Nice to see a round table discussion in Compendium of C.E. in
Dentistry , Jan/Feb 2009 edition, page46.

I would only agree with Thomas E. Van Dyke, DDS, Phd.  some
interesting quotes:

(1) "as our understanding of periodontal inflammation increases, our
current understanding of the microbiology of periodontitis becomes
less clear."

(2) "the role of specific bacteria is unknown."

(3) "our knowledge of the microbiology of peridiodontitis is based on
large cross-sectional and association studies.  ...however, not
possible to draw cause-and-effect inferences from these studies; the
implication of the 'red complex' as pathogens is an 'association.' "

(4) "the host inflammatory response dictates the composition of the
biofilm"

(5)  "the inflammatory response changes the microenvironment of the
biofilm and selects for specific organisms. What this means is that
the inflammatory response changes the microenvironment of the biofilm
and selects for specific organisms.  One might then argue that
P.gingivalis and T. forsythia overgrow in the periodontal pocket
because of  inflammation; the implication is that the inflammation
precedes the overgrowth.  What then initiates the disease?  Could it
be early, gram-positive colonizers that elicit a profound inflammatory
response in the susceptible host?"

(6)  "NO ORGANISMS WERE IDENTIFIED AS BEING PREDICTIVE OF FUTURE
ATTACHMENT LOSS,"  [my emphasis by capitalization] "Whereas gingival
inflammation did predict future attachment loss."    [ I would  say
Not true with cigarette smokers].

and (7) "Are 'traditional' peridontal pathogens the initiators of the
disease of do they result from the disease?"   [This is maybe how I
feel]

...David DiBenedetto, DMD, author of "Insider's guide to gum disease,
orthodontics, and dentistry. What is not taught in dental school."