gum surgery versus laser
gummybear
need flap surgery however i read laser is an option--i was wondering
if the laser would kill the bacteria where deep cleaning and root
planing could not get to (had that done versus the surgery two years
ago) some say that was option A but to me there is no option except
surgery after two years of researching and hearing what second,
third, fourth perios have to say--i think i still need surgery so any
thoughts or responses would be appreciated before heading for the
scalpel YIKES!!! ( i am definitely dentistphopia) due to childhood
experience three front teeth with NO ANESTHESIA OR NOVaCAINE
Joel344
Six dozen of one .... half of the other .... its marketing hype!
Show me someone who has been cured
of periodontitis and I will show you .. well you
get the idea.
--
Joel344
------------------------------------------------------------------------
Joel344's Profile: http://dentalcom.net/forum/member.php?userid=12
View this thread: http://dentalcom.net/forum/showthread.php?t=4681
gummybear
Joel344
Well, if you have gingivitis, and / or periodontitis (INFLAMMATION of
the supporting structures), then a thorough prophylaxis or tooth
cleaning, complete with ultrasonic Cavitron debridement will reduce
inflammation.
Home care is essential.
Now some dentists call this exact procedure SRP, scaling and root
planing at $600 a pop, others call it anything else and toss in
irrigation at $40 a quadrant, but all in all, periodontal concerns are
best addressed through prevention and home care.
Now the APA (Periodontists' Association ~ PERIODONTISTS!) dream up
classifications, treatment modalities, everything but please remember
this is a chronic disease. What this means is that 5 years or 10 years
goes by and its impossible to say "THIS HELPED," or "That DID NOT
help."
The studies themselves are flawed as I elaborated in hundreds of posts
right here. More about PerioChip, Periostat, and Arestin later, if you
have lots of stamina to read my posts!
Some of them that is. I hear there are around 46,000 of them!
Joely
gummybear
saying to skip surgery then? i had the Deep root planing &
scaling and went to see another perio for his consultation and he
recommend me to do surgery and bone grafting :shock: tks
cko...@eudoramail.com
My hygienist doesn't use the ultrasonic scaler ... Can you think of a
case(s) where scraping is preferred. (My old hygienist uses the
ultrasonic scaler, though.) Could it be a funding issue? ... my current
hygienist and dentist are members of a faculty group practice at USC.
Also, were you serious about being willing to look at x-rays from
posters?
Alexander Vasserman DDS
Translation analogy of what you are asking us.
My car has been diagnosed with advanced engine wear on 2 cylinders and
I need to get
it fixed by removing the engine however i read a power wrench is an
option--i was wondering if the power wrench would resurface the
breakdown in the engine where doing a thorough cleaning of the engine
would not fix the problem (had that done versus the taking the engine
apart two years ago) some say that was option A but to me there is no
option except taking the engine apart after two years of researching
and hearing what second, third, fourth mechanics have to say--i think i
still need to take the engine apart so any thoughts or responses would
be appreciated before heading for the traditional wrench YIKES!! (i am
definitely mechanicphobic) due to childhood experience with my tricycle
and no safety devices or Nike helmet.
Alexander Vasserman DDS
Your engine block is still worn despite you cleaning all the parts and
getting 4 consults on a very typical problem.
Don't you think you should address the resurfacing issue (bone grafting
and surgery) to get better performance and longer engine life???
Mark & Steven Bornfeld
> On 15 Jul 2006 00:24:42 GMT,
> victori...@yahoo-dot-com.no-spam.invalid (gummybear) wrote:
>
>
>>I have been diagnosed with advanced periodontitis on two quads and
>>need flap surgery however i read laser is an option--i was wondering
>>if the laser would kill the bacteria where deep cleaning and root
>>planing could not get to
>
>
> http://www.millenniumdental.com/research.html
>
> The first article, IMO , gives the best overview
> http://www.millenniumdental.com/pdf/MDT-GD-Sept-Oct-2004.pdf
> pay attention to figure 2, for pocket depths up to 10 mm, SRP does
> almost as well as perio-lase. Figure 3 compares the different
> treatments, including flap surgery
I have rarely if ever seen 10 mm pockets resolve with SRP. Yes, the
tissue tone will improve and there may be some tissue shrinkage, but not
pocket elimination to the extent that the remaining pocket (or sulcus,
if you will) is sustainable by the patient.
