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CONTROVERCONTROVER
SIES INSIES IN
PERIODONTIPERIODONTI
CSCS
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INTRODUCTIONINTRODUCTION
When a thing caeses to be a matter of controversy, it caeses to be a matter
of interest.
In reviewing past and present concepts and treatment modalities that areavailable, it becomes evident that there are no completely accepted
principles and techniques.
On this note, I would like to present my topic for seminar:
CONTROVERSIES IN PERIODONTICS.
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.
VIRAL BACTERIAL INTERACTIONS IN PERIODONTITISVIRAL BACTERIAL INTERACTIONS IN PERIODONTITIS
Recent studies have demonstrated various human viruses, especially cytomegalo
viruses and Epstein Barr Viruses type 1, seem to play a part in pathogenesis of
human periodontitis.
Parra and Slotes reported that HCMV was present in 60 % of patients and EBV- IN30%. Slots examined frequency of HCMV, EBV-2 and herpes simplex Viruses in
subgingival samples.
They reported 89% of samples yielded atleast one of three test viruses from deep
periodontal pockets and 56% yielded from shallow periodontal pockets
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Dual virus infection seems to be particularly pathogenic and they may
accentuate bacterial virulence factor.
HCMV resides in monocytes, macrophages, and T cells and EBV in B
cells, which has the potential to impair major defense mechanism of the
periodontium.
Tiny et al. reported that high rate of active HCMV infection in earlylocalized aggressive periodontitis.
They suggested that puberty is an important for HCMV and EBV primary
infection or reinfection.
Puberty related perturbation of immune system
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CMV has been shown to lead decreased Polymorphonuclear Leukocytechemotaxis, phagocytosis, oxidative burst and intracellular killing capacity and it
may increase the human susceptibility to bacterial infection.
HCMV infection of monocytes \ macrophage can induce prostaglandin E
2 production that may result in increased bone resorption and suppressed T
lymphocyte function.Mac Donald et al. emphasize the possible detrimental role of HCMV and EBV-1 in
periodontal repair.
Bacterial infection and other condition that promote diapedesis of
inflammatory cells in a tissue would increase possibility of initiating an HMCV
infection of the tissue.
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Contreras et al. in 1999 conducted a study to examine relation ship betweensubgingival herpes virus and periodontal disease and periodontopathogenic
bacteria
The study confirmed positive relationship between subgingival EBV-1, HCMV and
mixed herpes viral infections and clinical severity of periodontitis.
Viral infection promote subgingival pathogenic bacterial infection than vice versa.
Neutrophil dysfunction may serve to potentiate over growth and virulence of P
gingivalis and othermicrobes.
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WIDTH OF THE KERATINIZED GINGIVAWIDTH OF THE KERATINIZED GINGIVA
Attached gingiva is firm, resilient and tightly bound to underlying
periosteum of alveolar bone.
Distance between mucogingival junction and projection on external surface
of the bottom of the gingival sulcus
Keratinized gingiva includes marginal gingiva also.
No standard width of keratinized gingiva has been established.
It may be necessary to increase zone of healthy tissue if it is subjected to
trauma of the prosthetic treatment.
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For many years the presence of adequate zone of gingiva was considered
critical for maintenance of marginal tissue health and for prevention of
continues loss of connective tissue attachment.
Narrow zone of gingiva --
1) was in sufficient to protect periodontium from injury caused by frictional forcesencountered during mastication and to dissipate the pull on the gingival
margin created by muscles of adjacent alveolar mucosa.
2) it will favor sub gingival plaque formation
3) it will also favor attachment loss and soft tissue recession
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.
Goldman and Cohen outlined a tissue barrier conceptGoldman and Cohen outlined a tissue barrier concept
Dense collagenous band of connective tissue retards or obstructs the spread of
inflammation better than does the loose fiber arrangement of the alveolar
mucosa.
