Jan Lindhe. Clinical Periodontology

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status of diabetes in an individual patient, as in the

longer term metabolic control could indicate the

probable outcome of periodontal therapy. In addi-

tion, it is now accepted that periodontal therapy

can improve metabolic control in diabetics, mean-

ing that the relationship is two-way and periodon-

tal therapy is beneficial to the control of both dis-

eases.

Medications such as phenytoin, cyclosporin and

nifedipine may predispose to gingival overgrowth

in patients with gingivitis.

Genetic traits, which result in diseases that modify

the periodontal structures or change the immune

or inflammatory responses, can result in gross peri

odontal destruction in the affected individual and

although the destruction seen may imitate perio-

dontitis this is not etiopathologically chronic peri-

odontitis.

Stress

Stress and other psychosomatic conditions may have

direct anti-inflammatory and/or anti-immune effects

and/or behavior mediated effects on the body's de-

fenses. Hence both conditions may conceptually be

relevant to the etiology of chronic periodontitis and

necrotizing ulcerative conditions. Recent studies have

suggested that academic stress and financial stress

may be associated with an increased risk of periodon

tal disease. Most of the literature on stress and peri-

odontal conditions is quite old, however, and reports

of acute necrotizing ulcerative gingivitis (or trench

mouth) were made on stressed soldiers on the front

line during World War I. It is understood that stress

may be immunosuppressive and that acute necrotiz-

ing ulcerative gingivitis may occur in the immuno-

suppressed (also in HIV patients), but there is insuffi-

cient data as yet to substantiate the assumption that

psychosocial factors are indeed of etiological impor-

tance in chronic periodontitis.

Genetics

There is convincing evidence from twin studies for a

genetic predisposition to the periodontal diseases.

The twin studies have indicated that risk of chronic

periodontitis has a high inherited component but that

gingivitis is a general and common response which is

unlikely to be linked with particular genes. A great

deal of research is underway attempting to identify

the genes and polymorphisms associated with all

forms of periodontitis. It is likely that chronic perio-

dontitis involves many genes, the composition of

which may vary across individuals and races. Much

attention has focused on polymorphisms associated

with the genes involved in cytokine production. Such

polymorphisms have been linked to an increased risk

for chronic periodontitis but these findings have yet

to be corroborated.

SCIENTIFIC BASIS FOR

PERIODONTAL THERAPY

Periodontitis is initiated and sustained by microbes

which are present in supra and subgingival plaque in

the form of uncalcified and calcified (calculus)

biofilms. Initial periodontal therapy or basic treat-

ment of periodontitis involves the removal of both sub

and supragingival plaque. The clinical outcome is

largely dependent on the skill of the operator in re-

moving subgingival plaque and the skill and motiva-

tion of the patient in practising adequate home care.

A further variable is the innate susceptibility of the

patient which is related to the way in which their

innate, inflammatory and immune systems operate in

response to the microbial challenge. In addition, local

and systemic risk factors can influence the quantity

and quality of both the microbial challenge and the

host response to these pathogens. The relative contri-

bution of these risk factors has yet to be fully deter-

mined but their influence would be negated if the

periodontium was kept free of microbial plaque, and

thus subgingival debridement and patient's home

care are of vital importance.

Studies have been conducted which indicate the

relative importance of operator and patient-based in-

terventions (for further detail see Chapters 20 and 21)

and only a brief summary is presented below.

Tooth loss

There is an established literature strongly supporting

the concept that periodontal treatment of chronic pe-

riodontitis is effective, and numerous long term stud-

ies show low rates of tooth loss ( 0.1 tooth lost/year)

in treated and well-maintained periodontitis patients

(Lindhe & Nyman 1984, Nabers et al. 1988). Patients

who, following treatment, were not complying with

maintenance care had double the rate of tooth loss per

year (0.2 teeth/year) (Becker et al. 1984), and un-

treated patients lost approximately 0.6 teeth/year

(

Becker et al. 1979). Thus there is substantial evidence

supporting the concept that periodontal therapy and

subsequent maintenance care are beneficial in main-

taining the dentition.

Subgingival instrumentation and

maintenance

The effects of cause related periodontal therapy were

studied intensively during the 1980s and the work of

Egelberg and his colleagues will be described now.