One other thing--the diagrams in this paper illustrate suprabony
pockets. When you get over maybe 6-7 pockets most are infrabony. I
can't say specifically whether grafting/guided tissue regeneration are
used in combination with laser surgery (I wouldn't presume one way or
another) but many of these infrabony lesions will require grafting
and/or GTR, and possibly osseous recontouring for a good result.
Therefore, I would be careful about making sweeping judgements about the
suitability of laser surgery for individual patients whose situations
may well be different from those in this paper.
Steve
>
> As to treatment of periodontal disease, not all believe flap surgery
> is the best option. Loesche has done the most work on use of
> antibiotics. You can read his work here
> http://cmr.asm.org/cgi/content/full/14/4/727
>
> or the summary of the debate here
> http://query.nytimes.com/gst/fullpage.html?sec=health&res=9F02E6DB1230F932A15752C0A9659C8B63
>
> Clinical trials in the use of antibiotics (metronidazole ) and
> cleaning as alternatives to surgery continue,e.g., at the Forsythe
> institute
> http://www.clinicaltrials.gov/ct/gui/show/NCT00066001?order=3
>
> On a more personal note, I had a recommendation similar to yours,
> considered laser surgery as an alternative to flap surgery , and
> finally opted for SRP with better oral hygine. One year later no sign
> of deep pockets. I contacted Loesche by email ( he makes the offer of
> help somewhere on the net, I've lost the reference). He was very
> helpful in locating a local dentist that used antibiotic treatment as
> an alternative to surgery, though in my case it was not necessary.
>
>
>
--
Mark & Steven Bornfeld DDS
http://www.dentaltwins.com
Brooklyn, NY
718-258-5001
Mark & Steven Bornfeld
> On Tue, 25 Jul 2006 17:07:16 GMT, Mark & Steven Bornfeld
> <bornfe...@dentaltwins.com> wrote:
>
>
>>george1234 wrote:
>>
>>>You can read the research (such as it is) on perio-lase here
>>>http://www.millenniumdental.com/research.html
>
>
>> I have rarely if ever seen 10 mm pockets resolve with SRP. Yes, the
>>tissue tone will improve and there may be some tissue shrinkage, but not
>>pocket elimination to the extent that the remaining pocket (or sulcus,
>>if you will) is sustainable by the patient.
>> One other thing--the diagrams in this paper illustrate suprabony
>>pockets. When you get over maybe 6-7 pockets most are infrabony. I
>>can't say specifically whether grafting/guided tissue regeneration are
>>used in combination with laser surgery (I wouldn't presume one way or
>>another) but many of these infrabony lesions will require grafting
>>and/or GTR, and possibly osseous recontouring for a good result.
>
>
> I agree SRP is not the answer to all, the severity of the disease
> influences the selection of treatment. The conclusion the perio-lase
> author does reach is "It is evident from this comparison that pocket
> depth reductions from LANAP are similar to those obtained from ffalp
> and osseous resection and modified Widman flap surgical procedures"
>
>
>>Therefore, I would be careful about making sweeping judgements about the
>>suitability of laser surgery for individual patients whose situations
>>may well be different from those in this paper.
>
>
> Again we agree. My goal was to answer the question about laser
> surgery, and to cover alternatives to surgery. My intent was to point
> out alternatives that have an outcome similar to surgery, so that
> such alternatives could be explored. There are, of course, gradations
> in severity of the disease which requre different treatments.
>
> Leaving perio lase behind.... Then there is Loesch's opinion that the
> disease is caused by specific pathogens that can be treated with
> specific antibiotics. He also gives the reason why traditional
> treatment recommendations have not changed: in 8 of 10 cases
> traditional methods work.
Yes they "work", but patients hear these words and equate them with
"cure". Many chronic periodontal conditions are refractory because
patients think they have been cured.
>
> " If dental decay was a specific infection, why could periodontal
> diseasenot also be a specific infection resulting from the selection
> of bacteria that can grow in the stagnant pocket environment, using
> nutrients which leak into the pocket in the GCF as the result of the
> microbes' production of proinflammatory molecules? In the past 25
> years, over 200 studies have compared the flora of disease-associated
> plaques with the flora found in plaques associated with periodontal
> health. The results have generally shown a limited number of bacterial
> species mainly gram-negative anaerobes, to be significantly associated
> with periodontal disease.These findings have not changed the
> prevailing treatment philosophy in periodontal disease, because of the
> powerful legacy of the nonspecific plaque hypothesis in dictating
> treatment protocols that have become the standard of care in clinical
> dentistry. It is difficult to change a treatment approach whose 80%
> level of effectiveness is accepted by the clinician (111, 189, 190)
> and which provides the economic infrastructure of clinical
> periodontology. "
The basic premise here is actually pretty well-known. The more
interesting part is why these specific bacteria colonize some patients
and are difficult to impossible to eliminate long-term, while other
patients are resistant to these same strains establishing themselves in
the first place (even in the absence of oral hygiene).