Limits recession as result of inflammation
This view is indirectly supported by findings of Kennedy et al.after recall
evaluations of u patients from their 6 years longitudinal study of free
autogenous gingival grafts
ADEQUATE WIDTH OF GINGIVAADEQUATE WIDTH OF GINGIVA
Some authors suggested that less than 1 mm.
Apicocoronal height ought to exceed 3 mm
Third category of authors stated that adequate zone of gingiva is any dimension ofgingiva which ---1) is compatible with gingival health or 2) prevents retraction of gingival
margin during movements of the alveolar mucosa.
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Lang and Loe conducted a study to evaluate the significance of the gingival zone.
The results showed that despite of the fact that tooth surfaces were free from
plaque, all sites with less than 2 mm exhibited persisting clinical signs ofinflammation..
In contrast teeth possessing least attached tissue s (cuspid and bicuspids) are least
involved periodontally as compared to molars.
Incidence of disease is greater on palatal and lingual surfaces of molars where
amount of keratinized tissue is greatest
Wenstrom and Lindhe have shown that a free gingival unit supported by a loosely
attached alveolar mucosa is not more susceptible to inflammation than a free gingival
unit that is supported by a wide zone of attached gingiva.
.
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Miyasato et al. (1997) ceased oral hygiene for a period of 25 days andfound no difference in development of clinical signs of gingivalinflammation between areas with minimal and those with appreciable
width of gingiva.
Dorfman et al. examined 96 patients with bilateral side facial toothsurfaces exhibiting minimal keratinzed tissues, which has been treatedwith free gingival graft on one side and un treated control on other side.
Width of keratinized gingiva on grafted site was increased to 4mmfollowing the treatment.
The attachment level at grafted sites and control remained unchangedthrough out the years.
Thus narrow zone of gingiva has the same resistance to continuesattachment loss as wider zone of gingiva.
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TRAUMA FROM OCCLUSIONTRAUMA FROM OCCLUSION.
What is occlusal trauma?
The international workshop forclassification of periodontal disease andconditions in1999.
Occlusal Trauma - It is injury resulting in tissue changes within attachment
apparatus as a result of occlusal forces.
Primary Occlusal Trauma Injury resulting in tissue changes from excessive occlusal
forces applied to a tooth or teeth with normal support.
Secondary trauma from occlusion Injury resulting in tissue changes from normal or
excessive occlusal forces applied to a tooth or teeth with reduced support.
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Several early authors felt that occlusal forces were the initiating factor in
periodontal disease and led to ongoing progression of periodontal lesion.
In an attempt to demonstrate this relationship several animal studies on
sheep and monkeys were conducted
Later some investigators state that traumatic occlusion causes changes
in attachment apparatus without involving gingival unit.
They postulated that change in attachment apparatus is mainly due to reduced
blood supply to periodontal ligament
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Orban and Weinmann in 1933 using human autopsymaterial evaluated .They concluded that there was no relation ship between excessive occlusal force
and periodontal destruction.
Instead they suggested that gingival inflammation extending in to supporting bone
was the cause of periodontal destruction
During the same time Glickman and co workers published studies.
These studies demonstrated a phenomenon described as an altered pathway ofdestruction when an excessive occlusal force was present.
Change in orientation of gingival and periodontal fibers
Co destruction.
Vertical osseous defects
Based on this observation, use of occlusal adjustment was advocated as part of the
treatment of existing periodontal disease,
Occlusal adjustment to prevent periodontitis was not advocated
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Waertaug evaluated large number of human autopsy specimens to determinerelationship of morphology of osseous defect and excessive occlusal forces.
No relation between excessive occlusal force and vertical bone loss.
Polson and Lindhe conducted studies to evaluate effect of plaque and excessiveocclusal forces in animal models.
These studies agreed removal of plaque and control of inflammation would stopprogression of periodontal disease whether or not excessive occlusal forces are
present.
Meitner reported when squirrel monkeys was subjected to repeated mechanicalinjury in combination with marginal periodontitis, the connective tissue loss wasnot greater than that of specimen in which periodontitis alone was induced.
Thus these appeared to be no co destructive effect on connective tissueattachment.
