It has been very difficult to make the following points:  the purpose of my investigations was not to compare various therapeutic measures, and 2) I considered the use of untreated patients as controls to be highly unethical.  I had no interest whatsoever in comparing various therapeutic measures that might be used either professionally or by patients for self-care.  Although their pathogenicity was unknown, bacteria never found in healthy sites became therapeutic targets and their elimination was the end-point of therapy.  (make as a footnote: Since 1975 many refinements have been made in methods used to identify periodontal-disease-associated bacteria and the measures used to treat them.  However, no data published to date have shown that the targets and end-points I originally selected are not highly effective for arresting periodontopathic infections.)

 

In the fall of 1975, to a small audience attending a dental meeting in upstate New York I presented a paper in which I described the results I had observed in patients who had been treated with conservative anti-infective therapy.  Attendance at additional presentations was very small.  The first description of this therapeutic program appeared in Quintessence (Keyes et al.1978).

 

Several years later Scheffler and Rovin (1981 and 1982) reported at length on some of the findings available at that time, and stated that further studies were needed to determine the long-term results of what they named the “Keyes technique”. These investigators stated that in addition to reducing the cost of periodontal treatment “the Keyes technique may have other benefits in addition to the treatment and prevention of periodontal disease.  In some patients, there may also be a reduction in tooth loss. Furthermore, if surgery is avoided, the pain and discomfort associated with surgery are also avoided.  By involving patients in improving their oral health, the Keyes technique may improve their awareness of dental disease and encourage their use of dental services, while the disease is still treatable, often at reduced cost”.  Unfortunately many periodontists and others in the dental profession tried to discredit these reports, and the NIDR would not support a grant proposal, submitted by researchers at the University of Pennsylvania, which would have compared the results of conventional surgical treatment with conservative anti-infective therapy and settled much of the controversy.

 

Apparently, Sheffler and Rovin were unfamiliar with the dental literature on conservative anti-infective periodontal therapy.  Consequently, they mistakenly called the methods used by Keyes and his coworkers “new”.  The methods used were not new.  They were modifications of methods that had been used in past years.  The innovation in the system was the monitoring and modulating of therapy on the basis of microscopic findings in lesions and pockets.  Even this procedure had been suggested by   Clinical findings alone were not used for the making of decisions on what therapeutic measures would be used professionally and by patients for self-care. 

 

Scheffler and Rovin’s (1982) statement that “the Keyes technique is so new that long-tern efficacy and effectiveness studies have not been possible” was unintentionally incorrect and misleading.  The Scheffler-Rovin papers, and other favorable articles in the lay press, generated so much vehement criticism, largely from members of the American Academy of Periodontology, that I wrote a paper (Keyes, 1985) which described the background, rationale, and methods, which my colleagues and I had employed in the treatment of the patients we saw.

 

In 1984 this paper was submitted to the Journal of the American Dental Association, but publication was rejected because of irate criticisms that sounded very much like those previously voiced by periodontists.  However, in 1985 this paper was published under the title, “Microbiologically monitored and modulated periodontal therapy” (Keyes, 1985).  In retrospect a better title would have been:  “Anti-infective periodontal therapy monitored and modulated microbiologically”. This longer title would have made it more difficult for critics to distort and discredit the therapeutic measures that were used. As footnote: This paper has never been cited in any of the critical reviews published and circulated by the Academy of Periodontology.

 

 For the historical record some of statements which originally appeared in “General Dentistry” have been repeated here along with commentary of treated patients.


            “The intent of this report is to eliminate misconceptions about the “Keyes technique”, to enumerate the seven steps used in the system, and to discuss some of the background upon which this regimen is based.

            “The terms “Keyes technique” and “Keyes method” are misnomers.  Contrary to some opinions, the therapy used in the system does not rely upon particular therapeutic agents, instruments and procedures.  Clinicians may select any alternative deemed beneficial.

