Tài liệu Clinical Periodontology and Implant Dentistry 4th edition_2 doc

CHAPTER 24

Breath Malodor

DANIEL VAN STEENBERGHE AND MARC QUIRYNEN

Socio-economic aspects

Etiology and pathophysiology

Diagnosis

Patient history

Clinical and laboratory examination

Treatment

Conclusions

Breath malodor means an unpleasant odor of the ex￾pired air, whatever the origin may be. Oral malodor

specifically refers to such odor originating from the oral

cavity itself. A term like halitosis is synonymous with

breath malodor but is not always understood by the

general population. Breath malodor has long been a

matter of concern. There are references to it in the

Bible and in the Koran. Surprisingly enough, until

recently breath malodor has not been a matter of much

interest in periodontology, although its most frequent

causes are plaque-related gingivitis and periodontitis.

Even the literature concerning this subject is scarce.

There was only one book on this topic in the nine￾teenth century (Howe 1898) and it was not until the

end of the twentieth century that two more books were

devoted to the subject (Rosenberg 1995, van Steenber￾ghe & Rosenberg 1996). Joe Tonzetich from the Uni￾versity of British Columbia unfolded the biologic basis

for oral malodor (Tonzetich 1977) but his observations

received only limited attention from clinicians, even if

oral or breath malodor is frequently encountered in

any dental and especially periodontal office.

SOCIO-ECONOMIC ASPECTS

A transient breath malodor is noticed when waking up

in the morning in more than half the adult population

(Morris & Read 1949). It does not deserve special

attention since it is due to the xerostomia developed

during sleep, i.e. when salivary flow is reduced to a

minimum. This with the ongoing intra-oral putre￾faction explains the malodor when waking up. Morn￾ing breath odor disappears soon after the intake of

food or fluid. The intra-oral placement of a toothpaste

containing zinc salts and triclosan has the capacity to

reduce the odor for several hours, even in the absence

of toothbrushing (Hoshi & van Steenberghe 1996).

The real concern of the population is the breath

malodor which remains during the day and which can

cause social and/or relational problems. Unsubstan￾tiated press releases claim that breath malodor may

concern as many as 25 million people in the US alone.

Everyone has sometimes experienced, when a person

is speaking to them at close proximity, breath odor that

is unpleasant if not unbearable. Subjects who believe

they produce malodor can adopt avoidance patterns

such as keeping a distance when speaking to others or

holding their hand in front of the mouth while speak￾ing. There is also a tendency to constantly use rinses,

sprays, chewing gums or pills to mask the breath odor,

although many such items have no effect whatsoever

or at least no lasting effect.

Even more disturbing is the fact that a number of

subjects imagine they have breath malodor when they

may not have. This imaginary breath odor, also called

halitophobia (Oxtoby & Field 1994), has been associ￾ated with obsessive-compulsive disorders or hypo￾chondria. It has even led to suicide (Yaegaki 1995).

There are well-established personality disorder ques￾tionnaires such as the SCL-90 (Derogatis et al. 1973)

which allow the clinician to assess the tendency for

illusionary breath malodor among those where no

objective diagnosis of breath malodor can be made (Eli

et al. 1996). For such patients, the presence of a psy￾chologist/psychiatrist at the multidisciplinary mal￾odor consultation is essential.

Epidemiological investigations concerning breath

malodor are rare. There is a large-scale Japanese study

involving more than 2500 subjects aged 18 to 64 years

in which the malodor was measured by a portable

sulfide monitor (see section on diagnosis later in this

chapter) at several times during the day. The volatile

sulfur components reached high levels several hours

BREATH MALODOR • 513

after food intake and increased with age, tongue coat￾ing and periodontal inflammation. About one out of

four subjects exhibited volatile sulfur components (

VSC) values higher than 75 ppb, which is considered

the limit for social acceptance.

Thus one can conclude that the socio-economic

impact of breath malodor is considerable.

ETIOLOGY AND

PATHOPHYSIOLOGY

Findings from different investigations have docu￾mented that the vast majority of causes of malodor

relate to the oral cavity, with gingivitis (Persson et al.