.
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PROBLEM IN RELATING FINDING FROM ANIMALPROBLEM IN RELATING FINDING FROM ANIMAL
RESEARCH TO THE HUMAN DENTITIONRESEARCH TO THE HUMAN DENTITION
An ideal model on which to study occlusion is not yet to be found.
If a high crown on tooth of a dog or monkey, the tooth will intrude andrecognize a new position while human tooth gets progressively
mobile.Parafunctional habit is a major factor in human occlusal trauma,
monkeys and dogs not known to have such persistent habits
Periodontal disease naturally occurs in humans.
In the animals models the lesion of periodontal is induced artificially.
With treatment these artificially treated lesion repair more predictablythan naturally occurring lesions
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PERIODONTAL ENDODONTIC CONTROVERSYPERIODONTAL ENDODONTIC CONTROVERSY
Two questions have been raised and continue to be matters of dispute.
1) Is periodontal disease a cause of pulpal necrosis?
2) Can a pulpless tooth be cause of periodontal disease?
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The effect of periodontal disease andThe effect of periodontal disease and
procedures on the dental pulpprocedures on the dental pulp
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Periodontal diseasesPeriodontal diseases
Recent publications have suggested that periodontal disease is a direct
cause of Pulpal atrophy and necrosis.
The pathways for communication and therefore for the extension of
disease from a periodontal pocket to pulp are through patent dentinal
tubules, lateral canals, and apical foramina.
Many histological and clinical studies suggest, however, that such
relationships rarely, if ever, result in pulp necrosis.
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Kirkham examined 100 periodontally involved teeth and found only 2% had
lateral canals located in a periodontal pocket.
Tagger & Smukler removed roots from molar teeth so extensively involved
with periodontal disease that root amputation was required, and found that
none of the resected roots showed inflammatory changes.
Haskell et al also removed roots from maxillary molars with periodontal
involvement and found no inflammatory cells or very few inflammatory cells
present in the pulps of the periodontally involved resected roots.
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Czarnecki & Schilder performed a histological study of intact, caries freeteeth and compared the pulp of teeth, which had periodontal disease.
The pulp of the periodontally involved teeth were all histologically similar tocaries free teeth .
Teeth with extensive decay or extensive restortations showed evidence ofpulpal pathosis.
Ross & Thompson evaluated the progress of 100 patients with maxillary molarfurcation involvement over a period of 524 years.
Of the 387 maxillary molars, 79% had at least 50% or less bone supportaround one root prior to periodontal treatment.
Only 4% required root canal treatment subsequent to periodontal therapy. Nonewere ascribed to the effects of advanced periodontal disease in pulp.
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Jaoui et al. studied patients with advanced periodontal disease for 514
years after completion of active periodontal treatment .
Of the 571 teeth that did not have root canal treatment at time of completion
of periodontal treatment, only one tooth required root canal treatment over
the 5 to 14 year recall period.
Pulpal insult through patent dentinal tubules or the occasional exposed
lateral canal have relatively insignificant effect on the ability of the dental
pulp tissue to survive.
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Periodontal proceduresPeriodontal procedures
The clinical research studies by Ross Thompson, Bergenholtz , Nyman
and Jaoui et al evaluated patients who presented with advancedperiodontal disease, received periodontal treatment.
They received follow up maintenance for periods ranging from 4 to 24years. There were 1,623 teeth in the combined studies
Four percent required root canal treatment subsequent to periodontaltreatment, and follow up periodontal care.
Cause of pulp necrosis was mainly due to pulpal exposure.
Extension of periodontal disease to involve the root apices is also citedas a reason for root canal treatment
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In summary dental pulp is capable of surviving significant insults and
that the effect of periodontal disease as well as periodontal treatment is
on the dental pulp is negligible.