            “The “Keyes technique” is a quality-control system that begins with careful assessment of a patient’s periodontal-disease history, including the therapeutic adequacy of past professional care and the patient’s self-care measures, and then continues with monitoring and modulation of the therapeutic measures administered to all lesions disclose by the assessment.

            “The program requires: 1) The identification of specific therapeutic objectives and targets, 2) Treatment with measures that have a predictable antibacterial potential, and 3) Adjustments in therapy whenever therapeutic end-points, such as bringing bacterial co-factors under control, have not been attained.

            “Although almost all dental patients develop some form of periodontal disease, less than 1 percent of a general practitioner's effort may be directed to early diagnosis and treatment of periodontal pathoses (Douglass and Day, 1979).

Cohen (1983) stated: ‘General dentistry, identified principally with dental caries, has not been concerned with periodontics and the problems of periodontal diseases.  The large number of patients who have been receiving professional dental care on a regular basis but who nevertheless suffer from advanced periodontal; disease is tragic’.

“Cohen’s story is not new.  Arthur Merritt (1932), a highly respected New York Periodontist and one-time president of the American Dental Association noted: ‘Surgical periodontia is an indictment of the dental profession made necessary only because of its failure to live up to its responsibilities in the prevention and early treatment of periodontal diseases.

“Not surprisingly, some general dentists have had to defend themselves in malpractice suits, because serious periodontal disease has developed in patients under their care.  This professional failure can be attributed to the fact that most dentists and hygienists have not learned to identify incipient infections that must be controlled to prevent and arrest destructive periodontitis.

“Because dental clinicians have not used suitable diagnostic methods for disclosing disease activity (and risk factors) they often have failed to recognize periodontal disease activity before serious damage has occurred.

“ Page and Schroeder (1982) stated ‘periodontitis has no single accepted pathonomonic feature that can be used to accurately assess prevalence or incidence or severity, and no available methods (except for microscopy and the pocket microbiota) to distinguish active from inactive states.’

It should be obvious that the better clinicians can recognize specific therapeutic targets and endpoints the better they will be able to prescribe appropriate preventive and control measures.

For most of the 20th century, the principal therapeutic targets in the treatment of periodontal diseases were described as ‘poor oral hygiene’, ‘debris and calculus’, ‘plaque accumulations’ or ‘“schmutz’.  Very few clinicians, including periodontists, even recognized that periodontal diseases were infections caused by bacteria growing on root surfaces, in pockets and periodontal tissues.  Consequently, infection control was not the primary objective of periodontal therapy.  Unfortunately, over a period of many years this ignorance prevailed despite a number of perceptive reports by observant clinicians (Bass and Johns, 1915; Hartzell, 1932; Hartzell, 1941; Arnim, 1964: Socransky et al., 1982) Not only were these views not accepted but also they were rejected (Bunting, 1932; Kronfeld, 1939)

Keyes (1962) speculated “it is possible that specific microbes inhabit plaques when caries occurs and others contribute to periodontal disturbances’.  In 1963 Koch’s postulates satisfactorily implicated aerobic gram-positive periodontopathic microorganisms (Jordan and Keyes, 1964).  Strains of actinomyces strains were found to have a periodontopathic potential (Socransky et al., 1970: Jordan, Keyes, and Bellack. 1972).

“Actinomycotic populations now seem the most likely to initiate pocket formation and to provide the conditions, including surfaces on cell walls that permit the secondary colorizations associated with destructive periodontitis.  Indeed, some of the secondary invaders may be more pathogenic that the primary ones.

“Even without knowing the pathogenic potential of all the organisms that inhabit periodontal lesions, risk factors can be recognized and disease-associated populations established as therapeutic targets.  No data support the nonspecific plaque hypothesis upon which almost all periodontal therapy has been based.  Loesche’s review (Loesche, 1976) and other evidence support the specific plaque hypothesis.