1989, 1990), periodontitis (Yaegaki & Sanada 1992a)

and tongue coating (Yaegaki & Sanada 1992b) as pre￾dominant factors. On the other hand, since more than

90% of the population suffers from gingivitis and

periodontitis, there is a risk that such plaque-related

inflammatory conditions are always considered to be

the cause, while in fact more important pathologies,

such as a hepatic or renal insufficiency or a bronchial

carcinoma, may be the main etiological factor.

In a multidisciplinary breath odor clinic, it ap￾peared that 87% of the etiologies were intra-oral, 8%

in the oto-rhino-laryngological field and 5% from else￾where in the body or unknown (Delanghe et al. 1997)

Members of the oral anaerobic microbiota, espe￾cially species such as Treponema denticola, Porphyro￾nrrnras gingivalis and Prevotella intermedia, can produce

hydrogen sulfide and methylmercaptan from L-cyste￾ine or serum (Tonzetich 1977), i.e. proteins which are

consistently present in the oral cavity and in the cre￾vicular fluid. Chromatography (see section on diag￾nosis later in this chapter) revealed that crevicular

fluid contains hydrogen sulfide, methylmercaptan and

also dimethyl sulfide and even dimethyl disulfide (Coil

1996). When deep pockets are present the rela￾tionship with methylmercaptan/HZS increases (Coil

1996).

One should never forget that many components

besides sulfide components, e.g. diamines (putre￾scine, cadaverine) in the crevicular fluid and in saliva

can be malodorous (Goldberg et al. 1995). It is impor￾tant to realize that the latter odor-inducing compo￾nents cannot be detected by a portable sulfide monitor

(see section on diagnosis later in this chapter), which

is often used in breath odor consultations. All such

malodor-inducing components can only be perceived

when they become volatile. This means that as long as

they are dissolved in the saliva, they will not be ex￾pressed – just as a perfume only evaporates when the

skin becomes dry. This explains why xerostomia re￾veals a strong breath malodor, which otherwise might

only be a faint odor.

While on the one hand periodontitis favors the

production of malodorous components, the latter may

in their turn play a role in the ongoing periodontitis.

Volatile sulfur components, such as methylmercap￾tan, enhance the interstitial collagenase production,

the IL-1 production by mononuclear cells and the

cathepsin B production (Lancero et al. 1996, Ratkay et

al. 1996) and thus mediate connective tissue break￾down. Brunette et al. (1996) found that human gingi￾val fibroblasts grown in vitro showed an affected cy￾toskeleton when exposed to CH3SH. The same gas

altered cell proliferation and migration. These potent

biologic effects can be blocked by Zn", at least for the

influence of VSC on protein synthesis.

The tongue dorsum, because of itslarge surface, is a

prominent host for products that can cause malodor.

Desquamated cells, food remnants, bacteria, etc. accu￾mulate on the tongue and putrefy under the action of

bacteria (Bosy et al. 1994). There is six times more

tongue coating in patients with periodontitis than in

subjects with a healthy periodontium (Yaegaki &

Sanada 1992b).

Saliva plays a predominant role in the control/ex￾pression of malodorous components. After drying,

sulfur and non-sulfur-containing gases such as

cadaverine, skatole, indole, etc. are released (Klein￾berg & Codipilly 1995). The oral microbiology in￾volved in VSC production is well identified; Porphyro￾monas gingivalis, Prevotella intermedia, Fusobacteriurn

nucleatum, Porhyromonas endodontalis, Prevotella loesclrii,

Haemophilus para influenzae, Treponema denticola,

Enterobacter cloacae and many others have been

associated with malodoros gas production (Persson et

al. 1990, Kleinberg & Codipilly 1995, Niles & Gaffar

1995). The above are members of the oral microbiota,

are anaerobic and are Gram-negative.

The ear-nose-throat causes include chronic

pharyngitis, purulent sinusitis and postnasal drip.

