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/ Clin Periodontol }9%: 23: 240-250 Copyright ^- Munks^aarcl 1996

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periodoiitoloyy
ISS,\ IIM>.^-MT>

Niklaus P. Lang and


Periodontal diagnosis in treated Maurizio S. Tonetti
Department of Periodontology and Fixed
Prosthodontjcs, School ot Dental Medicine,

periodontitis Univereity of Beme, Berne, Switzertand

Why, when and how to use ciinical parameters


Lang NP, Tonetti MS: Periodontal diagnosis in treated periodontitis. Why, when
and how to use clinical parameters. J Clin Periodontol 1996: 23: 240-250.
© Munksgaard, 1996.

Abstract. The objective of clinical periodontal diagnosis in maintenance patients


is to monitor the risk for periodontal disease progression. Risk for progression
should be continuously monitored at the patient, tooth and site level at each
recall appointment. At the patient level, the significance of systemic diseases, ciga-
rette smoking, compliance with the recall program, loss of support m relation to
the patient"s age. full mouth plaque and/or bleeding scores, and prevalence of
residual pockets are of key importance. At the tooth and tooth-site levels, residual
periodontal support, inflammatory parameters and their persistence, presence
of ecological niches with difficult access such as furcations, and presence of iatro-
genic factors have to be put into proportion with the patient's overall risk profile.
The information gathered by clinical monitoring and continuous multilevel risk
assessment facilitates an immediate appreciation of the periodontal health status
Key words: diagnosis; risk assessment;
of an individual and the possible risk for further infection and/or disease pro-
periodontal diseases; clinicai moniioring;
gression in the dentition and at a particular tooth or site. periodontal maintenance

Clinical periodontal diagnosis relies (i,e. of untreated patients) thus repre-


Clinical Diagnosis for Different
upon the assessment of the signs and sents the clinical assessment of disease
Circumstances extent and severity by time.
symptoms mentioned in an attempt to
Periodontal diseases are a variety of establish the prevalence and severity of In this respect, a simple classification
pathological conditions of the tooth disease in a dentition. It has to be real- of periodontal conditions will include
supporting structures characterized by ized, however, that based on clinical (Attstrom & Van der Velden 1994); (i)
the presence of a bacterial challenge eli- parameters, periodontal diagnosis can gingigivitis; (ii) adult periodontitis; (iii)
citing a potentially destructive host re- only be established well after the bio- early onset periodontitis; (iv) necrotiz-
sponse. The pathognomonic feature of logic onset of the disease process (Fig. ing periodontitis. Additional secondary
periodontitis is the destruction of the 1). This, in turn, means that it is un- descriptors may further characterize the
coliagenous fibers of the periodontal known to the therapist, and somehow conditions provided that appropriate
ligament, which may result in loss of irrelevant, whether or not the disease is and relevant information is available
bone support of the tooth. Clinically, still "progressing". If the answer is yes, (Attstrom & Van der Velden 1994).
the condition is defined as measurable at which rate and in which sites of the Different diagnostic issues have to be
loss of clinical attachment in relation to dentition loss of attachment is induced raised following appropriate therapy.
the cemento-enamel junction. This is also remains obscure. Also, the time of These are based upon the long-term
associated with the presence of an in- onset is unknown as it is unknown overall objectives of periodontal ther-
whether or not the disease is in a period apy, i.e., the preservation of a function-
flammatory reaction which, clinically, is
of biological remission and thus char- ally adequate level of periodontai
recognized as bleeding, erythema,
acterized by stability of chnical par- attachment to maintain an individually
edema and occasionally suppuration
ameters. In essence, detection of disease acceptable dentition for a lifetime. It is
out of the marginal periodontal tissues.
mandates appropriate treatment and, generally accepted that such a treat-
Other commonly identified signs in-
with few exceptions, more sophisticated ment goal may be achieved through the
clude periodontal pocket formation, re- diagnostic procedures will not influence
cession of the gingival margin and pivotal role of combined efforts for op-
the treatment approach chosen by the timal regular plaque control by the pa-
eventually radiographic alveolar bone therapist. Initial periodontal diagnosis
loss. tient and the responsible professional
Clinica! periodontal diagnosis 241

Eatly Usual be understood that, so far, clinica! risk


Biologic Diagnosis Clinical Outcome assessment has also been demonstrated
Onset Possible Diagnosis to be very cost-effective {Axelsson &
Lindhe 1981a, b, Axelsson et al, 1991).
It should be recognized that, by vir-
tue of their previous disease prevalence,
all patients under a periodonta! main-
tenance regime represent a population
with a moderate to high risk for recur-
Clinical threshold rent periodontal infection. As opposed
of detection to the general population without such
a history, periodontal patients are re-
quired to participate in a well organized
recall system which should provide both
continuous risk assessment and ade-
quate supportive care. Without this, the
patients are most likely to experience
progressive loss of periodontal attach-
ment (Axelsson & Lindhe 1981a, Kent
Time
1981, Becker et al, 1984, Cortelhni et al.
Fig. I. Limitations of clinical diagnosis. Clinical diagnosis of periodontal disease requires 1994, Cortellini et ai, 1996). On the
presence of a loss of attachment greater than the clinical threshold of detection. The diagram other hand, it is important to determine
should not be interpreted to illustrate a specific pattern of disease progression.
the level of risk for progression in each
individual patient in order to be able to
determine the frequency and extent of
team. Frequently, it is observed that the the years to come. The relevant ques- necessary professional support to main-
professional teatn focuses on the mere tion would, therefore, be which clinical tain the attachment levels obtained fol-
execution of the retnoval of the etiologic parameters may serve as early indi- lowing active therapy The determi-
lactors and their retaining niches, here- cators for a new onset or recurrence of nation of such risk level would thus pre-
by forfeiting the clinically retrievable di- the periodontal disease process, i.e. re- vent undertreatment, but also excessive
agnostic information that is the scien- infection and progression of peri- overtreatment during maintenance
tific basis of supportive periodontal odontal breakdown of a once treated (Braggeret al, 1992).
care. periodonta] site. Significant factors for the multilevel
It is the purpose of this review to The objective of clinical diagnosis risk assessment will be discussed at the
elucidate the principles of clinical diag- during supportive care is to identify and subject, tooth and the tooth site level.
nosis during supportive care of peri- assess disease progression in a given pa- The sequence of enumeration does not
odontally treated patients. tient, a certain tooth or a particular site follow established priorities, but follows
of the dentition. Since in light of the the clinical sequence of their assess-
present knowledge, the biologic onset of ment.
Continuous Multilevel Risk disease progression cannot be deter-
Assessment mined with a single parameter (deter-
ministic model), an alternative ap- Subject Risk Assessment
As opposed to an initial periodontal di-
proach to the prediction of such events Systemic conditions
agnosis which considers the sequelae of
the disease process, i.e.. documents the must be based on probability calcu- The most substantiated evidence for
loss of periodontal attachment and the lations (probabilistic model). The latter modification of disease susceptibility
concomitant formation of periodontal approach is based upon the identifi- and/or progression o( periodontal dis-
pockets and development of inflam- cation and assessment of significant fac- ease arises from studies on insulin de-
mation, clinical diagnosis during sup- tors associated with disease pro- pendent and non-msulin dependent dia-
portive care has to be based on the vari- gression, i.e., risk factors or markers betes mellitus populations (Gusberti et
ations of the health status obtained fol- (Beck 1990). al. 1983. Emrich et al. 1991, Genco &
lowing successful active periodontal From a clinical point of view the sta- Loe 1993).
treatment. This, in turn, means that a bility of periodontal conditions reflects It has to be realized that the impact
new baseline will have to be established a dynamic equilibrium between bac- of diabetes on periodontal diseases has
once the treatment goals of active peri- terial aggression and effective host re- been documented in patients with un-
odontal therapy are reached and peri- sponse. As such, this homeostasis is treated periodontal disease, while, as of
odontal health is restored (Claffey prone to sudden changes whenever one today, no clear evidence is available for
1991). This baseline includes the level of of the two factors prevails. Hence, it is treated patients. It is reasonable, how-
clinical attachment achieved, while the evident that the diagnostic process must ever, to assume that the influence of the
inflammatory parameters are supposed be based on a continuous monitoring of systemic conditions may also affect re-
to be under control. Under optimal cir- the multilevel risk profile. The intervals currence of disease.
cumstances, supportive periodontal between diagnostic assessments must Research on the association and/or
care would maintain clinical attachment also be chosen based on the overall risk modifyitig influence in susceptibility
levels obtained after active therapy for profile and the expected benefit. It must and progression of periodontitis of
242 Lang & Tonetti

physical or psychological stress is (Pindborg 1949. Rivera-Hidalgo 1986).