“Bacterial mats (now called biofilms) removed from diseased sites differ qualitatively from specimens removed from healthy sites (Loesche, 1976, Socransky, 1977;  Slots, 1977; Listgarten and Hellden, 1978; Listgarten and Levin, 1981; Singletary et al., 1982; Keyes and Rams, 1982; Keyes and Rams 1982; Socransky, 1982).”  Culturing methods and microscopic examination of subgingival plaques available in the 1970s and ‘80s showed “that the microbiotae associated with periodontal diseases can be distinguished from those associated with periodontal health.”

“Disease-associated microbiotae should be considered bacterial risk factors that should not be given the benefit of doubt.  Clinicians need to expand the diagnostic system they use in determining whether patients are at risk of periodontal-disease associated microorganisms.

“If clinicians focus on specific therapeutic targets, they can improve office-methods used to eliminate disease-related pyogenic (biofilms) and develop self-care methods to maintain health-associated complexes in the periodontal milieu.

“These views are consistent with statements by Socransky et al. (1982).  They noted that although ‘periodontal diseases can be effectively controlled by periodic scaling and a variety of mechanical and chemical home-care procedures ----the fact that few, if any, other infections are treated in this manner should warn us that current therapy may not be optimal.  A more acceptable approach for periodontal treatment would be control or elimination of specific periodontal pathogens and their effects on the host’ 

“ ‘ The nature of therapy is changing for periodontosis and other forms of advanced disease, and treatment is beginning to include antimicrobial therapy directed specifically at the subgingival microbial complexes associated with different clinical entities.’


 
The Seven Steps



Step 1.  Clinical examinations and microbiological assessments.  This step includes a conventional clinical examination that includes tissue damage assessed by the extent of bleeding at gingival margins, suppuration, tooth mobility, probe insertion depths, attachment levels, radiographic findings and color photographs and a microbiological examination of bacterial biofilms.  A phase contrast microscope is used to examine subgingival plaque specimens.  The prevalence of white blood cells (WBCs) and disease-associated microorganisms (DAMs) are assessed in plaques removed from two or three of the most involved sites.  Findings related to WBCs, spirochetes, motile rods, bacterial organization, turbulence, amoebae, and trichomonads are noted on appropriate, and they may be videotaped for future reference. 

False positive findings are not possible in microscopic examinations, and occasional false negative findings are unlikely to affect the long-range treatment and prognosis of cases.  Repeated false negative findings are highly unlikely, if the most seriously involved sites are examined at every recall appointment. 

Critics of microscopic examinations have claimed that the findings are of no value, because the microorganisms seen cannot be positively identified, and it is impossible to know what sites to examine.  This criticism is specious.  Periodontists have never claimed that there is a problem selecting sites for culturing and other types of assays. The fact remains that microscopic examinations of bacterial biofilms give a lot of useful information, quickly, inexpensively, and vividly.   

Step 2.  Patient education.  Patients are informed that their disease has been caused by bacterial infections located on the necks and roots of their teeth.  A microscope-video system enables patients to see the various types bacteria that inhabited their pockets and to follow their progress of their treatment.  They are also told that the transfer of saliva transmits many of the bacteria seen from mouth to mouth, usually by kissing.  Consequently, patients are advised to have persons they are intimate with screened for DAMs.

Although “patient education” this step has listed as a separate step, in practice it can be combined with Step 4

Step 3.  Professional treatment.   The objective of in-office therapy is to disinfect root-surfaces and the pocket environment with various instruments and antibacterial irrigations. Today a wide variety of instruments and antibacterial agents are available for this purpose.  For patients treated at the NIH Clinical Center between 1975 and 1981, a 1% solution of chloramine-T was used before, during and after instrumentation.  The purpose of antibacterial pocket irrigation is not only to aid with disinfecting root surfaces and periradicular tissues but also to minimize bacteremias.

Periodontists who have criticized the use of pocket irrigation have claimed that this procedure does not significantly improve long-term healing. This procedure is comparable to that used in medicine in the treatment of infected wounds. Its primary benefit is to minimize the risk of bacteremias with microorganisms that might cause disease in other parts of the body.
    