The latter, rather frequent condition is associated with

regurgitation oesophagitis and is perceived by pa￾tients as a liquid flow in the throat which originates

from the nasal cavity (Rosenberg 1996). Ozena, which

is an atrophic condition of the nasal mucosa with the

appearance of crusts, leads to a very strong breath

malodor but is a rare disease.

Pulmonary causes include chronic bronchitis, bron￾chiectasis, and bronchial carcinoma (Lorber 1975,

McGregor et al. 1982).

Gastro-intestinal tract causes include:

• The Zenker diverticle: the accumulation of food and

debris in the pouch of the esophagus, not separated

from the oral cavity by any sphincter, can cause a

significant breath odor (Crescenzo et al. 1998).

• A gastric hernia can, especially when reflux eso￾phagitis occurs, lead to a disturbing breath odor.

Otherwise, the stomach never causes breath mal￾odor, contrary to a common opinion among the

public and even some clinicians (Norfleet 1993).

• Intestinal gas production can also play a role, prob￾ably because some gases such as dimethylsulfide

are poorly resorbed by the intestinal endothelium

and when transported by the blood they can reach

514 • CHAPTER 24

Fig. 24-1 The periodontologist, the

oto-rhino-laryngologist and the

psychologist listen to the patient.

Fig. 24-2. Two calibrated judges

evaluate the expired air and com

pare their rating.

the lung tissue and be exhaled in the breath air (

Suarez et al. 1999).

Other systemic causes (Leopold et al. 1990, Preti et al.

1995) of breath malodor include renal (uremia) (

Simenhoff et al. 1977), pancreatic (acetone) (Booth &

Ostenson 1966) and liver (ammonium) (Chen et al.

1970) insufficiencies which appear as breath malodors

with different characteristics that can be detected by

experienced clinicians.

Some medications such as metronidazole can by

themselves cause some breath malodor.

Periodontologists should keep these possible non￾oral causes in mind. Their role may be masked to the

clinician by the fact that a patient with such a disease

may also present, as the vast majority of adults do,

with gingivitis or periodontitis.

DIAGNOSIS

Patient history

There is a saying "Listen to the patient and he will tell

you the diagnosis". This is very true for patients with

breath odor complaints. Besides what is spontane￾ously told, the clinician should question about the

frequency of odor (e.g. does it happen only some

weeks), the time of appearance within the day (e.g.

after meals, which can indicate a hernia), whether

others (non-confidants) have identified the problem (

imaginary breath odour?), what kind of medications

are taken, whether dryness of the mouth is noticed,

etc. (Fig. 24-1).

Several of the points retrieved from this case his￾tory, which because of the emotional character of the

matter cannot be obtained by a written questionnaire,

must be used in the (differential) diagnosis of the

problem.

BREATH MALODOR • 515

Fig. 24-3. Nasal examination

should be done routinely when

the air expired through the nose is

malodorous.

Fig. 24-4. The oropharyngeal air is

sampled by an electronic appara￾tus which measures the volatile

sulfur components.

Clinical and laboratory examination

Organoleptic

Even though some instruments are now available, the

best method in the examination of breath malodor is

still the organoleptic assessment made by a judge,

who has been tested and calibrated for his/her smell￾ing acuity. This testing is done by determining the

threshold level for detecting a series of dilutions of a

malodorous compound such as isovaleric acid. The

discrimination power of the judge is evaluated by

presenting to him/her a series of odors for identifica￾tion (Doty et al. 1984).

The use of any fragance, shampoo or body lotion,

and smoking, alcohol consumption or garlic intake are

strictly forbidden 12 hours before the assessment is

made. This involves both the patient and the judge.

The judge will not wear rubber gloves, the odor of

which may interfere with the organoleptic assess￾ments. Assessments should be performed at several

appointments on different days, since breath odor

fluctuates dramatically from one day to the next. The

patient should be encouraged to bring a confidant to

the consultations to help him/her identify the odor

causing the problem. The judge will smell a series of

different air samples (Fig. 24-2):

• Oral cavity odor: the subject opens his/her mouth

and refrains from breathing; the judge places his

nose close to the mouth opening.