Steve
>
>
>>Steve
Steven Bornfeld
george1234 wrote:
> On Tue, 25 Jul 2006 18:52:42 GMT, Mark & Steven Bornfeld
> <bornfe...@dentaltwins.com> wrote:
>
>
>
>>>Leaving perio lase behind.... Then there is Loesch's opinion that the
>>>disease is caused by specific pathogens ...
>>
>> Yes they "work", but patients hear these words and equate them with
>>"cure".
>
>
> Loesch posits that specific anerobes are responsible for AP. He finds
>
> " a combination of metronidazole and doxycycline, followed if
> necessary by local delivery of antimicrobial agents to the pocket in
> an ethylcellulose film, resulted in an 80% reduction in the need for
> surgery and extraction (153). These results have been sustained for 5
> years or more "
>
> That is as much of a cure as traditional treatments
"Need for surgery" is a very, very fungible concept. Need for
extraction is somewhat less fuzzy. ;-)
I can tell you that there is nothing new in use of metronidazole,
docycycline, or intrasulcular medications. I can also tell you that in
the real world (experience of the periodontists I refer to), the results
have been underwhelming.
Certainly the fact that these men and women are surgeons could be seen
as a potential bias. ;-) Call me gullible; I believe them.
>
>
>>Many chronic periodontal conditions are refractory because
>>patients think they have been cured.
>
>
> It's pretty clear that re-infection will take place regardless of the
> method of dis-infection ( debridement, surgery, or antibiotic). There
> is no "cure", It is a more or less chronic condition, not a strict
> division into the sick and the well
>
> But I defer to your clinical experience here.
>
>
>>>" If dental decay was a specific infection, why could periodontal
>>>diseasenot also be a specific infection resulting from the selection
>>>of bacteria
>>
>
>> The basic premise here is actually pretty well-known. The more
>>interesting part is why these specific bacteria colonize some patients
>>and are difficult to impossible to eliminate long-term, while other
>>patients are resistant to these same strains establishing themselves in
>>the first place (even in the absence of oral hygiene).
>
>
> Well, yes that is interesting. not to put to fine a point on it, I
> think periodontists have only begun to scratch the surface (groan) The
> advance from non specific theory of infection infection to the
> identification of 4 to 10 anerobic species specifically associated
> with the disease is a recent result..
I am not up on the latest research, I'm afraid (I hang my head).
However, implication of specific anaerobes (as well as specific host
factors) was already being discussed during my dental school days (I
graduated in 1976), if not before. I don't doubt that the list of
implicated pathogens is longer now than it was then.
Steve
>
> --G
>
Steven Bornfeld
george1234 wrote:
> I'm slowly making my way through the Loesch paper quoted, but a
> partial explanation is offered
>
> However, the tooth surfaces cannot be completely "cleaned" of plaque
> species by these procedures, even when surgery to get access to the
> root surfaces is performed (318). If these residual organisms are
> enriched per"`centage-wise for the periodontopathic species, then the
> plaque community that returns could be as proinflammatory as the
> plaque that had just been suppressed. This would be especially true if
> there is an enrichment of the plaque flora by bacteria that are left
> behind on the root surface or that have invaded the dentinal tubules
> (2). Large numbers of bacteria invade these tubules and have been
> shown by electron microscopic examination to repopulate the root
> surfaces (3). This selection for periodontopathic species as a result
> of debridement, as well as the difficulty in controlling a biofilm
> such as dental plaque, might explain the failure rate of about 20%
> observed in clinical practice (111, 189).
>
>
Why would the residual bacteria be enriched percentage-wise for
specifically pathologic species?