Loss of periodontal support in relation to
sparse (Cohen-Cole et al. 1981. Green More recent evidence, however, has es-
tiie patient's age
et al. 1986, Freeman & Goss 1993). The tablished that smoking "per se" repre-
hormonai changes associated with these sents not only a risk marker, but prob- The extent and prevalence of peri-
condition, however, are well docu- ably a true risk factor for periodontitis odontal attachment loss (i.e. previous
mented (Selye 1950). (Ismail et al. 1983. Bergstrom 1989, disease experience and susceptibility),
Changes in female sex hormones Bergstrom et al. 1991, Haber et al. as evaluated by the height of the al-
during puberty and pregnancy have 1993). In a young population (19 to 30 veolar bone on radiographs, may repre-
also been shown to select for peri- years of age). 51 to 56% of the ob- sent the most obvious indicator of sub-
odontitis associated bacteria (Korn- served periodontitis was associated ject risk when related to the patient's
man & Loesche 1980. Mombelli et al. with cigarette smoking (Haber et al. age. In light of the present understand-
1990). However, no associations be- 1993). The association of smoking and ing of periodontal disease progression,
tween hormonally induced bacterial periodontitis has been shown to be and the evidence that both onset and
changes and the pathogenesis of peri- dose-dependent (Haber et al. 1993). It rate of progression of periodontitis
odontitis could be established in con- has also been shown that smoking will might vary among individuals and dur-
trolled clinical trials. affect the treatment outcome after ing different time frames (Van der
scaling and root planing (Preber & Veiden 1991), it has to be realized that
Bergstrom 1985). moditied Widman previous attachment loss in relation to
Compliance with a recall system flap surgery (Preber & Bergstrom the patient's age does not rule out the
1990), and regenerative periodontal possibility of rapidly progressing
Several investigations have indicated
therapy (Tanetti et ai. 1995). Further- lesions. Therefore, the actual risk for
that only a minority of periodontal pa-
more, a high proportion of so-called further disease progression in a given
tients comply with the prescribed sup-
refractory patients has been identified individual may occasionally be under-
portive periodontal care (Wilson et al.
to consist of smokers (Bergstrom & estimated. Hopefully, the rate of pro-
1984, Mendoza et al. 1991. Checchi et
Blomlof 1992). The impact of cigarette gression of disease has been positively
al. 1994, Demetriou et al. 1995). Since it
smoking on the long term effects of affected by the treatment rendered and
has been clearly established that treated
periodontal therapy in a population hence, previous attachment loss in re-
periodontal patients who comply with
undergoing supportive periodontal lation to patient's age may be a more
regular periodontal maintenance ap-
care has been recently reported. accurate indicator during supportive
pointments have a better prognosis
Smokers displayed less favorable heal- periodonta! care than before active
than patients who do not comply (Ax-
ing responses both at re-evaluation periodontal treatment. Given the hypo-
elsson & Lindhe 1981a. Kent 1981.
and during a 6 years period of sup- thesis that a dentition may be func-
Becker et al. 1984. Cortellini et al. 1994.
portive periodontal care (Baumert-Ah tional for the most likely life expectancy
Cortellini et al. 1996). non compliant or
et al. 1994). In spite of the paucity of for the subject in the presence of a re-
poorly compliant patients may be con-
evidence relating cigarette smoking duced height of periodontal support
sidered at higher risk for periodontal
with impaired outcomes during sup- (i.e. IS-Sff'A, of the root length), the risk
disease progression. A report that inves-
portive periodontal care, it seems assessment in treated periodonta] pa-
tigated the personality differences of
reasonable to incorporate heavy tients may represent a reliable prognos-
patients participating in a regular recall
smokers (>10 cigarettes/day) in a tic indicator for the stability of the
program as compared to patients who
higher risk group during maintenance. overall treatment goal of keeping a
did not. revealed that patients that did
With increasing age the general functional dentition for a lifetime (Pa-
not take part in a maintenance program
population is and will be exposed to in- papanou et al. 1988).
following periodontal therapy had
creasing numbers of medications for
higher incidence of stressful life events
prolonged periods of time. Some of
and less stable persona! relationships in
these drugs may affect the periodontal
their lives (Becker et al. 1988). Prospec- Oral hygiene (full mouth plaque record)
status by either directly interfering with
tive identification of non compliant pa-
the periodontal tissues, or indirectly af- Since bacterial plaque is by far the most
tients, however, has been elusive: pre-
fecting the host reponse or plaque for- important etiologic agent for the occur-
vious history of non compliance being
mation rates (Holm-Pedersen 1994). In rence of periodontal diseases (for re-
the best prognostic indicator.
spite of the fact that several studies on view, see Kornman & Loe (1993)), it is
immunosuppressed patients have been evident that the full mouth assessment
performed in the 1970s (Schuler et al. of the bacterial load must have a pivotal
Environmental exposures 1973), there is lack of sufficient data to impact in the determination of the risk
There is increasing evidence in the associate any medication with an in- for disease recurrence. It has to be real-
literature that consumption of tobacco, creased risk of disease progression dur- ized, however, that regular interference
predominantly in the form of smoking ing maintenance. On the other hand. It with the microbial ecosystem during
rather than snuffing or chewing, affects is evident that medically seriously com- periodontal maintenance will eventually
the susceptibility and the treatment promised patients may belong to a obscure such obvious associations. In
outcome of patients with adult peri- group of high risk patients in which patients treated with various surgical
odontitis. Classical explanations for control of periodontal infections is and non-surgical modalities, it has
these observations have included the aimed at prevention of .systemic compli- clearly been established that plaque in-
cations rather than preservation of the fected dentitions will yield recurrence of
association between smoking habits
dentition. periodontal disease in multiple loca-
and poor oral hygiene as well as un-
tions, while dentitions under plaque
awareness for general health issues
Clinical periodontal diagnosis 243