• Breath odor: the subject breathes out through the

mouth; the judge smells both the beginning (deter￾mined by the oral cavity and systemic factors) and

the end (originating from the bronchi and lungs) of

the expired air.

• Tongue coating scraping: the judge smells the tongue

scraping and also presents it to the patient or the

accompanying confidant to evaluate whether they

associate the smell from the scraping with the mal￾odor complaint.

• Breath odor when breathing out through the nose: when

the air expired through the nose is malodorous, but

the air expired through the mouth is not, a na￾sal/paranasal etiology should be suspected.

In the oro-pharyngeal examination, the clinician must

look for inflammation of the gingiva, or in the mucosa

under a prosthesis. Fresh extraction wounds or inter-

516 • CHAPTER 24

dental food entrapment can cause breath malodor. The

pharynx should be thoroughly inspected for the pres￾ence of inflamed tonsils. The tonsils often present with

crypts which may harbor anaerobic bacteria, pus and

even calculus (tonsilloliths).

Less obvious for a dentist is the examination of the

nostrils, although this is essential if the breath mal￾odor is noticed more clearly when the subject breathes

out through the nostrils (Fig. 24-3).

Portable volatile sulfide monitor

This is an electronic device that aspirates the air of the

mouth or expired air through a straw and analyses the

concentration of H2S (hydrogen sulfide) and CH3SH (

methylmercaptan), without discriminating between the

two (Fig. 24-4). It can also be used to measure the

headspace above incubated saliva (Rosenberg et al.

1991). The monitor is good for the detection of hydro￾gen sulfide but less good for methyl mercaptan. It

needs regular calibrations.

It should be stressed that this machine will not

detect malodorous components such as cadaverine,

putrescine, urea, indole, skatole and several others

which have been described in salivary headspace (

Kostelc 1981). Cadaverine (produced by bacteria

through decarboxylation of lysine to counteract the

unfavorable acidic growth conditions during gly￾colysis) and putrescine (from decarboxylation of orni￾thine or arginine) are both diamines the level of which

in air expired from the mouth does not, evidence

shows, correlate with VSC scores (Goldberg et al.

1994) but does correlate to a certain extent with tongue

coating and/or periodontitis.

Gas chromatography

This can analyse air or incubated saliva or crevicular

fluid for any volatile component (Goldberg et al. 1994).

Some hundred components were isolated, and mostly

identified, from saliva and/or tongue coating, from

ketones to alkanes and from sulfur-containing

compounds to phenyl compounds (Claus et al. 1996).

Gas chromatography is only available in specialized

centers and for identifying non-oral causes such as

intestinal (Suarez et al. 1999) or bronchial/pulmonary

causes.

TREATMENT

An etiologic treatment is to be preferred. The treat￾ment of oral malodor consists of the elimination of the

pathology present, such as deepened and inflamed

periodontal pockets and/or tongue coating. If another

underlying disease is suspected, or if clinical experts

in the different disciplines (internal medicine, perio￾dontology, ENT, psychology, etc.) are not available, it

is possible to rapidly (within 1-2 weeks) make a dif￾ferential diagnosis by performing a full-mouth one￾stage disinfection of the oro-pharynx, including the

use of chlorhexidine spray to deal with the pharynx (

Quirynen et al. 2000). Since all oral diseases which

cause malodor relate to microorganisms, this one￾stage professional approach reinforced by stringent

home care will dramatically reduce the oro-pharyn￾geal microbiota and the putrefraction they cause and

thus the malodour (Quirynen et al. 1998). If the symp￾toms do not disappear, the patient should be referred

to a specialized multidisciplinary center where gas

chromatography can help in the differential diagnosis.