In fact, most of the studies we've heard over the years followed an
experimental biofilm beginning with thorough debridement. Forgive, for
my memory is quite hazy. The first precipitant on the root surface is a
proteinaceous "salivary pellicle", which is itself non-bacterial but
provides an excellent medium for bacterial growth. The maturation of
plaque from this point on has been studied--the primary organisms to
populate the plaque are primarily gram-positive rods and cocci. These
are generally considered normal resident organisms. Only if the plaque
is left undisturbed for a longer period do you start seeing the
gram-negative bacteria, including the bulk of the usual suspects in
pathogenesis (in our day the professors always spoke of "spirochetes",
which I assume some of them are--for all I know maybe some treponema
were implicated at one time).
In any case, it certainly is believable that residual bacteria in the
sulcus, or even in the dentinal tubules could repopulate the plaque.
BTW, I consider a failure rate (again, what are the criteria for
failure) of 20% as exceptionally LOW.
Steve
Steven Bornfeld
george1234 wrote:
> On Wed, 26 Jul 2006 00:01:19 GMT, Steven Bornfeld
> <dentalt...@earthlink.net> wrote:
>
>
>
>> Why would the residual bacteria be enriched percentage-wise for
>>specifically pathologic species?
>
>
> I'm not sure.. I have not read the refeerences he cites. It may be
> that the electron microscope observation is that the the anerobic
> pathogens preferentially occupy the tubules, and that when you scrape
> the general population away when you debride, you leave the pathogens.
> However.. that does not conform to my undestanding of the
> symbiotic/ecological relation among the species. By that I mean the
> anaerobes don't show up until the aerobes have created the proper
> ecological niche.
It may just be that the intradentinal bacteria are in a relatively
anaerobic environment. That would make sense.
>
>
>
>> In fact, most of the studies we've heard over the years followed an
>>experimental biofilm beginning with thorough debridement. Forgive, for
>>my memory is quite hazy. The first precipitant on the root surface is a
>>proteinaceous "salivary pellicle", which is itself non-bacterial but
>>provides an excellent medium for bacterial growth. The maturation of
>>plaque from this point on has been studied--the primary organisms to
>>populate the plaque are primarily gram-positive rods and cocci. These
>>are generally considered normal resident organisms. Only if the plaque
>>is left undisturbed for a longer period do you start seeing the
>>gram-negative bacteria, including the bulk of the usual suspects in
>>pathogenesis
>
>
> That's my general understanding too
>
>
>>(in our day the professors always spoke of "spirochetes",
>>which I assume some of them are--for all I know maybe some treponema
>>were implicated at one time).
>
>
> Spirochetes are found in Acute necrotizing ulcerative gingivitis.(the
> trench mouth of ww1)as well as AP. Apparently the understanding of
> the "cause " shifted from the anerobic spirochetes to the
> microaerophilic A. actinomycetemcomitans and now back to the
> anerobes. Because their caracteristic structure is evident in a phase
> contrast microscope, Loesche suggests spirochetes be used as an
> indicator of AP. He says
>
> "The older literature identified anaerobic organisms such as
> spirochetes and black-pigmented Bacteroides species (now classified as
> Porphyromonas and Prevotella species), as putative periodontal
> pathogens "
>
> "With the identification of A. actinomycetemcomitans as a putative
> periodontal pathogen, emphasis shifted from anaerobes to this
> microaerophilic species. "
>
> "The findings shown in Tables 2 through 4, involving large numbers of
> samples and using diverse methods, indicate that anaerobes, rather
> than A. actinomycetemcomitans or other microaerophilic species, are
> more likely to be present or to dominate in plaques associated with
> EOP and AP. This would suggest that treatment strategies and tactics
> should be designed to selectively target certain anaerobic members of
> the plaque flora."
>
>
>> In any case, it certainly is believable that residual bacteria in the
>>sulcus, or even in the dentinal tubules could repopulate the plaque.
>> BTW, I consider a failure rate (again, what are the criteria for
>>failure) of 20% as exceptionally LOW.
>
>
> By failure he means preiodontitis
Most of the patients receiving (or who should receive) SRP already have
periodontitis.
>
> " 30% <of the gerneral poulation> have periodontitis as defined by the
> presence of three or more teeth with pockets of >= 4 mm ."
If you select for a population over 35-40 years of age, every survey
I've seen shows a far higher incidence. Certainly counting children in
your statistics would make things more grim.
Sadly, I would say the majority of my patients under the care of
periodontists (GOOD periodontists!) show relapse at some point, or more
or less acute exacerbations. This doesn't mean treatment is a failure,
but success must be viewed in less absolute terms. Certainly this is a
tough concept to sell to a patient--that losing your teeth in 20 years
rather than 10 (obviously a presumption) is a worthy goal.