control and regular supportive care this figure per se does not make much strated that tooth malposition within
maintain periodontal stability for many sense when considered as a sole par- the dental arch will lead to an in-
years (Rosling et al. 1976, Axelsson & ameter, the evaluation in conjunction creased risk for periodontal attach-
Lindhe 1981a, b). Similar observations with other parameters such as bleeding ment loss. It has to be realized, how-
were made following regenerative pro- on probing and/or suppuration will re- ever, that all the studies quoted incor-
cedures (Cortellini et al, 1994). Studies flect existing ecological niches from and porated patients with unknown risk
have, so far, not identified a level of in which re-infection might occur. It is, level for periodontal disease develop-
plaque infection compatible with main- therefore, conceivable to assume that ment, while patients in periodontal
tenance of periodontal health. How- periodontal stability in a dentition maintenance are, by definition, pa-
ever, in a clinical set-up, a plaque con- would be reflected in a minimal number tients who had experienced attachment
trol record of 20 to 40"/. might be toler- of residual pockets. Presence of high loss. Hence, for periodontal patients
able by most patients. It is important to frequencies of deep residual pockets during maintenance it is not known
realize that the full mouth plaque score and deepening of pockets during sup- whether or not tooth irregularities
has to be related to the host response of portive periodontal care has, in fact, within the dental arch play a signifi-
the patient, i,e,, compared to inflam- been associated with high risk for dis- cant role in disease progression. It is
matory parameters, ease progression (Badersten et al, 1990, understood that oral hygiene practices
Claffey et al. 1990). On the other hand, and accessibility of niches resulting
it has to be realized that an increased from tooth malposition are determin-
% of sites with bleeding on probing number of residual pockets does not ing factors for optimizing an individ-
Bleeding on gentle probing represents necessarily imply an increased risk for ual program for adequate oral hy-
an objective inflammatory parameter re-infection or disease progression, giene.
which has been incorporated into index since a number of longitudinal studies
systems for the evaluation of peri- has established the fact that, depending
on the individual supportive therapy Mesiai tipping of posterior teeth
odontai conditions (Loe & Silness 1963,
Muhlcmann & Son 1971) as well as provided, even deeper pockets may be
Tilted posterior teeth have often been
used as a parameter by itself. Although stable without further disease pro-
considered to create ecological niches
there is no established acceptable level gression for years (Knowles et al. 1979,
that will be conducive to colonization
of prevalence of bleeding on probing in Lindhe & Nyman 1984),
with presumptive periodontal patho-
the dentition above which a higher risk gens and hence, it was often proposed
for disease recurrence has been estab- by clinicians to eliminate these niches
lished, a BOP prevalence of 25"';. has Tooth Risk Assessment
by uprighting tilted molars (Stern et
been the cut-off point between patients Tooth position within the dentai arch al. 1981, Becker et al. 1982). In epide-
with maintained periodontal stability Early clinical surveys have associated miological studies, however, only mi-
for 4 years and patients with recurrent the prevalence and severity of peri- nor differences were found between the
disease in the same time frame in a pro- odontal diseases with malocclusion periodontal health of tipped and non
spective study in a private practice (Joss and irregularities of tooth position tipped molars (Geiger & Wasserman
et al. 1994), Further evidence of BOP (Ditto & Hall 1954, Bilimoria 1963), 1980). Another survey (Ehrlich & Jaffe
percentages between 20 and 30% deter- However, many subsequent studies 1983) could not establish increased
mining a higher risk for disease pro- using clinical evaluation methods risk for periodontal disease develop-
gression originates from studies of could not confirm these conclusions ment. More recently, a well designed
Claffey et al, (1990) and Badersten et (Beagrie & James 1962, Geiger 1962, intra-individual retrospective study
al, (1990). Gould & Picton 1966). Although a re- analyzed the conditions around tipped
In periodontal maintenance individ- lationship between crowding and in- and upright molars (Lundgren et al,
uals with low mean BOP percentages creased plaque retention and gingival 1992). Out of 450 adults, 69 subjects
{<10% of the surfaces) may be con- inflammation has been established (In- presented with molars tipped more
sidered as patients with a low risk for gervaO et al. 1977, Buckley 1980, Grif- than 30 degrees and controlateral up-
recurrent disease (Lang et al, i990), fiths & Addy 1981, Horup et al, 1987), right molars as controls. Besides the
while patients with mean BOP percen- no significant correlation between an- occurrence of plaque and gingivitis,
tages greater than 25% should be sched- terior overjet and overbite (Geiger et pocket probing depths and alveolar
uled for prophylactic supportive peri- al, 1973), crowding and spacing (Geig- bone levels were registered using clin-
odontal therapy more f^requently Of er et al, 1974) or axial inclinations and ical and radiographic parameters. Re-
course, the history and the response to tooth drifts (Geiger & Wasserman gardless of the variables tested, no sig-
therapy in relation to the patient's age 1980) on one side and periodontal de- nificant differences were revealed be-
should also be considered. struction, i,e,, attachment loss sub- tween tipped and upright molars when
sequent to gingival inflammation, compared over a 15-year period. This
could be established. It is evident from clearly indicates that tipped molars
Prevaience of residuai pockets greater the literature mentioned that crowding probably are not more susceptible to
Vnan 4 mm of teeth might eventually affect the periodontal disease progression than
amount of plaque mass formed in upright molars. But again, it remains
The enumeration of the residual dentitions with irregular oral hygiene unclear whether or not tipped molars
pockets with probing depth greater practices, thus contributing to the de- would be at increased risk in patients
than 4 mm represents, to a certain ex- velopment of chronic gingivitis, but, as treated for advanced periodontal dis-
tent, the degree of success of peri- of today, it remains to be demon- ease during maintenance.
odontal treatment rendered. Although
244 Lang & Tonetti

Retrospective analyses of large patient area for plaque retention, and there is
Mouth breathing and extreme overjet
populations in private periodontal prac- an abundance of association studies
Only few studies have attempted to tices of periodontal specialists (Hirsch- documenting increased prevalence of
correlate mouth breathing habits with feld & Wasserman 1978. McFall 1982) periodontal lesions in the presence of
periodontal disease development and have clearly established that multi-root- iatrogenic factors (for review see Leon
no studies are available about pen- ed teeth appear to be at high risk for 1977). Depending on the supragingival
odontal disease progression in treated tooth loss during the maintenance or subgingival location of such factors,
populations, it appears that extreme phase. The most impressive long term their influence on the risk for disease
anterior overjet (>6 mm) is associated documentation maintained 600 patients progression has to be considered. It has
with increased gingival inflammation for an average duration of 22 years, and been established that slightly subgingi-
(Geiger et al. 1973) and pocket forma- 10°/ii of these patients were even main- vally located overhanging restoration
tion (Helm & Petersen 1989). tained for more than 30 years (Hirsch- will, indeed, change the ecological niche
In mouth breathers a significant cor- feld & Wasserman 1978). While 83"',. of providing more favorable conditions for
relation between gingivitis and crowding the patients could be considered "well the establishment of a gram negative
was found, while nose breathers exam- maintained" and had lost only 0-3 teeth anaerobic microbiota (Lang et al.
ined by the same investigators showed no during the observation period, a patient 1983). There is no doubt that shifts in
such correlation (Jakobsson 1973). group of 4°'n (25) was identified with an the subgingival microflora towards a
Hence, it may be assumed that mouth extreme risk for disease progression and more periodontopathic microbiota. if
breathing may contribute to the develop- had lost between 10 and 23 teeth during unaffected by treatment, represent an
ment of gingivitis by dehydrating the a regularly scheduled maintenance pro- increased risk for periodontal break-
tissues, especially in dentitions with in- gram. Irrespective of the patient group down.
adequate plaque control. of low. moderate, and high risk for dis-
ease progression during maintenance the
majority of the teeth lost were furcation Residual periodontal support
Variations of tootti morphoiogy involved molars (Hirschfeld & Wasser-
Although clinicians often express feel-
man 1978). Similar results were obtained
The presence of variations in tooth in a study on 100 treated periodontal pa- ings as to teeth wdth reduced peri-
morphology, such as enamel pearls, en- tients maintained for 15 years or longer odontal support not being able to
amel projections, hngual grooves, and (McFall 1982). function either individually and hence,
root depressions have frequently been express a need for tooth extraction or
considered to be associated with devel- Prospective studies on periodontal splinting, there is clear evidence from
opment of periodontal disease. It is ob- therapy in multi-rooted teeth have also longitudinal studies that teeth with se-
vious that these aberrations provide revealed significant differences between verely reduced, but healthy, peri-
ecological niches which may or may not non molar sites and molar flat surfaces odontal support can function either in-
be conducive to the establishment of a on one side and molar furcation sites dividually or as abutments for many
microbiota associated with periodontal on the other, when looking at the treat- years without any further loss of
disease (for review, see Kornman & Loe ment outcomes evaluated as bleeding attachment (Nyman & Lindhe 1979,
(1993)). However, the accessibility of frequency, probing depth reductions Nyman & Ericsson 1982). Hence, suc-
such locations to cleaning devices and and levels of attachment (Nordland et cessfully periodontally treated teeth
the performance of adequate oral hy- al. 1987). Again, teeth with furcation can he maintained over decades and
giene practices in these areas would ren- involvement and original probing function as abutments in fixed bridge-
der these variations inconspicuous and depths >6 mm had reduced treatment work or as individual chewing units
insignificant for the disease process. outcomes. irrespective of the amount of residual
The question whether or not morpho- The assumption that the prognosis periodontal support, provided that
logical variations represent a higher risk for single rooted teeth and non fur- physiological masticatory forces do
for disease development and pro- cation involved multi-rooted teeth is not subject such teeth to a progressive
gression during maintenance has not better than the prognosis for furcation trauma which may lead to spon-
been addressed in controlled studies. involved multi-rooted teeth has also taneous extraction. Obviously, by
There are studies which attempted to been confirmed by Ramfjord et al. virtue of the already reduced support,
establish an association between e.g. en- (1987) in a prospective study over 5
amel projections and enamel pearls in should disease progression occur in
years. It has to be realized, however, severely compromized teeth, it may
multi-rooted teeth and the prevalence of that these results are not intended to
periodontal disease (Leib et al. 1967). lead to spontaneous tooth exfolia-
mean that furcation involved teeth tion.
However, no conclusive evidence was should be extracted, since all the pro-
provided by this and subsequent spective studies have documented a
studies. rather good overall prognosis for such Mobility
teeth if regular supportive care is pro- In the light of the discussion of abut-
vided by a .well-organized maintenance ment teeth with severely reduced, but
Furcation involvement program. healthy periodontal support, tooth mo-
It is evident that multi-rooted teeth with bility may be an indicator for progress-
periodontal lesions extending into the ive traumatic lesions, provided that the
latrogenic factors
furcation area have been subject to in- mobility is increasing continuously
tensive therapeutic studies for many Overhanging restorations and ill-fitting (Nyman & Lang 1994). When assessing
years (Kalkwarf & Reinhardt 1988). crown margins certainly represent an tooth mobility, it has to be realized that
Clinical periodonlal diagnosis 245