Masking of breath malodor should be distin￾guished from etiological treatment. It is well establ￾ished that zinc-containing mouthrinses have the prop￾erty to complex the divalent sulfur radicals, reducing

this important cause of malodor. Thus it appears that

the application of a zincchloride/triclosan-containing

toothpaste on the tongue dorsum reduces the oral

malodor for some 4 hours (Hoshi & van Steenberghe

1996). Baking soda containing dentifrices (> 20%) con￾fers a significant odor-reducing benefit for up to 3

hours (Brunette et al. 1998). The use of hydrogen

peroxide rinse also offers positive perspectives (Suarez

et al. 2000). To deal with the tongue coating it appears

that tongue brushing with chlorhexidine, be-sides

oral rinses with the same antiseptic, reduces the

organoleptic scores significantly (Loesche & De Bo￾ever 1996). Whether the beneficial effect of tongue

brushing is related to the removal of bacteria and/or

to the reduction of their substratum, remains an open

question.

Hardly efficient are mints and other short acting "

anti-breath" odor components. Most of them have not

been properly tested in a blind way against a placebo.

A recent review compared the efficiency of oral rinses,

toothpastes and cosmetics for breath odor therapy (

Quirynen et al. 2002).

When dryness is at stake, any measure to increase

the salivary flow may be beneficial. This can mean a

proper fluid intake or the use of chewing gum to

trigger the periodontal-parotid reflex, which origi￾nates from the mechanoreceptors in the periodontal

ligament of molar teeth (lower) and has the parotid

gland as a target (Hector & Linden 1987). The presence

of these molars is therefore crucial before advocating

the use of chewing gum to enhance salivary secretion.

The pH of the saliva can also be reduced to increase

the solubility of malodorous components (Re￾ingewirtz et al. 1999). Evidence shows that the effect

is short-lived.

CONCLUSIONS

Breath malodor has important socio-economic conse￾quences. A proper diagnosis and determination of the

etiology allows the proper etiological treatment to be

instituted quickly. Although gingivitis, periodontitis

and tongue coating are by far the most common

causes, other more challenging diseases should not be

BREATH MALODOR • 517

overlooked. This can be dealt with either by a trial full-mouth one-stage disinfection) or by a multidisci￾therapy to deal quickly with intra-oral causes (the plinary consultation.

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van Steenberghe, D. & Rosenberg, M. (1996). Bad Breath: a mul￾tidisciplinary approach. Leuven: Leuven University Press, p.

287.

Yaegaki, K. (1995). Oral malodor and periodontal disease. In:

Rosenberg, M., ed. Bad Breath: Research perspectives. Tel-Aviv:

Ramot Publishing, Tel-Aviv University, pp. 88-108.

Yaegaki, K. & Sanada, K. (1992a). Biochemical and clinical factors

influencing oral malodor in periodontal patients. Journal of

Periodontology 63, 783-789.

Yaegaki, K. & Sanada, K. (1992b). Volatile sulfur compounds in

mouth air from clinically healthy subjects and patients with

periodontal disease.Journal of Periodontal Research 27, 233-238.

CHAPTER 25

Periodontal Surgery:

Access Therapy

JAN L. WENNSTROM, LARS HEIJL AND JAN LINDHE

Techniques in periodontal pocket surgery

Gingivectomy

Flap procedures

Regenerative procedures

Distal wedge procedures

Osseous surgery

General guidelines for periodontal surgery

Objectives, indications, contraindications Local

anesthesia

Instruments

Selection of surgical technique

Root surface instrumentation

Root surface conditioning/biomodification

Suturing

Periodontal dressings

Postoperative pain control

Postsurgical care

Outcome

Since most forms of periodontal disease are plaque￾associated disorders, it is obvious that surgical access

therapy can only be considered as adjunctive to cause

-related therapy (see Chapter 20). Therefore, the vari￾ous surgical methods described below should be

evaluated on the basis of their potential to facilitate

removal of subgingival deposits and self-performed

plaque control and thereby enhance the long-term

preservation of the periodontium.

The decision concerning what type of periodontal

surgery should be performed and how many sites

should be included is usually made after the effect of

initial cause-related measures has been evaluated. The

time lapse between termination of the initial cause-re￾lated phase of therapy and this evaluation may vary

from 1 to 6 months. This routine has the following

advantages:

• The removal of calculus and bacterial plaque will

eliminate or markedly reduce the inflammatory cell

infiltrate in the gingiva (edema, hyperemia, flabby

tissue consistency), thereby making assessment of

the "true" gingival contours and pocket depths pos￾sible.