Understandably patients aren't happy.
Thanks for the info--this is an interesting article.
Steve
>
>
>>Steve
>
> --George
Steven Bornfeld
george1234 wrote:
> On Tue, 25 Jul 2006 23:52:04 GMT, Steven Bornfeld
> <dentalt...@earthlink.net> wrote:
>
>
>
>> I am not up on the latest research, I'm afraid (I hang my head).
>>However, implication of specific anaerobes (as well as specific host
>>factors) was already being discussed during my dental school days (I
>>graduated in 1976), if not before. I don't doubt that the list of
>>implicated pathogens is longer now than it was then.
>
>
> The paper is a survey paper and he does summarize the work of others.
> I'm not schooled enough in the art to identify Loesche's unique
> contirbution.
>
> I found the list of pathogens studied suprisingly small. At one point
> he cites more thatn 400 species in the plaque. When he summarizes
> earlier studies in table 2 and 5 he concentrates on 10. In his
> conclusion he callls out only 3 (P. gingivalis, B. forsythus, and T.
> denticola)
>
> Bacterial species that were monitored listed in tables 2 and 5
>
> A. actinomycetemcomitans;
> Aa, A. actinomycetemcomitans;
> Cr, C. rectus;
> Ec, E. corrodens;
>
> Anerobic
> Pg, P. gingivalis;
> Bf, B. forsythus;
> Td, T. denticola;
> Pi/Pn, P. intermedia/nigrenscens;
> Fn, F. nucleatum;
> Eub. Sp. = Eubacterium species;
> Spir, spirochetes;
> Tv, T. vincentii.
>
>
> BTW... I hope my summaries have not mis represented Loesche's view.
> I'll let him speak for himself in the conclusion to his survey paper
>
> "The evidence presented in this review indicates that most, if not
> all, forms of periodontal disease are specific, albeit chronic,
> infections. Regardless of whether the host is genetically predisposed
> to periodontal disease, as in Papillon-LeFevre syndrome or Down
> syndrome, or if the host is compromised by leukocyte defects as in LJP
> or diabetes, or is a smoker, or has poor oral hygiene, or has simply
> aged, the clinical symptoms are almost always significantly associated
> with the overgrowth of a finite number of anaerobic species, such as
> P. gingivalis, B. forsythus, and T. denticola in the subgingival
> plaque. This overgrowth can be periodically suppressed by mechanical
> debridement over a lifetime, the current treatment paradigm, or the
> flora can be altered by the judicious short-term usage of
> antimicrobial agents targeted against the specific anaerobes. This
> latter approach, while supported by several double-blind clinical
> studies (147), goes contrary to centuries of dental teaching which
> states that periodontal disease results from the overgrowth of plaque
> on the tooth surfaces, i.e., a "dirty mouth." The challenge lies not
> in proving that periodontal disease is an infection but in
> implementing treatment procedures based on the fact that it is an
> infection. The antimicrobial treatment of periodontal infections will
> benefit from studies suggesting that periodontal disease may be a risk
> factor for cardiovascular disease and stroke. If an antimicrobial
> approach is as effective as a surgical approach in the restoration and
> maintenance of a periodontally healthy dentition (147, 153), this
> would give a cardiac or stroke patient and his or her physician a
> choice in the implementation of treatment seeking to improve the
> patient's periodontal condition so as to reduce and/or delay future
> cardiovascular events.
>
I remember the A. actinomycetemcomitans and Eichenella sp. as the ones
they harped on the most.
Does "Micro-aerophilic" equal facultative anaerobe? I'm unfamiliar
with the term.
Steve
Alexander Vasserman DDS
an analogy of what was being asked.
george1234 wrote:
> On 15 Jul 2006 21:35:06 -0700, "Alexander Vasserman DDS"
> <purple...@yahoo.ca> wrote:
>
> >
> >My car has been diagnosed with advanced engine wear on 2 cylinders and
> >...YIKES!! (i am
> >definitely mechanicphobic) due to childhood experience with my tricycle
> >and no safety devices or Nike helmet.
>
> You know, most people in need of help don't come to this forum with
> advanced degrees in medicine or dentistry, skilled in the art of
> succinct medic al history presentation. They pose their questions in a
> conversational manner, and some times meander about the point. You can
> choose to help by answering the underlying question, or to belittle
> the manner in which the question was posed