Badersten et al. (1984) utilized patients with severe

chronic periodontitis to study the effects of cause re-

lated periodontal therapy. The patients had a multi-

tude of sites with deep pockets (up to 12 mm). Initial

oral hygiene instruction was provided at two to three

CHRONIC PERIODONTITIS • 213

Clinical changes between 0-24 months in sites with different initial probing depths

Fig. 8-3. Data from the Badersten et al. (1984) study showing the clinical changes at 2 years according to baseline

pocket depth.

visits during the first month of the study. Additional

instruction and reinforcement of self-performed

plaque control was provided, as required, during the

2 years of the study. Subgingival debridement was

performed at 3, 6 and 9 months and the results were

evaluated over 2 years. Only minimal improvements

in the periodontal indices occurred during the first 3

months in which no scaling and root planing was

performed. Following supra and subgingival instru-

mentation, and gradually up until 12 months from

baseline, the periodontal indices improved markedly.

In the final 12 months of the 2-year period, no signifi

cant further improvements in the clinical condition

occurred. These results demonstrate that chronic pe-

riodontitis can be treated successfully by intensive

initial non-surgical periodontal therapy and this out-

come can be maintained over time with supportive

periodontal therapy (SPT).

Fig. 8-3 shows further data from the Badersten et al.

(1984) study and reports the clinical changes at 2 years

according to baseline pocket depth. It can be seen that

pocket depth reduction after therapy is an arithmetic

combination of gingival recession and gain or loss of

clinical attachment. At the end of the study the mean

pocket depth reduction was 1.5 mm although it is clear

from Fig. 8-3 that the initially deeper pockets had the

largest reduction in pocket depth over the 2 years and

the greatest clinical attachment gain. An interesting

feature is the fact that the sites with initially shallow

pockets tended to lose clinical attachment over the

study period. Several theories have been proposed to

explain this fact. The most plausible explanation for

the loss of clinical attachment at shallow sites is the

trauma caused by subgingival instrumentation to the

supracrestal connective tissue attachment and the

subsequent remodeling of the marginal tissues. The

best predictor of further clinical attachment loss was

residual deep pockets that occurred after treatment.

Thus, Claffey and Egelberg (1995) found that at re-

evaluation, patients with multiple sites with residual

probing depth >_ 6mm after active treatment had a

greater risk for additional attachment loss than pa-

tients with mainly shallow sites.

EFFECT OF SURGICAL

TREATMENT

Surgical treatment of chronic periodontitis lesions

permits visualization and access to the root surfaces

and thus has clear advantages over a non-surgical

approach for the cleaning of root surfaces. Tissues may

also be manipulated and lesions modified, or granu-

lation tissue surgically removed. The efficacy of sur-

gical periodontal therapy compared within the vari-

ous surgical treatment modalities and compared to

non-surgical therapy has to be considered from the

extensive scientific literature on these matters (for

further detail see Chapter 25).

COMPARISONS OF SURGICAL

AND NON-SURGICAL THERAPY

Kaldahl et al. (1993) reviewed a large body of work on

the advantages of different periodontal treatment mo-

214 • CHAPTER 8

dalities over others. Although the best assessment of

clinical outcome is achieved from longer-term studies,

actually following patients over the long term creates

new confounding problems and these can reduce the

benefit imparted by the longitudinal element of the

investigation. For example, the patient drop-out in-

creases over time which may increase the bias in the

selection of the final group for analysis (usually the

less motivated patients or less successfully treated

patients will drop out). In addition, tooth loss may

occur for which we do not know the reason and sites

associated with such teeth are lost for longitudinal

analysis. Nevertheless, useful long-term studies have

been conducted over 5 to 8 years and have typically

made intra-patient comparisons of different peri-

odontal treatment modalities using split mouth de-

signs. In the Kaldahl et al. (1993) review, some com-

prehensive summary statements were arrived at. In

general:

1. Surgical and non-surgical periodontal therapy can

improve periodontal clinical outcome measures.

Surgical therapy created greater short-term reduc-

tions in probing depth than non-surgical therapy

although longer-term results varied between main-

taining greater probing depth reduction or show-

ing no differences with non-surgical therapy.

Flap surgery with and without osseous resection

gave variable probing depth reductions in the short

term. Some studies favored osseous resection

whilst others showed no difference in probing

depth reduction.

Flap surgery without osseous resection tended to

produce greater better short and long-term gains in

attachment levels.

In both short and long-term studies, surgery pro-

duced a greater loss of probing attachment in sites

with initially shallow pockets. In sites with deeper

pockets short and long-term studies reported no

difference in attachment level change for non-sur-

gical and surgical therapy.

Supragingival plaque control alone gave markedly

inferior results to plaque control combined with

subgingival root debridement.

REFERENCES

Badersten, A., Nilveus, R. It Egelberg, J. (1984). Effect of nonsur-

gical periodontal therapy. II. Severely advanced periodonti-

tis.