• The reduction of gingival inflammation makes the

soft tissues more fibrous and thus firmer, which

facilitates surgical handling of the soft tissues. The

propensity for bleeding is reduced, making inspec￾tion of the surgical field easier.

• A better basis for a proper assessment of the prog￾nosis has been established. The effectiveness of the

patient's home care, which is of decisive importance

for the long-term prognosis, can be properly evalu￾ated. Lack of effective self-performed care will often

mean that the patient should be excluded from

surgical treatment.

TECHNIQUES I N PERIODONTAL

POCKET SURGERY

Over the years, several different surgical techniques

have been described and used in periodontal therapy.

A superficial review of the literature in this area may

give the reader a somewhat confusing picture of the

specific objectives and indications relevant for various

surgical techniques. It is a matter of historical interest

that the first surgical techniques used in periodontal

therapy were described as means of gaining access to

diseased root surfaces. Such access could be accom￾plished without excision of the soft tissue pocket ("

open-view operations"). Later, procedures were de￾scribed by which the "diseased gingiva" was excised (

gingivectomy procedures).

The concept that not only inflamed soft tissue but

also "infected and necrotic bone" had to be eliminated

called for the development of surgical techniques by

520 • CHAPTER 25

Fig. 25-1. Gingivectomy. The straight incision technique

(Robicsek 1884).

Fig. 25-2. Gingivectomy. The scalloped incision tech￾nique (Zentler 1918).

a b

Fig. 25-3. Gingivectomy. Pocket marking. (a) An ordinary periodontal probe is used to identify the bottom of the

deepened pocket. (b) When the depth of the pocket has been assessed, an equivalent distance is delineated on the

outer aspect of the gingiva. The tip of the probe is then turned horizontally and used to produce a bleeding point at

the level of the bottom of the probeable pocket.

which the alveolar bone could be exposed and re￾sected (flap procedures). Other concepts such as (1) the

importance of maintaining the mucogingival complex

(i.e. a wide zone of gingiva) and (2) the possibility for

regeneration of periodontal tissues have also prompted

the introduction of "tailor-made" surgical techniques.

In the following, surgical procedures will be de￾scribed which represent important steps in the devel￾opment of the surgical component of periodontal ther￾apy.

Gingivectomy procedures

The surgical approach as an alternative to subgingival

scaling for pocket therapy was already recognized in

the latter part of the nineteenth century, when Robic￾sek (1884) pioneered the so-called gingivectomy proce￾dure. Gingivectomy was later defined by Grant et al. (

1979) as being "the excision of the soft tissue wall of a

pathologic periodontal pocket". The surgical proce￾dure, which aimed at "pocket elimination", was usu￾ally combined with recontouring of the diseased

gingiva to restore physiologic form.

Robicsek (1884) and, later, Zentler (1918) described

the gingivectomy procedure in the following way: The

line to which the gum is to be resected is determined

first. Following a straight (Robicsek; Fig. 25-1) or scal￾loped (Zentler; Fig. 25-2) incision, first on the labial

and then on the lingual surface of each tooth, the

diseased tissue should be loosened and lifted out by

means of a hook-shaped instrument. After elimination

of the soft tissue, the exposed alveolar bone should be

scraped. The area should then be covered with some

kind of antibacterial gauze or be painted with disin￾fecting solutions. The result obtained should include

eradication of the deepened periodontal pocket and a

local condition which could be kept clean more easily.

Technique

The gingivectomy procedure as it is employed today

was described in 1951 by Goldman.

• When the dentition in the area scheduled for sur￾gery has been properly anesthetized, the depths of

the pathologic pockets are identified with a conven-

PERIODONTAL SURGERY: ACCESS THERAPY • 521

Fig. 25-4. Gingivectomy. (a) The primary incision. (b) The incision is terminated at a level apical to the "bottom"

of

the pocket and is angulated to give the cut surface a distinct bevel.