two factors may contribute to so called the future may be predicted for sites re- cussed: (i) dimension of the periodontal
hypermobility: (l) a widening of the peatedly positive for bleeding on prob- probe; (ii) placement of the probe and
periodontal ligament as a result of uni- ing (Badersten et al. 1985, Lang et al. obtaining a reference point: (iii) crude-
or multi-directional forces to the crown, 1986, Vanooteghem et al. 1987, Bad- ness of the measurement scale: (iv) prob-
high and frequent enough to induce re- ersten et al. 1990. Claffey et al. 1990, ing force; (v) gingival tissue conditions.
sorption of the alveolar bone walls: (ii) Vanoothegem et al. 1990).
the height of the periodontal support- Obviously, bleeding on probing is
ing tissues. If this is reduced due to Dimensions of tiie periodontal probe
rather sensitive to different forces ap-
prior periodontal disease, but the width plied to the probe. An almost linear It is obvious that different sizes of peri-
of the periodontal ligament is un- relationship (if=0.87) existed between odontal probes will yield different pene-
changed, the amplitude of root mobility the probing force applied and the per- tration depths into the periodontal
within the remaining periodontium is centage of bleeding sites in a study on tissues, even if all other variables are
the same as in a tooth with normal healthy young adults (Lang et al. controlled. Hence, the use of probing
height, but the leverage on the tooth 1991). If the probing force exceeded instruments with standardized dimen-
following application of forces to the 0.25 N (25 g), the tissues are trauma- sions is a prerequisite for repeated
crown is changed. Therefore, it has to tized and bleeding is provoked as a re- probing depth measurements. Usually,
be realized that all teeth that had lost sult of trauma, rather than as a result periodontal probes with a point diam-
periodontal support have increased of tissue alterations due to inflam- eter of 0.4-0.5 mm have been used suc-
tooth mobility as defined by crown dis- mation. To assess the 'true' percentage cessfully.
placement upon application of a given of bleeding sites due to inflammation,
force. Nevertheless, this so called hyper- a probing force of 0.25 N or less
mobility should be considered as physi- should be applied which clinically Placement of the probe and obtaining a
ologic (Nyman & Lindhe 1976). means a light probing force. This has reference point

Since tooth mobility is probably also been confirmed for patients who Manual probing involves the variability
more frequently affected by reduced have experienced loss of attachment, of the measurements generated by dif-
periodontai height rather than uni- or i.e. with successfully treated advanced ferent angulation and site localization
multi-directional application of forces periodontitis (Karayannis et al. 1991. of the probe and by the difficulty in ob-
onto the tooth, its significance for the Lang et al. 1991). taining a fixed landmark as a reference
evaluation of the periodontal con- Since absence of bleeding on probing point. Recently, electronic probes have
ditions has to be questioned. Several at 0.25 N indicated periodontal stability been developed to automatically locate
studies have indicated that tooth mo- with a negative predictive value of 9S"A>- the cemento-enamel junction (Jeffcoat
bility varies greatly before, during and 99% (Lang et al. 1990), this clinical par- et al. 1991) which are able to measure
after periodontal therapy (Persson ameter is most reliable to monitor pa- attachment levels to a sensitivity of 0.1
1980, 1981a, b). From these studies it tients over time in daily practice. Non- mm. This technique is still subjected to
can be concluded that periodontally in- bleeding sites may be considered as chnical trials and. in the light of other
volved teeth showed a decrease in mo- periodontally stable. On the other variables, its advantage over conven-
bility following non-surgical and/or sur- hand, bleeding sites seem to have an in- tional probing cannot be determined at
gical periodontal procedures. However, creased risk for progression of peri- this time.
following surgery, tooth mobility may odontitis. especially when the same site
temporarily increase during the healing is bleeding at repeated evaluations over
phase and may resume decreased values time (Lang et al. 1986. Ciafley et al. Crudeness of the measurement scale
later on. Provisional splinting as an ad- 1990). Probing depth measurements are gener-
junct to non-surgical or surgical ther- It is. therefore, advisable to register ally assessed to the nearest millimeter
apy does not seem to affect the final re- the sites which bleed on probing (BOP) (Glavind & Loe 1967). It is evident that
sult of tooth mobility. in a dichotomous way using a constant even a measurable loss of attachment of
force of 0.25 N. This allows the calcu- 0.5 mm accepts a high incidence of false
lation of the mean BOP for the patient, negative values. This, in turn, means
Site Risk Assessment but yields also the topographical loca- that "true" disease progression may ac-
Bleeding on probing tion of the bleeding site. Repeated tually occur, but only to a small extent
Absence of bleeding on probing is a re- scores during maintenance will yield the which is not revealed by the crudeness
liable parameter to indicate periodontal surfaces at higher risk for loss of of the measurement scale.
stability if the test procedure for as- attachment.
sessing bleeding on probing has been
Probing force
standardized (Lang et al. 1990). Pres-
Probing depth and loss of attachment
ence of bleeding upon standardized Probing force is a significant variable
probing will indicate presence of gingi- Clinical probing is the most commonly which should be controlled in order to
val inflammation. Whether or not re- used parameter both to document loss obtain reproducible measurements of
peated bleeding on probing over time of attachment and to establish a diag- probing depth. Although a wide range
will predict the progression of a lesion nosis of periodontitis. There are. how- of 0.03-1.35 N has been identified for
is, however, questionable (Lang et al. ever, some sources of error inherent to examiners with different experience
1986, Vanooteghem et al. 1987, Lang et this method which contribute to the (Gabathuler & Hassei! 1971) in a study
a l 1990). Nevertheless, a 30% prob- variability in the measurements. Among of 58 subjects, different professionals in
ability for attachment loss to occur in these, the following factors are dis- periodonties probed with an average of
246 Lang & Tonetti