Step 4. Patient training in self-care.  Patients need to use self-care measures that have a dependable anti-infective potential.  Consequently, their self-care program is customized for their needs.  They are shown step by step how to use various types of toothbrushes, irrigation equipment, toothpicks, “stimulator” tips, etc. 

While watching what they do in a mirror, they use these mechanical devices to deliver appropriate pastes, powders, solutions, and gels to all vulnerable sites.

Agents such as salts (sodium chloride, sodium bicarbonate, magnesium sulfate) can be beneficial adjutants for bacterial control, e.g., patients may use sodium bicarbonate moistened with 3% hydrogen peroxide. The catalase in plaques rapidly breaks down the peroxide into oxygen and water.  When patients use this agent, the effervescence produced by this breakdown helps to disorganize and disperse the adhesive bacterial mats (biofilms) attached to tooth surfaces. Properly delivered to infected sites, a combination of sodium bicarbonate and hydrogen peroxide will effectively disorganize, disperse, detoxify, and devitalize many DAMs. (DeRenzis, 1981: Chasens, 1978: Newburn et al., 1984; Fletcher et al., 1984)


Step 5.  Assessment of results.  Two to four weeks after completion of steps 3 and 4, results are assessed clinically and microbiologically.  If counts of WBCs are at low levels (5-25/field) and disease-associated microorganisms are not detected, patients are placed on a maintenance program.  However, if adequate control has not been attained, as is usually the case when pockets are more than 5 mm deep and there is furcation involvement, clinicians need to modulate their treatment by prescribing appropriate antibiotics systemically for 7-14 days. 

If examinations of subgingival biofilms removed from lesions reveal poor control of WBCs and DAMs, bacterial culturing or other methods for identifying presumptive pathogens should assess infected sites.  On the basis of these microbiological findings clinicians can prescribe appropriate antibiotics.

 

Step 6.  Modulation of therapy. Appropriate systemic antibiotics should be used immediately: 1) for patients at risk of bacterial colonization of cardiac valves and implants in other parts of the body, 2) for patients in pain associated with periodontal abscesses and severe gingival inflammation,

Tetracycline (250 mg. four times daily for 14 days) can be effective in controlling WBC migration and suppressing DAMs (Rams and Keyes, 1983; Hawley, Lee and LeBlanc, 1980).  Little risk appears to be associated with the taking of tetracycline, but other antibiotics may be used.  Metronidazole (250g three times daily for seven to ten days) has been highly effective in controlling periodontal lesions (Loesche et al., 1981) and eventually may become an agent of choice when used alone or in combination with other antibiotics.

The use of surgical measures is also considered in the modulation stage.

When the combination of measures described in the above steps controls WBC migration and eliminates DAMs, excellent healing occurs (Rams and Keyes, 1983).

Sept 7.  Recall appointments.  The frequency of recall appointments should be based on the individual needs of patients. Clinical findings alone are not used to evaluate the status of infection control and for modulating therapy.  Decisions regarding the need for adjustments in in-office and self-care treatment are based more on microbiological (microscopic) findings than on clinical features.

 

Discussion

Contrary to the mistaken opinions and disingenuous criticisms of persons who have commented on “MMPT” none of the measures used in this rationale is new, and none is experimental.  All of the measures, including the use of systemic antibiotics, have been described before.

In 1683 Van Leeuwenhoek used his little microscopes to monitor the effect of vinegar rinses on the motile microorganisms he observed in the “white matter” that was growing on the surfaces of his teeth  (Burnett and Scherp, 1968).  In 1925, Beckwith (Beckwith, 1925) recommended the use of the dark-field microscope to monitor treatment of periodontal lesions, because “progression in healing of the open lesions of pyorrhea is attended by marked diminution of the bacterial forms present.”  Beckwith believed that the microscope was “a valuable accessory to the dentist’s equipment, since it gives valuable information regarding the conditions of the lesion itself”.