Fig. 25-6. Gingivectomy. The detached gingiva is re￾moved with a scaler.

Fig. 25-5. Gingivectomy. The secondary incision through

the interdental area is performed with the use of a

Waerhaug knife.

Fig. 25-7. Gingivectomy. Probing for residual pockets.

Gauze packs have been placed in the interdental spaces

to control bleeding.

Fig. 25-8. Gingivectomy. The periodontal dressing has

been applied and properly secured.

tional periodontal probe (Fig. 25-3a). At the level of

the bottom of the pocket, the gingiva is pierced with

the probe and a bleeding point is produced on the

outer surface of the soft tissue (Fig. 25-3b). The

pockets are probed and bleeding points produced at

several location points around each tooth in the

area. The series of bleeding points produced de￾scribes the depth of the pockets in the area sched￾uled for treatment and is used as a guideline for the

incision.

• The primary incision (Fig. 25-4), which may be made

by a scalpel (blade No. 12B or 15; Bard￾Parker®) in either a Bard-Parker handle or an angu￾lated handle (e.g. a Blake's handle), or a Kirkland

knife No. 15/16,should be planned to give a thin and

properly festooned margin of the remaining gingiva.

Thus, in areas where the gingiva is bulky, the

incision must be placed at a level more apical to the

level of the bleeding points than in areas with a thin

gingiva, where a less accentuated bevel is needed.

The beveled incision is directed towards the base of

the pocket or to a level slightly apical to the apical

extension of the junctional epithelium. In areas

where the interdental pockets are deeper than

522 • CHAPTER 25

the buccal or lingual pockets, additional amounts of

buccal and/or lingual (palatal) gingiva must be

removed in order to establish a "physiologic" con￾tour of the gingival margin. This is often accom￾plished by initiating the incision at a more apical

level.

• Once the primary incision is completed on the buc￾cal and lingual aspects of the teeth, the interproxi￾mal soft tissue is separated from the interdental

periodontium by a secondary incision using an Or￾ban knife (No. 1 or 2) or a Waerhaug knife (No. 1 or

2; a saw-toothed modification of the Orban knife;

Fig. 25-5).

• The incised tissues are carefully removed by means

of a curette or a scaler (Fig. 25-6). Remaining tissue

tabs are removed with a curette or a pair of scissors.

Pieces of gauze packs often have to be placed in the

interdental areas to control bleeding. When the field

of operation is properly prepared, the exposed root

surfaces are carefully scaled and planed.

• Following meticulous debridement, the den￾togingival regions are probed again to detect any

remaining pockets(Fig. 25-7). The gingival contour is

checked and, if necessary, corrected by means of

knives or rotating diamond burs.

• To protect the incised area during the period of

healing, the wound surface must be covered by a

periodontal dressing (Fig. 25-8). The dressing

should be closely adapted to the buccal and lingual

wound surfaces as well as to the interproximal

spaces. Care should be taken not to allow the dress￾ing to become too bulky, since this is not only un￾comfortable for the patient, but also facilitates dis￾lodgement of the dressing.

• The dressing should remain in position for 10-14

days. After removal of the dressing, the teeth must

be cleaned and polished. The root surfaces are care￾fully checked and remaining calculus removed with

a curette. Excessive granulation tissue is eliminated

with a curette. The patient is instructed to properly

clean the operated segments of the dentition, which

now have a different morphology as compared to

the preoperative situation.

Flap procedures

The original Widman flap

One of the first detailed descriptions of the use of a

flap procedure for pocket elimination was published

in 1918 by Leonard Widman. In his article "The opera￾tive treatment of pyorrhea alveolaris" Widman de￾scribed a mucoperiosteal flap design aimed at remov￾ing the pocket epithelium and the inflamed connec￾tive tissue, thereby facilitating optimal cleaning of the

root surfaces.

Technique

• Sectional releasing incisions were first made to de￾marcate the area scheduled for surgery (Fig. 25-9).