The weight of evidence in literature shows that clinical significance of
the relationship between periodontal disease and dental pulp has been
exaggerated in historical and much of the current periodontal
endodontic literature
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Effect of endodontically involved teeth on periodontalEffect of endodontically involved teeth on periodontal
health and healinghealth and healing
. Only in recent years the potential effect of a tooth with a necrotic pulp ora tooth that had root canal treatment was considered as a risk factor in
the initiation of periodontal disease.
Pulpless tooth with a periapical lesion promotes the initiation of
periodontal pocket formation and interfere with healing of periodontal
lesion after periodontal treatment.
Jansson et al. state that teeth teeth with periapical lesion had lost more
proximal bone .
0.19 mm\ year vs 0.06mm\ year for teeth with no periapical lesion orwhere there is evidence of reduction in lesion size.
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Sanders et el. reported in 1983 that after the use of freeze dried bone
allografts 65% of teeth that did not have root canal treatment showed
complete or greater than 50% bone fill in periodontal osseous defects.
While only 33% of teeth which had root canal treatment prior to
periodontal surgical procedure had complete or greater 50% bone fill.
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ROLE OF LYMPHOCYTES IN PERIODONTITISROLE OF LYMPHOCYTES IN PERIODONTITIS
Inflammatory cells, predominantly lymphoid cells and macrophagesthought to be engaged in controlling bacterial challenge.
Participation of these cells in a major way in process of tissue
destruction had not yet been conceived.
In 1970 antibodies to cell surface markers became available which
allowed sub categorization of T lymphocytes in to two major
subsetsCD4and
CD
8.
. CD4 molecules serves as a co receptor for major histocompatibilityclass two molecules on antigen presenting cells.
CD8 molecule is a co receptor for MHC class one molecules of the
target cells.
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Phenotypic AnalysisPhenotypic Analysis
Phenotypic analysis shows that there are no numerical abnormalities of
T helper cells or major cells.
There may be altered ratios of CD4 to CD8 in periodontal lesions of
aggressive periodontitis patients
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Functional studiesFunctional studies
T and B-lymphocytes are present in lesions of early onset periodontitis
patients.
Two accepted activities of the lymphocytes are.
1) They may provide protection against host from infectious agents.
2) they contribute to host tissue damage.
B cells and their linear descendents secrete immunoglobulins (IgG) that
may inactivate bacterial toxins, prevent bacterial adherence and
promote bacterial phagocytosis by polymorphonuclear leukocytes.
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Juvenile periodontitis patients frequently have elevated levels of serumIgG antibodies against AA antigens.
But still there has been controversy that whether these antibodies wereprotective or not.
IgG2 antibodies are the predominant sub class presented.
IgG2 antibodies are not been thought to be effective direct opsonins, oractivators of direct classical pathway.
IgG2 antibodies can kill AA only when neutrophil has the properallotypic form of fc receptor.
Abnormal lymphocyte function in early onset periodontitis asmanifested by lower than normal levels of non stimulated DNAsynthesis in cultured peripheral blood mononuclear cells.
This reaction has been called autologous mixed lymphocyte function(AMLR )
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In some of the studies of periodontal disease patient AMLR returned to
normal after periodontal treatment.
It is not known how diminished AMLR relates to early onset
periodontitis.It has been suggested that reduced AMLR relate to
improper regulation of B cell responses.
In 1974 Langer et al. reported that peripheral blood lymphocyte from juvenile periodontitis patients exhibited reduced blastogenic response
to dental plaque and gram ve bacteria.
Several other studies following this early reports found that
lymphocytes from periodontitis patients exhibited more exacerbated
than normal blastogenic response to mitogens and bacterial antigens.
This phenomenon remains with no strong scientific evidence although it
may be related to reduce AMLR via reduced population of suppressor
inducer T cells.
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ROOT - CONDITIONINGROOT - CONDITIONING
Exposed root surface as result of periodontitis has undergonesubstantial alteration and may no longer serve as an appropriatesubstrate for cell attachment.
Loss of collagen fiber insertion, contamination of root surface bybacteria and alteration in mineral density.
Root surface also lack chemotactic stimuli for migration of cell capableof producing periodontal regeneration.