About 1000 years ago, Albucasis (Spink and Lewis, 1973; Herschfeld, 1987) described instruments for removing “ugly matter” on tooth surfaces and advised that debridement should be carefully repeated on successive days “until the desired purpose is obtained”.

Since then the value of meticulous scaling and root planning has been described many times.  Arcolani (1557) recommended using special sticks, salts, and vinegar to clean the teeth immediately after eating, even after little things.  In the 16th century the same advice on oral hygiene appears in series of anonymous booklets published in Germany (Zene Artzneis, 1530, 1570) 

Allen (1685) warned that the slimy stuff and scale on the teeth should be removed by someone skilled in the art lest the treatment be worse that the disease itself. He also recommended various salts and ashes as adjutants to oral hygiene.

For well over a hundred years a few physicians and dentists have implicated microorganisms in the cause of periodontal lesions, and they have tried to use various antimicrobial measures for treating such lesions.    Harlan (1883) described hydrogen peroxide as highly beneficial in controlling bacteria associated with “pyorrhea alveolaris” which he believed was the result of infection.  Stern (1919) first reported favorable results with the use of chloramines-T to irrigate periodontal pockets.  Stralfors (1942) reported that chloramines-T applied in vinyl applicators killed 99 percent of the microorganisms he isolated from supragingival plaques.  Sweet et al (1978) reported that presurgical rinsing with a 1% solution of chloramine-T significantly reduced bacteremias associated with extractions.

For 25 years Hartzell (1916, 0) repeatedly emphasized the need to control “germ life” on tooth surfaces to prevent dental caries and “pyorrhea”.  He described the antibacterial measures he and his patients used.  In his paper, “The patient’s needs” (Hartzell 1930) he recommended that patients learn about the role of microorganisms in the pathogenesis of periodontal and systemic disease and suggested that they be taught to use measures that would detoxify and control pyogenic germ-lie attached to tooth surfaces.

The anti-infective measures used in MMPT embrace well-accepted medical procedures to improve the diagnosis and treatment of periodontopathic infections.  However, even without recognizing the infectious nature of periodontal diseases, clinicians have, over the past 1000 years, discovered empirically the benefits that may follow careful debridement of root surfaces and good oral hygiene.  

Data available in 1985 (Knowles et al, 1980; Linde et al. 1982; Pihlstrom et al., 1983; Badersten et al., 1984; Isidor et al., 1984) helped to quantify clinical findings, which prior to that time had been largely anecdotal, and they showed that conservative, nonsurgical methods were as effective as surgical methods in the treatment of periodontal infections.

Between 1975 and 1981 a number of patients were referred to the NIH dental clinic, because their disease had not been controlled by periodontal surgery, regular maintenance care, and excellent supragingival plaque control.  High counts of WBCs and disease-associated microorganisms were found in subgingival plaques removed from all of these patients (Keyes et al., 1978; Keyes, 1984).  In all of these patients anti-infective therapy brought disease-related bacteria under control, and arrested all the clinical signs of periodontal infection (Keyes, 1982, 1984; Keyes and Rams 1983, 1984).

A conservative quality control system, inappropriately called he “Keyes technique” enables clinicians to assess any of the many therapeutic alternatives that may be used to prevent and arrest periodontopathic infections.  Regular clinical examinations and microbiological assessments can reveal whether the therapy used by professionals and by patients has adequately controlled the microorganisms that cause periodontitis.

“Therapeutic programs with modulations based on microbiological findings rather than on clinical features alone, improve the prognosis of periodontal therapy by informing patients about microorganisms associated with periodontal disease, by offering therapeutic measures with reliable antibacterial potentials, and by reducing the possibility of incomplete infection control.”

 

Discussion
ANTI-INFECTIIVE PERIODONTAL THERAPY


 
Over a period of many years Hartzell (1925, 1939, 1941) described the need for bacterial control and the use of conservative antibacterial measures for the prevention and treatment of “pyorrhea”. In his paper entitled “Patient’s Needs”   (Hartzell, 1930) he also stressed the importance of teaching patients how to control the bacteria that not only caused dental caries and “pyorrhea” but also diseases in other parts of the body.