0.44 N (Glavind & Loe 1967. Gabathul- reliable parameter for the evaluation of the orifice of a pocket. This criterion of
er & Hassell 1971. Freed et al. 1983). the periodontal tissues. It has to be real- suppuration may be recognized while
No significant differences were found in ized that increased probing depth and clinically probing the lesions or prefer-
probing forces applied among the dif- loss of probing attachment are par- ably, by using a ball burnisher (Singh et
ferent professional groups (students, ameters which reflect the history of al. 1977|. Several longitudinal studies
general practitioners, periodontists. periodontitis rather than its current on the results of periodontal therapy
dental hygienists). Significant differ- state of activity. In order to obtain a have evaluated clinical parameters, in-
ences were found, however, when inter- more realistic assessment of the disease cluding suppuration, for the prediction
and intra-examiner variability was ana- progression or. more commonly, the of future loss of attachment (Badersten
lyzed. If a probing force of 0.25-0.3 N healing following therapy, multiple et al. 1985. Badersten et al. 1990. Claf-
is applied, the apical termination of the evaluations should be performed. Obvi- fey et al. 1990). In all these studies the
probing tip lies usually within the junc- ously, the first evaluation prior to ther- presence of suppuration increased the
tional epithelium in healthy gingival apy will yield results confounded by positive predictive value for disease pro-
tissues (Armitage et al. 1977. greater measurement error than evalu- gression in combination with other clin-
Robinson & Vitek 1979. Poison et al. ations following therapy. The reference ical parameters such as bleeding on
1980. Fowler et al. 1982). This is the point (cement enamel junction) may be probing and increased probing depth.
reason why probing forces in this order obstructed by calculus or by dental res- Hence, following therapy a suppurating
of magnitude have generally been ac- torations, and the condition of the gin- lesion may provide evidence that the
cepted when using electronic pressure gival tissues may allow an easy penetra- periodontitis site is undergoing a period
sensitive probes. If treatment effects are tion of the periodontal probe into the of exacerbation (Kaldahl et al. 1990).
to be monitored the probing force will tissues, even though the probe position
influence the clinical attachment levels. and force applied are standardized.
Also, it has been demonstrated that at These biological variables (tissue con- Clinical Implementation and Utility of
least 0.25 N of probing force has to be ditions and calculus) may be minimized Continuous Multilevel Risk
applied in order to yield treatment re- following initial periodontal therapy Assessment
lated differences in clinical attachment and hence, repeated periodontal evalu-
levels (Mombeili et al. 1992). ations using probing will improve the Practically all longitudinal studies on
metric assessment. Therefore, the first periodontai therapy have documented
periodontal evaluation after healing fol- that successful treatment outcomes such
lowing initial periodontal therapy as resolution of inflammation, reduction
Gingival tissue conditions
should be taken as the baseline for long of probing pocket depths, and gain in
Several studies have documented that term clinical monitoring (Claffey 1994). clinical attachment levels can only be
attachment level measurements are sig- maintained by supportive therapy (for
nificantly influenced by the density of Periodontal probing is best per- review, see Wachtel (1994)). These
the connective tissue collar around the formed at six sites around each tooth.' studies have implemented regular visits
teeth (Armitage et al. 1977, Fowler et root (mesio-buccal. buccal. disto-buc- for professional tooth cleaning as the
al. 1982). cal, disto-lingual. lingual and mesio-lin- most important pre-requisite to assure
In healthy tissues, or in slight gingi- gual) in two steps: (i) Determination of treatment results over time. All of these
vitis, the probe tip generally reaches the the distance from the free gingival mar- studies, however, have u,sed stereotype
most apical cell of the junctional epi- gin (FGM) to the cemento-enamel and standardized maintenance sched-
thelium. In a periodontal pocket, how- junction (CEJ) to the nearest milli- ules and protocols. There is no doubt
ever, the probe tip routinely exceeds the meter. For recognition of the CEJ. the that, in some of the patients, the stan-
level of the connective tissue attach- periodontal probe is angulated at 45° to dardized supportive therapy for a clin-
ment, penetrates into the inflamed the long axis the root surface and ical trial may represent overtreatment.
tissue and is hindered in its apical pro- guided towards the CEJ. If recession is while in others it may not suffice. The
liferation by intact connective tissue present the value becomes negative, (ii) present review attempted to focus on the
fibers or eventually by the alveolar bone Assessment of the probing pocket depth evaluation of the risk of the individual
crest (Armitage et al. 1977). In gingival (PPD) from the FGM to the bottom of patient following periodontal treatment
health, however, the most apical cell of the pocket or sulcus to the nearest milli- as a pre-requisite to guarantee mainten-
the junctiona! epithelium may not al- meter. The periodontal probe is only ance of periodontal attachment.
ways be reached if a tight adaptation of slightly angulated (about 10°) and
The 3 levels of risk assessment pre-
the gingival tissues is obtained as a re- guided along the root surface until the
sented represent a logical sequence of
sult of therapy (long junctional epithel- first resistance of the gingival connec-
clinical evaluation to be performed
ium). The significant influence of the in- tive tissues is felt. Preferably, a stan-
prior to rendering treatment during
flammatory infiltrate on probing depth dardized force (e.g. 0.25 N) is applied.
maintenance. The information gathered
measurements has, therefore, clearly from a stepwise evaluation should not
Probing attachment levels (PAL) are
been documented. impinge but rather improve the efficacy
calculated by algebraically subtracting
the values of step 1 (FGM-CEJ) from of secondary prophylactic peridontal
the values of step 2 (PPD). care and treatment. A logical sequence
Ciinical probing of checks and examinations may be eas-
In spite of the recognized method errors ily obtained in a short period of time
Suppuration and at no extra cost for laboratory
inherent to clinical probing, this diag-
nostic procedure has not only been the In a proportion of periodontal lesions tests. The information obtained from
most commonly used, but also the most pus will develop and may drain through clinical monitoring and multilevel risk
Clinical periodontal diagnosis 247