Apical migration of junctional epithelium along root surface over
connective tissue following surgical therapy also appear to inhibitregeneration
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Scaling and root planning is effective in removing bacterial deposits as wellas removing endotoxins from exposed root surface.
How ever it results in formation of smear layer is thought to serve as aphysical barrier between periodontal tissues and root surface and mayinhibit formation of new connective tissue attachment to root surface.
Root conditioning of these periodontally involved root surface will eliminate
cytotoxic materials, will dematerializes the planed root surface,will alsoexpose and enlarge opening of dentinal tubules and will dematerializes theinter tubular dentin.
Exposed collagen matrix of dentin is chemotactic for PMN, macrophageand fibroblasts.
It can also support the attachment and migration of fibroblast.
Root surface demineralization will also enhance healing
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HISTOLOGICAL AND CLINICAL SUTDIESHISTOLOGICAL AND CLINICAL SUTDIES
College of dentistry --Columbus asses the efficacy of root surface
biomodification through tetracycline citric acid or EDTA in patients with
chronic periodontitis.
They included all the studies evaluating histological and clinical effects
of citric acid, tetracycline and EDTA.
They excluded studies evaluating effects of extra cellular matrix protein,
enamel matrix protein or growth factors applied to root surface.
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Main resultsMain results
Thirty-four studies incorporating total patient population of 575 wereanalyzed, 26 for citric acid, 5 for tetracycline and 3 EDTA treatment.
Four of eight human histological studies represents regeneration with
use of citric acid and only 1 of 18 clinical studies reported attachmentgain.
Of 5 studies using tetracycline, 1 histological study and 1 clinical studyreported attachment gain.
No regeneration was reported in the 3 studies evaluating use of EDTA.
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Reviewers conclusionReviewers conclusion
Evidence to data suggests that use of citric acid, tetracycline and EDTAto modify root surface provides no benefit of clinical significance to
regeneration in patients with chronic periodontitis
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Root conditioning delays wound healing?Root conditioningdelays wound healing?
Selvig et al. examined wound healing in experimental fenestration
defects following conditioning of defects walls with either saline or citric
acid.
Following elevation of mucoperiosteal flaps, fenestral defects where
covered with polytetrafluroethylene membrane.
Post surgically after 14 days healing appears to be delayed in citric
acid treated site as compared to the control.
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RESTORATION OR IMPLANT PLACEMENT: ARESTORATION OR IMPLANT PLACEMENT: A
growing treatment planning quandarygrowing treatment planning quandary
Regardless of the implant system, the placement and functional success of
endosseous implants is greater than 90%.
Is a tooth with questionable prognosis restored or intervened with dental
implant?
Should a tooth with large post and core restoration and failing endodontic
procedure is re treated conventionally or should it be extracted?
Is it better to replace such a tooth with an implant?
If the implants fail to integrate or if restoration is an esthetic failure, would it
have been better to retain the tooth?
Answering such questions is a challenge for clinicians. Clinical and economic
factors should be considered in making such decisions.
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Clinical factorsClinical factors
The heavily restored toothThe heavily restored tooth
These teeth may have been restored multiple times, have minimal
external coronal dentin for an adequate restorative ferrule.
The post space can be so large that internal dentinal walls of the
preparations are too thin.
If greater force is to be exerted on a tooth, increase in the resistance
form should be made.
Crown lengthening can increase resistance but at the expense of
removing bone of adjacent teeth.
Orthodontic extrusion can also be considered but extrusion adds both
additional financial cost and increased time to treatment.
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Immediate implant placement along with single stage surgical placement
limits number of procedures.
Before the acceptance of sinus augmentation procedures, the choice mighthave been to retain teeth with root resective and endodontic retreatment procedures.
Previously it was thought that implants in posterior maxillae or mandiblewas less ideal.
.
Decision for implant placement may change if patient is a heavy smoker orif they are an uncontrolled diabetic, factors which could compromiseimplants
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The Furcation involvementThe Furcation involvement
Reducing attachment levels for crown lengthening or for root resective
procedures may have a negative long-term impact.
