Recent letters to the editor in the Journal of American Dental Association:

Reprinted with permission from the Amerian Dental Associatiom, JADA,

December 2014, 145,1212.

Defining Oral Health

I would like to applaud Dr. Michael Glick and Dr. Daniel Meyer’s June JADA commentary, “Defining Oral Health: A Prerequisite for Any Health Policy” (JADA 2014;145[6]:519–520). How do we define oral health objectively? My objective list would include the following items: decayed, missing or filled teeth; bone loss around the teeth; issues with salivary flow and composition; problems with occlusion (lack of anterior guidance) and presence of tooth mobility; the presence of any airway restriction that could be improved by jaw repositioning; pain; pathology of soft tissues; problems with speech, swallowing or chewing; unusual wear, chipping or positioning of the teeth; any issues with overall facial appearance and smile; radiographic findings; and mouth odor.

The problem comes in objectively defining periodontal disease and gingivitis. Bone loss is not periodontal disease. Is gingivitis a disease or a symptom? How can gingivitis be defined objectively? How do we define periodontal disease objectively? These are important questions that would help define oral health.

Good epidemiology requires objective data. With objective data we then can know if oral health influences general health, and if general health influences oral health.

We know general health improves with cigarette smoking cessation, but how do we document it with oral health?

David C. DiBenedetto, D.M.D.


Reprinted with permission from the American Dental Association, JADA October 2012 143(10): 1069-1071

Endodontics in General Practice

After reading Dr. Susan Bernstein and colleagues' May JADA article, “Outcomes of Endodontic Therapy in General Practice: A Study by the Practitioners Engaged in Applied Research and Learning Network” (Bernstein SD, Horowitz AJ, Man M, et al. JADA 2012;143[5]:478-487) and Dr. Xi Chen and colleagues' June JADA article, “Length of Tooth Survival in Older Adults With Complex Medical, Functional and Dental Backgrounds” (Chen X, Clark JJJ, Supawadee N. JADA 2012;143[6]:566-578), I was disappointed that functioning occlusion was neglected by all the authors in both important articles.

It would have been nice to see the type of occlusion the patients had with endodontic failures. Did group function contribute to multirooted failures of endodontically treated teeth?

In the older adults study, it would have been nice to observe whether those entering the study had group function or anterior guidance with normal type I jaws and which posterior teeth were lost. Do individuals with group function have a greater chance of losing their posterior teeth than those with anterior guidance? It would have been nice to see the longevity of teeth with Angle Class III, with and without an open bite.

David DiBenedetto, DMD

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DiBenedetto,DC. Letter to the editor and author's response. JADA 2011;142(4)368-9. Copyright 2011. American Dental Association.  All rights reserved. Reproduced by permission.

 
    The Journal of the American Dental Association April 1, 2011 vol. 142 no. 4 368

I read Dr. Brian Bresnahan and colleagues’ October JADA article, “Quality of Life and Economic Burdens of Malocclusion in U.S. Patients Enrolled in Medicaid (Bresnahan BW, Kiyak HA, Masters SH, McGorray SP, Lincoln A, King G. JADA 2010; 141[10]:1202–1212), and wondered how the authors would define malocclusion.

Is malocclusion like pornography? You know it when you see it?

Malocclusion must be defined before we can decide whether it interferes with the quality of one’s life, and then, what is the economic cost if it is not resolved? In today’s difficult economic times, when should public funds pay for treatment of malocclusions that some would say are quite subjective?

Angle’s classification of occlusion is a static relationship. Static relationships help define esthetics. Crooked teeth may be unpleasing to look at, but how crooked do teeth have to be before treatment is necessary?

As a restorative dentist, functioning occlusion is more important than Angle’s classification for maintaining the health of the temporomandibular joint and the perodontium. I feel orthodontics has neglected the functioning occlusion facet in determining what a malocclusion is.

Lastly, I was surprised that there was no mention of obstructive sleep apnea caused by a skeleton imbalance of the jaws. Surely this type of malocclusion, even though a static relationship, would greatly interfere with long-term quality of life.


David C. DiBenedetto, D.M.D.


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 J Am Dent Assoc, Vol 140, No 12, 1467-1468.
© 2009 American Dental Association
    
LETTERS
A SYMBIOTIC RELATIONSHIP

I took great interest in reading Dr. Christoph Schaudinn and colleagues’ August JADA cover article, "Periodontitis: An Archetypical Biofilm Disease" (Schaudinn C, Gorur A, Keller D, Sedghizadeh PP, Costerton JW. JADA 2009;140[8]:978–986).