assessment facilitates an immediate ap- Patient A Patient A


preciation of the periodontal health sta- FMBS=7% FMBS=7%
tus of an individual and the possible 5 residual pockets 5 residual pockets
Patient C
ron smoker non smoker
risk for further infection and/or disease #11 distal #16 mesial
Blood glucose
150mg/100mL
progression. absence of BOP persistent BOP
Smoker (20/day)
PPD = 4 mm PPD = 6 mm
Most longitudinal studies published FMBS=50%
up to date have been based on single #43 distal
Patient B persistent BOP
level, i.e. site or tooth risk assessment, Ff^BS=42% PPD = 7 mm
rather than accounting for the most evi- Smoker (20/day)
#21 distal
dent factor in risk assessment: the pa- persistent BOP
tient. Ample evidence indicates that a PPD = 4 mm
minority of patients will continue to 100
present problems and. hence, com-
pletely differ from the maintenance pat-
tern visualized in the majority of the
patients. Even in the studies where this
fact has been explicitly addressed
(Hirschfeld & Wasserman 19781. the
Leve! of Risk for Disease Progression
factors which determined whether or
not a patient belonged to a well main- Fi^. 2. Continuous Multiievel Risk Assessment. Subject, tooth and site parameters are com-
tained group or to a group with con- bined to establish the clinical risk for disease progression. Please note that different sites in
tinuous loss of periodontal attachment the same patient may have a different level of risk. Subject based risk factors or markers are
used to put the tooth and/or site risk assessment in perspective.
have not been identified.
Based on the evidence emerging from
recent and ongoing studies this review
suggested risk factors to consider in or- sofortige Beurteilung des parodontaien Ge-
Acknowledgements sundheitszustandes ernes einzelnen Patienten
der to optimize the therapeutic efforts
during supportive periodontal therapy. Supported in part by Swiss National und erlauben eine Abschatzung des mogli-
It is evident that some of the aspects Foundation for scientific research grant chen Risikos einer Reinfektion und/oder ei-
proposed have not yet been validated in nes weiteren Fortschreitem der Erkrankung
32-37763.93 and by the Clinical Re-
im ganzen Gebiss. an einem Zahn oder an
well controlled studies, but are being search Foundation for the Promotion einer einzelnen Stelle.
addressed in a number of ongoing in- of Oral Helath, University of Berne,
vestigations around the world. Switzerland.
For the time being, it is suggested to Resume
evaluate patients on the three different Diagnostic parodontal chez les patients paro-
levels mentioned. At the patient level loss Zusammenfassung
dontaux traites. Powquoi. quand et eomment
of support in relation to patient age. full Partuhmak' Dlagtwstik in hehandeiren Paro- etjjphver Ics parametres cliniques
mouth plaque and/or bleeding scores, donuus-Falk'jiten. Warum, wie und wami nr'f- Le but du diagnostic parodontal chez les
prevalence of residual pockets are evalu- den klhUM'he Parameter augewendcf patients en phase de maintien, est de sur-
ated together with the presence of sys- Das Ziel der klinischen parodontalen Dia- veiller le risque de progression de la mala-
gnostik bei Patienten in der Betreuungsphase die parodonlale. Ce risque de progression
temic conditions or environmental fac-
ist das Aufzeigen von Risikofaktoreti eines devrait etre continuellement surveille au ni-
tors, such as smoking, which can influ- weiteren Fortschreitens der parodontalen Er- veau de patient, de la dent et du site lors de
ence the prognosis. The clinical utility of krankung. Die Risikofakloren sollte konti- chaque visite de maintien. Chez le patient.
this first level of risk assessment influ- nuierlich bei Jeder Recallsitzung patienten-. 1 influence de tnaldies systemiques. du taba-
ences primarily the determination of the zahn- und stellenbezogen erfasst werden. Auf gisme. de sa compliance au programme de
recall frequency and time requirements. der Ebene des Patienlen sind die Bedeutung maintien. la perte de tissu de soutien en
It should also provide a perspective for der systemischen Erkrankungen, das Rau- fonction de son age. la presence de plaque
the evaluation of risk assessment con- chen, die Mitarbeit des Patienten wahrend et'ou de saignement ainsi que la prevalence
der Erhaltungsphase, der Verlust von paro- des poches residuelles ,sont d'une importan-
ducted at the tooth and site level.
dontalem Stutzgewebe im Verhaltnis zum ce capitale. Au niveau de la dent et du site,
At the tooth and tooth site levels, re- Alter des Patienten, die Plaque- und Gingi- le tissu de soutien parodontal, les paramet-
sidual periodontal support, inflamma- valindizes und die verbleibenden parodonta- res inflammatoires ei leur persistance, la
tory parameters and their persistence. len Resttaschen von entscheidender Bedeu- presence de niches ecologiques d'acces dif-
pre.sence of ecological niches with diffi- tung. Im Zusammenhang rtiit dem allgemein- ficile, telles que des furcations, et enfin la
en Risikoprofil des Patienten mtissen die presence de facteurs iatrogenes sont a met-
cult access such as furcations, and pres-
zahn- und stellenbezogenen Parameter wie tre en proportion avec le profil global de
ence of iatrogenic factors have to be put restliches parodontales Attachment. Entzun- risque du patient. Les informations recueil-
into proportion with the patient's over- dungszeichen und ihr Fortbestehen. das Vor- ties iors de la surveillance clinique et I'eva-
all risk profile (Fig. 2). The clinical util- handensein von okologischen Nischen mit er- luation continuelle des risques a tous les ni-
ity of tooth and site risk assessment re- schwertem Zugang. wie z.B. Furkationen. veaux, facilitent I'appreciation immediate de
lates to rationale allocation of the recall und die Anwesenheit von iatrogen Faktoren la sante parodontale d un individu et le ris-
time available for therapeutic inter- gebracht werden. Die durch klinische Unter- que eventuel qu'il eticourt de contracter une
vention to the sites with higher risk, and suchungen und standiges Erfassen der Risi- nouvelle infection evou de progression de la
possibly to the selection of different kofaktoren auf den verschiedenen Ebenen maladie. au niveau de la dentition et meme
gewonnenen Informationeii ermoglichen eine d'une dent ou d'un site particulier.
forms of therapeutic intervention.
248 Lang & Tonetti

refractory periodontat disease. Journal of Ehrlich, J & Jaffe, A, (1983) The effect of
Dental Research 71 (spec, issue), p. 297 first molar loss on the dentition and peri-
References
#1530 (LADR abstr.). odontium. Journal of Prosthetic Dentistry
Armitage. G. C . Svanberg. G. K. & Loe. H. Bergstrom, J., Eliasson, S. & Preber, H. 50, 830-832.
(1977) Microscopic evaluation of clinical (1991) Cigarette smoking and periodontal Emrich, L., Sclossman, M. & Genco, R.
measurements of connective tissue attach- bone loss. Journal of Periodonlology 62. (1991) Periodontal disease in non-insulin
ment levels. Journal of Clinical Periodonlo- 242-246. dependent diabetes meJlitus. Journal of
Iogy4. 173-190. Bilimoria, K. (196,'') Malocclusion. Its role in Periodomology 62, 123-130.
Attstrom, R. & Van der Velden. U. (!994) the causation of periodontal disease. Fowler, C , Garrett, S,, Crigger, M. & Egel-
Consensus report of session 1. In: Proceed- Journal of the All-India Dental Association berg, J. (1982) Histologic probe position in
ings of ihe Isl European Workshop in Pcr'i- 35, 293-300. treated and untreated human periodontal
odomology. eds. Lang. N. & Karring, T. Bragger, U., Hakanson, D. & Lang, N. tissues. Journal of Clinical Periodontoiogy
pp. t20-126. Berlin: Quintessence. (1992) Progression of periodontal disease 9. 373-385.
Axelsson, R & Lindhe. J. (19Sla) Effect of in patients with mild to moderate adult Freed, H. K.., Gapper, R. L. & Kalkwarf, K.
controlled oral hygiene procedures on periodontitis. Journal of Clinical Periodon- L. (1983) Evaluation of periodontal prob-
caries and periodontal disease in adults. toiogy 19, 659-666. ing forces. Journal of Periodontoiogy 54.
Results after 6 years. Journal of Clinical Buckley. L. (1980) The relationship between 488^92.
Periodonlology 8. 239-248. irregular teeth, plaque, calculus and gingi- Freeman, R. & Goss, S. (1993) Stress meas-
Axelsson. P. & Lindhe. J. (1981b) The sig- val disease, A study of 300 subjects. British ures as predictors of periodontal disease:
nificance of maintenance care in the treat- Denial Journal 148, 67-69. a preliminary communication. Community
ment of periodontal disease. Journal of Checchi, L., Pellicioni, G., Gatto, M. & Itel- Dentistrv and Oral Epidemiologv 21, 176-
Clinical Periodimtoiogy 8. 281-294. escian, L. (1994) Patient compliance with 177.
Axelsson, P.. Lindhe. J. & Nystrom. B. (1991) maintenance therapy in an Italian peri- Gabathuler, H. & Hassell, T (1971) A press-
On the prevention of caries and peri- odontal practice. Journal of Clinical Peri- ure-sensitive periodontal probe, Helvetica
odontal disease. Results of a 15-year-longi- odontoiogy 21. 309-312. Odontotogica Acta 15, 114-117,
tudinal study in adults. Journal of Clinical Claffey, N, (199!) Decision making in peri- Geiger, A, (1962) Ocdusal studies in 188
Periodontoiogy 18. 182-189. odontal therapy. The re-evaluation. consecutive cases of periodontal disease.
Badersten, A., Nilveus, R. & Egelberg. J. Journal of Clinical Periodontoiogy 18, 384- American Journal of Orihodontics 48, 330-
(1985) Effect of non-surgical periodontal 389. 360.
therapy. (VII) Bleeding, suppuration and Claffey, N. (1994) Gold Standard, Clinical Geiger. A. & Wasserman, B, (1980) Relation-
probing depths in sites with probing and radiograpbic asses,sment of disease ac- ship of occlusion and periodontal disease.
attachment loss. Journal of Clinical Peri- tivity. In: Proceedings of the 1st European Part XI. Relation of axial inclination (me-
odontology 12. 432-440. workshop on Periodontologv. eds, Lang, sial-distal) and tooth drift to periodontal
Badersten, A., Nilveus. R. & Egelberg, J. N. & Karring, T. pp, 42-53. Berlin: status. Journal of Periodontoiogy 51, 283-
(19901 Scores of plaque, bleeding, suppu- Quintessenz Verlag. 290.
ration and probing depth to predict prob- Claffey, N,, Nylund, K., Kiger, R., Garrett, Geiger, A., Wasserman, B. & Turgeon, L.
ing attachment loss. Journal of Clinical S. & Egelberg. J, (1990) Diagnostic pre- (1973) Relationship of occlusion and peri-
Periodontoiogy 17, 102-107. dictability of scores of plaque, bleeding, odontal disease. Part VI. Relation of an-
Baumert-Ah. M., Johnson, G., Kaldahl. W., suppuration, and probing pocket depths terior overjet and overbite to periodontal
Patil, K. & ICalkwarf, K. (1994) The effect for probing attachment loss. 3 1/2 years of destruction and gingival inflammation.
of smoking on the response to periodontal observation foilowing initial therapy. Journal of Periodontoiogy 44, 150-157.
therapy. Journal of Clinical Periodontologv Journal of Clinical Periodontoiogy 17, 108- Geiger, A., Wasserman, B. & Turgeon, L.
21, 9i-97. 114, (1974) Relationship of occlusion and peri-
Beagrie. G. & James, G. (1962) The associ- Cohen-Cole S,, Cogen, R., Stevens, A,, Kirk, odontal disease. Part VIL Relationship of
ation of posterior tooth irregularities and K,, Gaitan, E., Hain, J. & Ereeman, A. crowding and spacing to periodontal de-
periodontal disease, British Dental Journal (1981) Psychosocial, andocrine and im- struction and gingival inflammation.
113,239-243. mune factors in acute necrotizing ulcer- Journal of Periodonlology 45, 43—49.
Beck, J. (19901 Risk assessment in dentistry. ative gingivitis. Psychosomatic Medicine Genco, R, & Loe, H. (1993) The role of sys-
Chapel Hill. North Carolina: University of 43,91. temic conditions and disorders in peri-
North Carolina Oral Ecology, Cortellini, P., Pini-Prato. G. & Tonetti, M, odontal disease. Periodontoiogy 2000 2,
Becker, A., Zalkind, M. & Stern, N. (1982) (1994) Periodontal regeneration of human 98-116.
The tilted posterior tooth. Part II: Bio- infrabony defects (V). Effect of oral hy- Glavind, L. & Loe, H. (1967) Errors in the
mechanical therapy. Journal of Prosthetic giene on long term stability. Journal of clinical assessment of periodontal destruc-
Dentistry^, 149-155. Clinical Periodontoiogy 21, 606-610. tion. Journal of Periodontal Research 2,
Becker, B., K.arp, C , Becker, W. & Berg, L. Cortellini, P,, Pini-Prato, G. & Tonetti, M. 180-184.
(19881 Personality differences and stressful (1996) Long term stability of clinical Gould, M. & Picton, D. (1966) The relation
life events. Differences between treated attachment following guided tissue re- between irregularities of teeth and peri-
periodontal patients with and without generation and conventional therapy. odontal disease. British Dental Journal
maintenance. Journal of Clinical Periodon- Journal of Clinical Periodontoiogy 23, in 12i, 20-23.
toiogy 15, 49-52. press. Green, L., Tryon, W, Marks, B. & Huryn, J.
Becker, W., Becker, B. & Berg, L. (1984) Peri- Demetriou, N., Tsami-Pandi, A. & Parashis, (1986) Periodontal disease as a function of
odontal treatment without maintenance. A A. (1995) Compliance with supportive life events stress. Journal of Human Stress
retrospective study in 44 patients. Journal periodontal treatment in private peri- 12, 32-36.
of Periodontoiogy 55, 505-509, odontal practice. A 14 year retrospective Griffith, G. & Addy, M. (1981) Effects of ma-
Bergstrom, J. (1989) Cigarette smoking as a study. Journal of Periodontologv 66, 145- lalignment of teeth in the anterior seg-
risk factor in chronic periodontal disease. 149. ments on plaque accumulation. Journal of
Journal of Clinical Periodontologv 17, 245- Ditto, W. & Hall, D, (1954) A survey of 143 Clinical Periodontoiogy 8, 481-490.
247, periodontal cases in terms of age and mal- Gusberti, F. A., Syed, S. A., Bacon, G.,
Bergstrom, J, & Blomibf, L. (1992) Tobacco occlusion. American Journal of Orthodont- Grossman, N. & Loesche, W. J. (1983) Pu-
smoking major risk factor associated with ics 40. 234-^243. berty gingivitis in insulin-dependent dia-
Clinical peiiodonla! diagno.m 249