Journal of Clinical Periodontology

11, 63-76.

Becker, W., Becker, B.E. & Berg, L.E. (1984). Periodontal treatment

without maintenance. A retrospective study in 44 patients.

Journal of Periodontology

55, 505-509.

Becker, W., Berg, L. & Becker, B.E. (1979). Untreated periodontal

disease: a longitudinal study.

Journal of Periodontology

50,

234-244.

Claffey, N. & Egelberg, J. (1995). Clinical indicators of probing

attachment loss following initial periodontal treatment in

advanced periodontitis patients.

Journal of Clinical Periodon-

tology

22(9), 690-696.

Flemmig, T.F. (1999). Periodontitis. Annal of Periodontology 4,

32-38.

Kaldahl, W.B., Kalkwarf, K.L. & Patil, K.D. (1993). A review of

longitudinal studies that compared periodontal therapies.

Journal of Periodontology 64,

243-253.

Kinane, D.F. & Chestnutt, I. (2000). Smoking and Periodontal

Disease. Critical Reviews Oral Biological Medicine 11, 356-365.

Lindhe, J. & Nyman, S. (1984). Long-term maintenance of pa-

tients treated for advanced periodontal disease.

Journal

Clinical Periodontology

11(8), 504-514.

Nabers, C.L., Stalker, W.H., Esparza, D., Naylor, B. & Canales, S. (

1988). Tooth loss in 1535 treated periodontal patients.

Journal

Periodontologi

59(5), 297-300.

Socransky, S.S., Haffajee, A.D., Goodson, J.M. & Lindhe, J. (1984).

New concepts of destructive periodontal disease.

Journal of

Clinical Periodontology

11, 21-32.

CHRONIC PERIODONTITIS • 215

CHAPTER 9

Aggressive Periodontitis

MAURIZIO S. TONETTI AND ANDREA MOMBELLI

Classification and clinical syndromes

Epidemiology

Primary dentition and permanent dentition

Screening

Etiology and pathogenesis

Diagnosis

Clinical, microbiologic, genetic

Principles of therapeutic intervention

Periodontitis is an infection that can manifest itself

with polymorph clinical presentations. This has led to

the recognition of different clinical syndromes. Until

recently, the question of whether or not these dissimi

lar clinical presentations represented different forms

of disease has been open to discussion. Today several

lines of evidence support the existence of truly differ-

ent forms of periodontitis. These include:

The growing clinical consensus of differential prog-

nosis and need for specific treatment approaches

for the various syndromes

Heterogeneity in etiology with possible therapeu

tic

implications

Heterogeneity in genetic and environmental sus-

ceptibility

At the 1999 international classification workshop, the

different forms of periodontitis were reclassified into

three major forms (chronic, aggressive and necrotiz-

ing forms of periodontitis) and into periodontal mani-

festations of systemic diseases. This chapter deals

with aggressive, type 1, periodontitis. Until recently,

this group of diseases was defined primarily based on

the age of onset/diagnosis and was thus named early

onset periodontitis (EOP). Features of this form of

disease, however, can present themselves at any age

and this form of periodontitis is not necessarily con-

fined to individuals under the arbitrarily chosen age

of 35.

Aggressive periodontitis (AgP) comprises a group

rare, often severe, rapidly progressive forms of

periodontitis often characterized by an early age of

clinical manifestation and a distinctive tendency for

cases to aggregate in families. At the above mentioned

classification workshop, AgP periodontitis was char-

acterized by the following major common features

(

Lang et al. 1999):

•

Non-contributory medical history

•

Rapid attachment loss and bone destruction

•

Familial aggregation of cases

Frequently AgP presents early in the life of the indi-

vidual; this implies that etiologic agents have been

able to cause clinically detectable levels of disease over

a relatively short time. This fact is central to the current

understanding of these diseases, since it implies infec

tion with a highly virulent microflora and/or a high

level of subject susceptibility to periodontal disease.

AgP, however, can occur at any age. Diagnosis of AgP

requires exclusion of the presence of systemic diseases

that may severely impair host defences and lead to

premature tooth loss (periodontal manifestations of

systemic diseases).

The existence of specific forms of AgP has also been

recognized based on specific clinical and laboratory

features: localized aggressive periodontitis (LAP, for-

merly known as localized juvenile periodontitis or

UP)

and generalized aggressive periodontitis (GAP,

formerly termed generalized juvenile periodontitis

(

GJP) or generalized early onset periodontitis, G-EOP)

(

Tonetti & Mombelli 1999).