Periodontally involved molars are the most common teeth lost.
Furcation and concavities associated with them make them difficult to
treat.
Resecting roots can improve debridement acess but literature differs asto success of root amputations or hemisections.
Reasons for failures were current decay, endodontic failure,root
fractures and less commonly, recurrent periodontal dis
Resection may require osseous removal to the adjacent teeth, as
crown lengthening does. If osteoplasty \ ostectomy is not performed then plaque retentive
areas are created
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HemisectionHemisection
Hemisection, the length of root trunk affects how much bone is
removed to create positive osseous architecture.
To create a positive osseous architecture a large amount of bone must
be removed on remaining root and adjacent tooth..
If the patients anatomy requires sinus augmentation, then clinician
may reconsider treating tooth with root resection.
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Difficult anterior esthetic casesDifficult anterior esthetic cases
The use of dental implants to replace anterior teeth is one of the lastareas to gain acceptance by dental profession.
The greatest benefit is avoidance of unnecessary preparations of non-restored teeth adjacent to an implant.
Professional acceptance of implants in esthetic zone has increased
because they are
Better pre-surgical planning guidelines.
More option in diameter of implants fixtures.
Great variety of abutments.
Better techniques for preparing edentulous ridge.
Better prosthetic techniques to produce a high esthetic final restoration.
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ECONOMIC FACTORSECONOMIC FACTORS
Clinician as well as patients many times elects best economic option
than best treatment option.
Some still argue that the long-term success rates of implants are not
high enough and that questionable teeth should be maintained until
they become hopeless.
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Hand versus Ultrasonic InstrumentationHand versus Ultrasonic Instrumentation
Partial removal of cementum became established as a therapeutic
procedure over one century ago.
Mergenhen and Hampp were the first to demonstrate that plaque
related gram-negative bacteria produce the complex lipo-polysachride
endotoxins described by Boe in 1941
Aleo and De Renzius scientifically proved the significance of root
cementum bound endotoxin removal in periodontally diseased teeth.
In 1974 they showed that cementum of these involved teeth contains
endotoxins and also found that this lipo-polysachride is toxic to cells invitro.
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ComparisonComparison
Many investigators have compared hand and ultrasonicinstrumentation.
Nishimine and O Leary showed that root planning was more effectivethan ultra sonic scaling in removing endotoxins from periodontally
involved root surfaces.
Two investigations evaluated the smoothness of root surfaces at anulrtastructural level following hand and ultrasonic instrumentation.
One study reported a much smoother root following ultrasonic scaling.
The second study reported opposite results.
Luiggi and Gian conducted a study to compare efficacy of ultrasonicand hand instrumentation.
They found no significant differences between fibroblast growth on
periodontally involved root surfaces treated with hand instruments andwith ultra sonic scalers.
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Several studies reported on an increased efficiency of subgingivalinstrumentation with both sonic and ultra sonic scalers, since manual
instrumentation takes longer to achieve the same clinical results(Dargoo 1992,Copulos et al. 1993).
Power driven instruments have been shown to be superior in treatmentof class 2 and class 3 furcations (Leon & Vogel 1987).
Development of heat at scaler tip when water-cooling is not sufficient.This increased temperature may cause injury to pulpal and periodontaltissues.
Another draw back is formation of pathogenic bacterial aerosols andthe reduced tactile sensation in comparison to hand instruments.
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NONSURGICAL ANDNONSURGICAL AND
SURGICAL PERIODONTALSURGICAL PERIODONTAL
THERAPYTHERAPY
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NONSURGICALNONSURGICAL
PERIODONTAL THERAPYPERIODONTAL THERAPY
Conventional nonsurgical periodontal therapy consists of mechanical supra andsubgingival tooth debridement
Reducing the bacterial load and altering the microbial composition towards aflora more associated with health,which in turn result in lower levels of
inflammation and relative stability in periodontal attachment levels.