Here is a paraphrase of what he was saying in 1927:  If we could prevent the growth of bacteria on and around the teeth, we would prevent dental caries and periodontal disease.   The multitude of bacteria that grow in the mouth has confused dentists to so great a degree that they refuse to accept the fact that the destruction of the teeth and their supporting tissues is a bacterial matter.  And because they do not know which of the multitude to credit with this destruction, they discredit all bacteria.


In his discussion of patient’s needs in 1930 he makes the following points. The first need of patients is to understand that the vast bacterial mass growing on the teeth not only destroys the teeth and their foundation, but also, when it diffuses to other parts of the body, may cause disease in those parts where the bacteria may lodge.   With this understanding in mind patients need to apply modern methods of tooth cleaning and to employ detoxifying agents that will neutralize the bacterial poisons around the teeth.  One these detoxifying agents was sodium ricinoleate, the soap of castor oil.  Another product Hartzell’s patients used was a solution of zinc phenol sulfonate.  When applied to the margins of infected pockets, this powerful astringent alone helps to dislodge subgingival bacteria and pus.

At this time the American Dental Association’s Council on Dental Therapeutics stated that the sole function of a dentifrice is to aid in the removal of food particles from tooth surfaces.

In his paper on prophylaxis Hartzell stated that 30 years of observation had convinced him that bacterial control would prevent and cure caries and destructive periodontitis.  Commenting on this presentation, Russel Bunting, then Dean of the Dental School at Michigan, stated that Hartzell’s concept is quite unacceptable as is his statement that he is able to prevent and cure pyorrhea by reducing bacteria in the mouth.

In 1940 in his presidential address to the American Academy of Periodontology Hartzell stated that it would be as impossible for pyorrhea to exist around human teeth were it not for pus germs growing on the teeth as it would be to have wheat growing in a field, without the planting of seeds.

At the same time Kronfeld stated in his textbook, “Histopathology of the Teeth”, that microorganisms have no etiological relationship to pyorrhea.  In 1997 at the annual meeting of the AAP its then president, Dr. James Mellonig was quoted as saying  “Today’s general concept of periodontal disease as an infection will be shown to be untrue”

Throughout the history of periodontics there has controversy and disagreement about methods clinicians have used to diagnosis and treat disease.  To make maters worse - until recently dental education included little or nothing regarding periodontal infections.  Millions of teeth have been lost as a consequence.  Unlike views that prevailed for most of the last *century, today no well-informed dentist or hygienist questions the role of bacteria in the pathogenesis of periodontal lesions.  Opinions still differ widely in regard to diagnosis, treatment, and end points.    

 
CONCLUSIONS AND SPECULATIONS

 
If we can look dispassionately, and this is not easy to do, at the role dentists and hygienists play in the prevention and control of the bacterial infections that cause caries and periodontal lesions, we have to recognize that our input as professionals has had inherent limitations.  We are not in the position of physicians who can often cure patients with surgical procedures and other therapeutic measures.

One's dental health depends, almost entirely, on how well the things that get into one's mouth get out. 

These things include substances that one eats, drinks, sucks and chews, and most important of all, the types of microorganisms that one acquires from another parson’s saliva, primarily by kissing.  There are very few things that clinicians can do to compensate for self-care not having an adequate bactericidal potential.

The disappointing and unpredictable results in disease control that have often occurred in patients who have sought professional care can be attributed to the lack of interest and guessing game that many clinicians have played in the management of dentobacterial infections.

Industries that manufacture products used for dental hygiene are intensively engaged in producing dentifrices, oral-hygiene solutions, instruments, and programs that will aid in the control of the pathogenic biofilms that grow on surfaces of teeth.  This means that methods that can prevent and control dentobacterial infections will become more and more available for persons who want to preserve their dental health. 

The dental profession needs to give careful consideration to how it can accommodate to this inevitable trend. 

(Re-printed with permission by Dr. Paul Keyes.)

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