betic children (I). Cross-sectional obser- Shick, R. A., Morrison. E. C. & ing. Attachment gain in relation to prob-
vations. Journal of Periodoiitotogv 54. Ramfjord. S. P (1979) Results of peri- ing force. Journal of Clinical Periodonto-
714-720. odontai treatment related to pocket depth logy 19. 295-300.
Haber, J.. Wattles. J.. Crowley, M.. Mandell. and attachment level. 8 years. Journal of Muhlemann. H. R, & Son, S. (1971) Gingival
R.. Joshipura. K. & Kent. R. (1993) Evi- Periodontology 50. 225-233. sulcus bleeding - a leading symptom in in-
dence for cigarette smoking as a major Kornman, K. & Loe. H, (1993) The role of itial gingivitis. Helvetica Odontologica
risk factor for pcriodontitis. Journut of local factors in the etiology of periodontai Acta 15. 107-113.
Periodonlohgy 64. 16-23. diseases. Periodonlohgy 2000 2. 83-97, Nordiand. P.. Garret, S.. Kiger, R., Vanoot-
Heltti. S. & Petersen, P. (19S9) Causal re- Kornman. K, S. & Loesche. W. J. (1980) The eghem. R.. Hutchetts, L. & Egelberg,
lationship between malocclusion and peri- subgingival microbial flora during preg- J. 11987) The effect of plaque control
odontal health. Ada Odonwhgka Scandi- nancy. Journal Periodontai Research 15, and root debridement in molar teeth.
mvica 47. 223-228. 111-'122. Journal of Clinical Periodontology 14, 231-
Hirschfeld. L. & Wasiserman. B, (1978) A Lang. N.. Kiel. R, & Anderhalden, K. 11983) 236,
long-term survey of tooth loss in 600 Clinical and microbiological effects of Nyman, S, & Ericsson, I, (1982) Tbe capacity
treated periodonta! patients. Journal of subgingival restorations with overhanging of reduced periodontai tissues to support
Periodonlohgy 49. 225-^237, or clinically perfect margins. Journal fixed bridgework. Journal of Clinical Peri-
Holm-Pedersen. P (1994) Gerodontic aspects of Clinical Periodontology 10. 563- odontology 9, 409^14,
of Periodontology. In: Proceedings of ihe 578. Nyman. S. & Lang, N, (1994) Tooth mobility
1st European Workshop in Periodoniohgw Lang, N. P.. Joss. A,, Orsanic, T . Gusberti. and biological rationale for splinting teeth.
eds. Lang. N. &. Karring. T. pp. 462^75. F. A. & Siegrist. B. E. (1986) Bleedmg on Periodontology 2000 4. 15-22.
Berlin: Quintessenz Verlag. probing, A predictor for the progression Nyman. S. & Lindhe. J, (1976) Persistent
Horup. N.. Melsen. B. & Terp. S, (19g7| Re- of periodontai disease'' Journal of Clinical tooth hypermobility following completion
lationship between malocclusion and Periodontology 13. 590-596, of periodontai treatment. Journal of Clin-
maintenance of teeth. Communily Den- Lang, N, P, Adier, R., Joss, A. & Nyman, S. ical Periodontology 3. 81-93.
ti.'ilry and Oral Epidemiology 15. 74-78, (1990) Absence of bleeding on probittg. Nyman, S. & Lmdhe, J. (1979) A long-
lngervall, B., jacobsson. U. & Nyman. S. An indicator of periodontai stability. itudinal study of combmed periodontai
(1977) A clinical study of the relationship Journal of Clinical Periodontology 17. 714- and prosthetic treatment of patients
between crowding of teeth, plaque and 721. with advanced periodontai disease.
gingiva! condition. Journal of Clinical Lang. N, P. Nyman. S.. Senn. C. & Joss. A. Journal of Periodontology 50. 163-
Periodontologv 4. 214-222. (1991) Bleeding on probing as it relates to 169.
Ismail. A. 1.. Burt. B. A. & Eklund. S. A. probing pressure and gingival heaUh, Papapanou, P.. Wennstrom, J. & Grondal, K,
(1983) Epidemiologic patterns of smoking Journal oj Clinical Periodoniology 18, 257- (1988) Periodontai status in relation to age
and periodontai disease in the United 261, and 100th type. A cross-sectional radio-
States. Journal of the Alabama Dental .4,v- Leib, A.. Berdon. J, & Sabes. W. (1967) Fur- graphic study. Journal oj Clinical Period-
sociatkm 106. 617-621. cation involvements correlated with en- ontology 15. 469^78,
Jakobsson. L. (1973) Mouth breathing and amel projections from the cemento-enamel Persson, R, (1980) Assessment of tooth mo-
gingivitis. Journal of Periodonial Research junction. Journal of Periodontology 38. bility using small loads Hi). Effect of oral
8. 269-277. 330-335. hygiene procedures. Journal of Clinical
Jeffcoat. M. K.. Jeffcoat. R. L. & Captain. Leon, A, (1977) A periodontium and restora- Periodontology 7, 506-515.
K. (1991) A periodontai probe with auto- tive procedures. A critical review. Journal Persson, R. {1981a) Assessment of tooth mo-
mated cemento-enamel junction detection- of Oral Rehabilitation 4, 105-117. bility using small loads (III). Effect of
design and clinical trails. IEEE Trans- Lindhe. J, & Nyman. S, (1984) Long-term periodontai treatment including a gingi-
actions on Biomedical Engineering 38. 330- maintenance of patients treated for ad- vectomy procedure. Journal of Clinical
333. vanced periodontai disease. Journal of Periodontology 8, 4—11, ,
Joss, A.. Adler. R. & Lang. N. (1994) Bleed- Clinical Periodontology 11. 504-514. Persson, R. (1981b) Assessment of tooth mo-
ing on probing. A parameter for monitor- Loe, H, & Silness, J. (1963) Periodontai dis- bility using small loads (IV). The effect of
ing periodontai conditions in clinical prac- ease in pregnancy (I), Prevalence and se- periodontai treatment including gingivec-
tice. Journal of Clinical Periodontology 21, verity. Acta Odontologica Scandinavia 21, tomy and flap procedures. Journal of Clin-
402-408. 533-551, ical Periodontology 8. 88-97.
Kaldahl. W, Kalkwarf, K.. Patil, K. & Mol- Lundgren, D., Kurol, J,, Thorstensson, B, & Pindborg. J. (1949) Correlation between con-
var. M. (1990) Evaluation of gingival sup- Hugoson. A. (1992) Periodontai con- sumption of tobacco, ulcero-membranous
puration and supragingival plaque follow- ditions around tipp>ed and upright molars gingivitis and calculus. Journal of Detital
ing 4 modalities of periodontai therapy in adults. An intraindividual retrospective Research 2&.4b\^i(iy.
Journal of Clinical Periodonlohgy 17, 642- study. European Journal of Orthodontics Poison, A. M.. Caton, J. G.. Yeaple. R. N &
649. 14, 449.^55. Zander, H. A. (1980) Histologica! determi-
Kalkwarf. K. & Reinhardt, R. (1988) The McFall, W. T, (1982) Tooth loss in 1(K) nation of probe tip penetration into gingi-
furcation problem: current controversies treated patients wilh periodonlal di.sease va] sulcus of humans u.sing an electronic
and future directions. Dental Clinics of in a long-term study. Journal of Periodon- pressure-sensitive probe. Journal of Clin-
North America 22, 243-266. /Hto^?.r 53. 539-549, ical Periodontology 1. 479^88.
Karayannis. A.. Lang. N. P.. Joss, A, & Ny- Mendoza. A., Newcomb, G, & Nixon, K. Preber. H, & Bergstrom. J. (1985) The effect
man, S, (1991) Bleeding on probing as il (1991) Compliance with supportive peri- of non-surgical treatment on periodontai
relates to probing pressures and gingival odontai therapy. Journal of Periodontology pockets in smokers and non smokers.
health in patients with a reduced but 62.731-736, Jourtial of Clinical Periodontology 12. 319-
healthy periodontium. A clinical study. Mombelli. A.. Lang. N. P.. Burgin. W. B. & 323.
Journal of Clinical Periodontologv 19, 471- Gusberti, F .\. (1990) Microbial changes Preber, H. & Bergstrom. J, (1990) EfTect of
475. associated with the development of pu- cigarette smoking on periodontai healing
Kent. N. (1981) Treatment of chronic peri- berty gingivitis. Journal of Clinical Period- followmg surgical therapy Journal of Clin-
odontitis. 45'!'i> failure rate. Britlth Dental ontology 25. 331-338. ical Periodontology 17. 324-328,
Journal 150. 222-224. Mombelli. A., Muhle, T. & Frigg. R. (1992) Ramfjord. S., Caffesse. R.. Morrison. E.,
Knowles. J, W., Burgett. F. G., Nissie. R. R., Depth-force patterns of periodontai prob- Hill, R,, Kerry, G,, Appleberry, E,, Nissie,
250 Lang & Tonetti