In spite of its rare occurrence AgP has been the focus

of many investigations aimed at understanding its

etiology and pathogenesis. Difficulties in gathering

sufficiently large populations, however, have resulted

in few clinical studies addressing both diagnostic and

therapeutic procedures for these subjects. Utilization

of both clinical and advanced diagnostic procedures

as well as of a variety of treatment approaches remains

largely anecdotal and somehow based on the specific

218 • CHAPTER 9

Fig. 9-1. (a-c) Clinical appearance of the periodontal tissues of a 15-year-old girl suffering from localized aggressive

periodontitis. Note the proper oral hygiene conditions and the scalloped outline of the gingival margin. In the

lower

anterior region, the interdental papilla between teeth 31 and 32 has been lost. Intraoral radiographs (d) show

the

presence of localized angular bony defects, associated with clinical attachment level loss, at the mesial aspect of

tooth

46, 36 and at the distal aspect of tooth 31. No significant bone loss and/or attachment loss was detectable in

other

areas of the dentition. Diagnosis: localized aggressive periodontitis (LAP).

loss at primary molars in 20-52% of the cases, suggest

EPIDEMIOLOGY

ing that at least some LAP cases may initially affect the

primary dentition (Sjodin et al. 1989, 1993). Further-

more, in LAP subjects an association between the Given the recent definition of AgP and the fact that it

number of

lesions and the age of the subject has been does not represent just a new term for the previously

described,

suggesting an age-dependent shift from defined EOP, epidemiological studies available relate

localized to generalized

forms of AgP (Hormand & primarily to EOP. Relatively few investigations em-

Frandsen 1979, Burmeister et al.

1984).

ploying different epidemiological techniques have es-

Fig. 9-1. (e-g) Clinical appearance of the 14-year-old sister of the proband depicted in (a-d). Note that in spite of

the excellent oral hygiene status, bleeding on probing was provoked in the mesial of the molars, where deep

pockets were present. (h) Angular bone loss is evident on the mesial of 16, 26 and 46.

timated the prevalence and the progression of EOP in the employed epidemiological methodologies and the

primary and permanent dentition(s) of children definition of EOP.

and young adults. All available investigations, how-

ever, indicate that early onset (aggressive) forms of

periodontal diseases are detectable in all age and eth- Primary dentition

nic groups (Papapanou 1996). Wide variation in

prevalence, however, has been reported, with some Little evidence is available concerning the prevalence

studies showing up to 51.5% affected individuals. of AgP affecting the primary dentition. In the few

These differences are probably due to differences in studies from industrialized countries, marginal alveo-

AGGRESSIVE PERIODONTITIS • 219

220 • CHAPTER 9

Fig. 9-2. (a-c) Clinical presentation in 1990 of a 32-year-old female with generalized severe bone loss and clinical at

tachment loss, recession of the gingival margin and presence of deep periodontal pockets. Presence of local

factors, and intense inflammation and edema of the gingival margin are evident.

lar bone loss has been found to affect the primary

dentition of 5 to 11 year olds with frequencies ranging

from 0.9-4.5% of subjects (Sweeney et al. 1987, Bim-

stein et al. 1994, Sjodin & Mattson 1994). In this respect,

it should be emphasized that periodontitis affecting

the primary dentition does not necessarily mean pres-

ence of an aggressive form of periodontitis, but may

indicate a chronic form of disease with relative abun-

dance of local factors (plaque and calculus). A clinical

case of localized periodontitis affecting the primary

dentition is illustrated in Fig. 9-3. More severe cases

affecting the primary dentition and leading to tooth

exfoliation early in life are usually interpreted as peri-

odontal manifestations of systemic (hematologic) dis-

eases, such as leukocyte adhesion deficiency (see

Chapter 2 and Fig. 9-4).

Permanent dentition

In the permanent dentition of 13 to 20-year-old indi-

viduals, the majority of studies have reported a preva-

lence of periodontitis of less than 1% (usually 0.1-0.2%

in Caucasian populations). The risk of developing

periodontitis at such an early age, however, does not

seem to be shared equally in the population: among

US schoolchildren 5-17 years of age, the prevalence of

periodontitis has been estimated to range from about

0.2% for whites to about 2.6% for blacks (Loe & Brown

1991). Furthermore, in these young age groups higher

prevalence of periodontitis has been reported in stud-

ies from some developing countries (see Chapter 2).