In the past, endotoxin or lipopolysacchairde derived from cells of gram-negativebacteria was though to be so firmly attached to the root surface.
More recent studies on extracted teeth indicate that endotoxins are superficiallybound and can be removed by such means as brushing.
Thus systematic root planing to remove cementum does not seem warranted.
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Furcation opening is often less than 1 mm, too small to be effectivelyreached with relatively larger curettes.
Most of the new ultrasonic tips are approximately 0.50mm in diameter,which may favor ultrasonics as the instruments of choice for furcationsites.
One study on instrumentation of furcations with and without surgicalaccess indicates that no major differences were observed between useof curettes or ultrasocics in the closed treatment groups and in widefurcations.
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PERIODONTAL SURGERYPERIODONTAL SURGERY
The following have been proposed as the aims of periodontal surgery:
Accessibility to previously in accessible root surfaces.
Production of healthy dento-gingival junction that would enable thepatient to practice a high level of plaque removal.
Reduction of probing depths to allow - a) effectively deliveredmaintenance and home care and b) the monitoring and or diagnosis ofrecurrent inflammation and progressive periodontal disease.
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COMPARISON OF SURGICAL AND NONSURGICALCOMPARISON OF SURGICAL AND NONSURGICAL
TREATMENT MODALITIESTREATMENT MODALITIES
An early study employing a split-mouth design was that of knowles etal.
. Three modalities were tested sub-gingival curettage, modified Widmanflap surgery and pocket elimination surgery
After evaluation for eight years all techniques resulted in favorable
changes in the means of the clinical parameters measured The surgical techniques resulted in slightly more pocket reduction in
deep pockets. The modified Widman flap resulted in the greatest clinical attachment
gain.
In studies comparing the effects of root planing and modified Widmanflap surgery over 6 years of observation,.
The modified Widman flap resulted in more pocket reduction in initiallydeep pockets, although mean attachment levels were similar.
In summary following points may be deducedIn summary
following points may be deduced
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In summary, following points may be deducedIn summary, following points may be deduced
from available literature.from available literature.
Both non-surgical and surgical therapies have been shown to resultin similar mean improvements of clinical scores.
Data for the possible adjunctive effect of surgical procedures onpatients/sites unresponsive to initial therapy are scarce.
Data for the possible adjunctive effect of surgical procedures onpatients believed to be at high risk to ongoing attachment loss arescarce.
Other than studies on regenerative techniques data for thecomparable effects of different surgical modalities on furcation areas
are also scarce.
Data for long-term outcome measures, such as tooth loss andquality of life issues, are scarce.
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PERIODONTITIS PERIODONTITIS
SYSTEMIC DISEASESYSTEMIC DISEASE
ASSOCIATIONS IN THEASSOCIATIONS IN THE
PRESENCE OF SMOKING PRESENCE OF SMOKING CAUSAL ORCAUSAL OR
COINCIDENTAL?COINCIDENTAL?
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No Current issue in periodontal research is more visible or controversialthan the relationship between periodontitis and systemic diseases.
Four lines of evidence suggests that the observed periodontitis-systemicdisease associations are in part a result of confounding by smoking
First, no periodontitis-systemic disease associations have been identifiedamong neversmokers.
Second, periodontitis and smoking mimic one another with respect to thetypes of diseases with which they are associated (e.g. lung cancer andParkinsons disease).
Third, only studies with inadequate adjustment for smoking report
significant periodontitis-systemic disease associations.
Lastly, elimination of dental infection, unlike smoking cessation, does notreduce coronary heart disease risk.
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Smoking, the epidemoiologists perspectiveSmoking, the epidemoiologists perspective
Individuals with periodontitis are more likely to be current or pastcigarette smokers.
When individuals with and without periodontitis are compared it is to beexpected that individuals with periodonititis will have more smoking-related diseases, such as coronary heart disease, lung cancer, low-birth weight babies etc.,..
Statistical adjustment of control for confounding is possible.
Such statistical adjustment can be used to eliminate some but not allof the bias caused by the smokers.