R. & Stults, D. (19S7) 4 modalities of peri- The suppurative index: an indicator of ac- and root debridement. Journal of Clinical
odontai treatment compared over 5 years. tive periodontal disease. Journal of Dental Periodontology 17, 580-587.
Journal oJCIinftvl Periodontoiagv 14, 445- Research 56, p. 200 #593. Wachtel, H. (1994) Surgical periodontal ther-
452, Stern, N., Revah, A. & Becker, A. (19«1) The apy. In: Proceedings of the Ist European
Rivera-Hidalgo, F. (1986) Smoking and Peri- tilted posterior tooth. Part 1: Etiology, syn- Workshop on Periodontology, eds. Lang,
odotital disease. Journal of Periodontolugy drome and prevention. Journal og Pros- N. & Karring, T, pp. 159-171. Berhn:
57, 617-624. thetic Dentistry 4*, 404-^07. Quintessenz Verlag.
Robinson, F J. & Vitek, R. M. (1979) The Tonetti, M., Pini-Prato, G. & Cortellmi, P. Wilson, T , Glover, M., Schoen, J.. Baus,
relationship between gitigival inflam- (1995) Effect of cigarette smoking on peri- C. & Jacobs, T. (1984) Compliance with
mation and resistance to probe penetra- odontal healing following GTR in maintenance therapy in a private peri-
tion. Journal of Periodontal Research 14, infrabony defects. A preliminary retro- odonta! practice. Journal of Periodonto-
239-243. spective study. Journal of Clinical Period- logy 55, 468^73,
RosHng, B,, Nyman, S. &. Lindhe, J. 11976) ontology 22, 229-234.
The effect of systematic plaque control on Van der Velden, U. (199[) The onsel age of
bone regeneration in infrabony pockets. periodontal destruction. Journal of Clin-
Journal of Clinical Periodontologv X 38-53. ical Periodontology T8. 380-383. .Address:
Schuler, R, Freedman, H. & Lewis. D. (1973) Vanooteghem, R., Hutchens, L. H., Garrett, Niklaus P. Lang
Periodontal status of renal transplant pa- S., Kiger. R. & Egelberg, J. (1987) Bleed- Department of Periodontology and Fixed
tients receiving immunosuppressive ther- ing on probing and probing depth as indi- Prosthodontics
apy. Journal of Periodomoiogr 44, 147- cators of the response to plaque control University of Bern
170. and root debridement. Journal of Clinical Friihiirgstrasse 7
Selye, H. (1950) The physiology and pathol- Periodontohgv 14, 226-230, CH-3010 Bern
ogy of stress: a treatise based on the con- Vanoothegem, R.. Hutchens, L.. Bowers, G.. Switzerland
cepts of the general-adaptation-syndrome Kramer. G., Schallhorn, R., Kiger, R..
and the diseases of adaptation, pp. 203. Crigger, M. & Egelberg, J. (1990) Subjec- Tel.: +41-31-632-2577
Montreal: Acta Medical Publishers. tive criteria and probing attachment loss Fax: +41-31-3SI-7H34
Singh, S,, Cianciola, L. & Genco. R. (1977) to evaluate the effects of plaque control e-mail: tonettiiii ZMK.unibe.ch

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