Longitudinal studies of disease progression in ado-

lescents indicate that subjects with signs of destructive

periodontitis at a young age are prone to further dete-

rioration. Such deterioration appears to be more pro-

nounced at initially affected sites, and in patients di-

agnosed with LAP and from low socio-economic

classes. Deterioration of the periodontal status in-

volves both an increase in extent (number of lesions

within the dentition) and an increase in severity of

lesions (further alveolar bone loss at initially diseased

sites, Fig. 9-5) (Clerehugh et al. 1990, Lissau et al. 1990,

Albandar et al. 1991a,b, 1993, Aass et al. 1994).

Some epidemiological investigations have re-

ported high prevalence of attachment loss in adoles-

cents and young adults that did not fit the charac-

teristics of recognized periodontitis clinical syn-

dromes. Such occurrences have been termed incidental

attachment loss, and have been reported in 1.6-26% of

the subjects. This group is thought to comprise both

initial forms of periodontitis (including AgP) and a

variety of defects such as recession due to traumatic

tooth-brushing, attachment loss associated with re-

moval of impacted third molars, etc.

Conclusion

A small but significant proportion of children and

AGGRESSIVE PERIODONTITIS • 221

Fig. 9-2. (d-f). Previous radio-

graphic examinations were avail-

able from 1984 and 1987. Compari

son of the radiographs obtained

over the 6-year period from 1984

to 1990 indicates that most of the

periodontal destruction occurred

during the last 3 years. The pa-

tient had been smoking 20 ciga-

rettes/day for more than 10 years.

Diagnosis: Generalized aggressive

periodontitis (GAP) in a cigarette

smoker.

young adults is affected by some form of periodonti-

tis. A substantial proportion of these subjects is

thought to be affected by AgP. Given the severity of

these forms of periodontal diseases and their tendency

to progress, early detection of periodontitis, and AgP

in particular, should be a primary concern of both

practitioners and public health officers. The whole

population, including children and young adults,

should receive a periodontal screening as part of their

routine dental examination.

Screening

Given the low prevalence of AgP patients within the

population, cost-effective detection of cases requires

utilization of a sensitive screening approach, i.e. the

application of a diagnostic approach able to correctly

identify most of the cases with disease. The objective

of screening is the detection in a population of possi-

bly diseased subjects that would require a more com-

prehensive examination. In periodontology, the most

sensitive diagnostic test for the detection of periodon-

titis is the measurement of attachment loss by probing.

Application of this diagnostic procedure in the mixed

dentition and in teeth that are not fully erupted, how-

ever, may be difficult.

In younger subjects, therefore, a currently utilized

screening approach is the measurement of the dis-

tance between the alveolar crest and the cemento-

enamel junction on bite-wing radiographs. An advan-

tage of this approach relates to the fact that in most

industrialized countries bite-wing radiographs of

children and young adolescents in mixed dentition are

routinely taken for caries prevention programs; these

radiographs should therefore be screened not only for

carious lesions but also for the presence of marginal

alveolar bone loss.

Recent investigations have attempted to determine

the "normal" distance between the cemento-enamel

222 • CHAPTER

Fig. 9-3. Seven-year-old African-American female presenting with radiographic alveolar bone loss and probing at-

tachment loss at the primary molars and permanent first molars and incisors: (a-c) clinical photographs, buccal

view; (d-e) bite-wing radiographs. Clinical presentation shows moderate plaque accumulation, localized gingival

inflammation, with ulceration of the gingival margin and loss of the interdental papilla mesial of #65. 4-6 mm pock-

ets with bleeding on probing were present in the primary molar regions. Bone loss and attachment loss were lim-

ited to the molar region. The mesial aspects of the first permanent molars are also initially involved. Radiographic

subgingival calculus is evident. Note that the upper left posterior sextant seems to be more severely affected than

the other posterior segments. Diagnosis: localized aggressive (type 1) periodontitis.

junction and the alveolar crest of primary and perma-

nent molars in 7 to 9-year-old children (Sjodin &

Mattson 1992, Needleman et al. 1997). Median dis-

tances at primary molars were 0.8 to 1.4 mm. These

values were in agreement with those previously re-

ported for primary molars of 3 to 11-year-old children

(Bimstein & Soskolne 1988). The cemento-enamel

junction of permanent molars was 0 to 0.5 mm apical

to the alveolar crest in 7 to 9 year olds. These values

were age-dependent, and related to the state of erup-

tion of the tooth. In general, however, it should be

noted that the majority of children present with dis-

tances significantly smaller than the 2-3 mm consid-

ered normal for the completely erupted dentitions of

adults. In children, significantly greater distances have

been detected at sites with caries, fillings or open

contacts, indicating that these factors may contribute

to bone loss in similar ways to in adult patients. Fur-

thermore, presence of one of these local factors may

suggest a local cause of bone loss, other than perio-