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The imperfect smoking questionnaires,the inability to ask questions or otherwise
obtain information on important characteristics of smoking, all make it virtually
impossible to have perfect statistical adjustment for smoking.
Wherever past or current smokers are included in the analyses, biased
periodontitis systematic disease associations will be reported.
Therefore, primary analyses should be limited to healthy never-smokers both
because smoking is such a strong risk factor and because the magnitude of
smoking cannot be well measured.
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Effect of smoking on Periodontitis cannot beEffect of smoking on Periodontitis cannot be
distinguished from the effect of smoking ondistinguished from the effect of smoking on
systemic diseasessystemic diseases Periodontitis-systemic disease associations have not been identified
among never-smokers.
Periodontitis and smoking are associated with similar health risks.
Conflicting study results can be explained in terms of statisticaladjustment for tobacco smoking.
Dental infection elimination through complete tooth removal, unlikesmoking cessation, does not reduce health risks.
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Periodontitis and chronic obstructivePeriodontitis and chronic obstructive
pulmonary disease (COPD)pulmonary disease (COPD)
Among past and current smokers, periodontitis significantly increased
the risk for COPD.
When the analysis included past, current, and never smokers with
adjustment for reported smoking dose and duration, the HR for COPDdecreased by 7%.
Finally, when the analysis was limited to never-smokers, periodontitis
was associated with a small and insignificant increased risk for COPD.
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Periodontitis and lung cancerPeriodontitis and lung cancer
Among past and current smokers, periodontitis significantly increasedthe risk for lung cancer
When the analysis included never, past, or current smokers, withadjustment for smoking the HR for lung cancer associated withperiodontitis decreased by 49%.
When the analysis was limited to never-smokers, the oppositeassociation was present.
Periodontitis was associated with a decreased risk for lung cancer, notan increased risk.
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P i d titi d h t di (CHD)P i d titi d h
t di (CHD)
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Periodontitis and coronary heart disease (CHD)Periodontitis and coronary heart disease (CHD)
Among past and current smokers, periodontitis significantly increased the riskfor CHD by 26%.
Among past, current and never-smokers the HR for CHD associated withperiodontitis was 1.13.
Finally, when the analysis was limited to never-smokers, the HR for CHDassociated with periodontitis became insignificant).
Imperfect adjustment for smoking history is inducing associations betweenperiodontitis and smoking related diseases.
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There is also hope that periodontal treatments can reverse anincreased CHD risk..
Findings from the same cohort study indicated that completeelimination of all dental infections by extraction does not decreaseCHD risk..
Then why would an incomplete, imperfect and reversible decreasing ofthe bacterial load by means of periodontal treatments decrease CHDrisk?
Some have offered the explanation that the risk, once established, isnot reversible and therefore primary periodontitis prevention trialsrather than secondary prevention should be initiated.
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Dental infection elimination through completeDental infection elimination through
complete
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Dental infection elimination through completeDental infection elimination through complete
tooth removal does not reduce health riskstooth removal does not reduce health risks
There is certainly hope that secondary prevention of CHD events canoccur through periodontal treatment.
Current epidemiological evidence does not support the hope thatperiodontitis plays a role in secondary heart disease prevention.
A cohort study in the US population suggests that periodontitis doesnot increase the risk for secondary heart disease events.
Individuals with periodontitis and pre-existing heart disease were foundto be at the same risk for developing a secondary heart disease eventas the individuals with pre-existing heart disease but withoutperiodontitis.
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There is also hope that periodontal treatments can reverse anincreased CHD risk..
Findings from the same cohort study indicated that a definitive,irreversible, and complete elimination of all dental infections by
extraction does not decrease CHD risk.
Then how incomplete, imperfect and reversible decreasing of thebacterial load by means of periodontal treatments decrease CHD risk?
Some have offered the explanation that the risk, once established, isnot reversible and therefore primary periodontitis prevention trialsrather than secondary prevention should be initiated.
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CONCLUSIONCONCLUSION
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THANK YOUTHANK YOU