We forget that much of the bacteria that colonize our bodies do it in their own ecosystem, which we call "biofilm." Our bodies comprise about one trillion cells, and the bacteria that colonize us appear to be about 10 trillion. We live in a symbiotic relationship with these bacteria. It would appear that our bodies need these bacteria, and that these biofilms are necessary for our survival. We all should be aware that the lacto-bacilli lining our urogenital and gastrointestinal tracts act as a protective biofilm.

Cystic fibrosis is an inheritable disease, and the authors point out that a biofilm causes pneumonia in patients with cystic fibrosis. Study results show that there is less periodontal disease in cystic fibrosis.1,2 If periodontal disease is a biofilm disease, why is there less periodontal disease in patients with cystic fibrosis? Does cystic fibrosis affect dental plaque?

The authors point out that middle-ear infections are another biofilm disease. Middle ear infections are mostly a young children’s disease, and most children outgrow these infections. Healthy children do not get periodontitis, even though healthy children get plenty of gingivitis. Why? How does biofilm as a cause of disease explain this—that healthy children don’t get periodontitis, but they get middle-ear infections?

The authors think Koch postulates3–5 are outmoded because all organisms cannot be cultured, and that many organisms acting together act differently. One hundred years ago, Koch needed to perform culturing because it would eliminate any doubt that specific organisms would cause specific diseases. We need to know when specific entities cause disease. Koch did not have tools that we have today that can identify organisms without culturing, such as polymerase chain reaction. Koch postulates gave rise to germ theory, and germ theory makes no distinction in whether one is an adult or a child.

If biofilm causes disease, then we should be able to transfer biofilms to susceptible hosts to cause disease. Where has this been done with periodontitis? Biofilm may be unique to its host. The host may be responsible for its own biofilm. Environmental factors also play a role in colonization. We also know that normal biofilms become opportunistic and cause pathology when the host is stressed and has diseases such as AIDS and uncontrolled diabetes. The questions we should ask for adults are how, when and, for epidemiology, how often do biofilms cause periodontitis?
REFERENCES

    Blacharsh C. Dental aspects of patients with cycstic fibrosis: a preliminary clinical study. JADA 1977;95(1):106–110.[Abstract]

    Kinirons MJ. Dental health of patients suffering from cystic fibrosis in Northern Ireland. Community Dent Health;1989;6(2): 113–120.[Medline]

    Donlan RM, Costerton JW. Biofilms: survival mechanisms of clinically relevant microorganisms. Clin Microbiol Rev 2002; 15(2):167–193.[Abstract/Free Full Text]

    Inglis TJ. Principia aetiologica: taking causality beyond Koch’s postulates. J Med Microbiol 2007;56(Pt 11):1419–1422.[Abstract/Free Full Text]

    Grimes J. Koch’s postulates: then and now. Microbe 2006;1(5):223–228.

    David DiBenedetto, DMD
    Pembroke, Mass.




    The Journal of the American Dental Association December 1, 2009 vol. 140 no. 12 1467-1468

  

 
© 2007 American Dental Association
    
LETTERS
OCCLUSION AND PERIODONTAL DISEASE

I took great interest in reading the October JADA Point/Counterpoint regarding the role of occlusion in periodontal disease.1,2 However, many problems exist in deciding whether occlusion causes or contributes to periodontal disease.

    – How do we define periodontal disease? Is bone loss the same as periodontal disease? Do we confuse bone loss with periodontal disease?
    – What is normal occlusion? What is occlusal trauma? What are occlusal discrepancies?
    – Is the periodontal ligament different from other ligaments in the body that are overworked? We know other ligaments in the body break down when they get overused. Easier questions that we might be able to answer are the following:
    – Do dentitions that have canine guidance have more buccal recession on maxillary canines than dentitions with group function?
    – Do patients with Class III occlusion have less gingival recession than others?

It is also interesting to note that Dr. Gordon Christensen, later in the same October issue ("Implant Therapy, Versus Endodontic Therapy," JADA 2006;137(10):1440–3), feels that implants have questionable success when extreme occlusal forces are placed on them.
REFERENCES

    Harrel SK, Nunn ME, Hallmon WW. Is there an association between occlusion and periodontal destruction?: Yes—occlusal forces can contribute to periodontal destruction. JADA 2006;137(10):1380–92.[Free Full Text]

    Deas DE, Mealey BL. Is there an association between occlusion and periodontal destruction?: Only in limited circumstances does occlusal force contribute to periodontal disease progression. JADA 2006;137(10): 1381–9.[Free Full Text]

    David C. DiBenedetto, DMD


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