These incisions were made from the mid-buccal

gingival margins of the two peripheral teeth of the

treatment area and were continued several millime￾ters out into the alveolar mucosa. The two releasing

incisions were connected by a gingival incision

which followed the outline of the gingival margin

and separated the pocket epithelium and the inflamed

connective tissue from the non-inflamed gingiva. Simi-lar

releasing and gingival incisions were, if needed,

made on the lingual aspect of the teeth.

• A mucoperiosteal flap was elevated to expose at least

2-3 mm of the marginal alveolar bone. The collar of

inflamed tissue around the neck of the teeth was

removed with curettes (Fig. 25-10) and the exposed

root surfaces were carefully scaled. Bone

recontouring was recommended in order to achieve

an ideal anatomic form of the underlying alveolar

bone (Fig. 25-11).

• Following careful debridement of the teeth in the

surgical area, the buccal and lingual flaps were laid

back over the alveolar bone and secured in this

position with interproximal sutures (Fig. 25-12).

Widman pointed out the importance of placing the

soft tissue margin at the level of the alveolar bone

crest, so that no pockets would remain. The surgical

procedure resulted in the exposure of root surfaces.

Often the interproximal areas were left without soft

tissue coverage of the alveolar bone.

The main advantages of the "original Widman flap"

procedure in comparison to the gingivectomy proce￾dure included, according to Widman (1918):

• less discomfort for the patient, since healing oc￾curred by primary intention and

• that it was possible to reestablish a proper contour

of the alveolar bone in sites with angular bony

defects.

The Neumann flap

Only a few years later, Neumann (1920, 1926) sug￾gested the use of a flap procedure which in some

respects was different from that originally described

by Widman.

Technique

• According to the technique suggested by Neumann,

an intracrevicular incision was made through the

base of the gingival pockets, and the entire gingiva (

and part of the alveolar mucosa) was elevated in a

mucoperiosteal flap. Sectional releasing incisions

were made to demarcate the area of surgery.

• Following flap elevation, the inside of the flap was

curetted to remove the pocket epithelium and the

granulation tissue. The root surfaces were sub￾sequently carefully "cleaned". Any irregularities of

the alveolar bone were corrected to give the bone

crest a horizontal outline.

• The flaps were then trimmed to allow both an opti￾mal adaptation to the teeth and a proper coverage

Fig. 25-9. Original Widman flap. Two releasing incisions

demarcate the area scheduled for surgical therapy. A

scalloped reverse bevel incision is made in the gingival

margin to connect the two releasing incisions.

Fig. 25-10. Original Widman flap. The collar of inflamed

gingival tissue is removed following the elevation of a

mucoperiosteal flap.

Fig. 25-11.Original Widnian flap. By bone recontouring,a

"physiologic"

contour of the alveolar bone may be

reestablished.

Fig. 25-12. Original Widman flap. The coronal ends of

the buccal and lingual flaps are placed at the alveolar

bone crest and secured in this position by interdentally

placed sutures.

of the alveolar bone on both the buccal/lingual (

palatal) and the interproximal sites. With regard to

pocket elimination, Neumann (1926) pointed out

the importance of removing the soft tissue pockets,

i.e. replacing the flap at the crest of the alveolar

bone.

PERIODONTAL SURGERY: ACCESS THERAPY • 523

524 • CHAPTER 25

Fig. 25-13. Modified flap operation (The Kirkland flap).

-tracrevicular incision.

Fig. 25-14.Modified flap operation (The Kirkland flap). The

gingiva is retracted to expose the "diseased" root sur￾face.

Fig. 25-15.Modified flap operation (The Kirkland flap). The

exposed root surfaces are subjected to mechanical de￾bridement.

Fig. 25-16.Modified flap operation (The Kirkland flap). The

flaps are replaced to their original position and sutured.

The modified flap operation

In a publication from 1931 Kirkland described a surgi￾cal procedure to be used in the treatment of "periodon￾tal pus pockets". The procedure was called the modified

flap operation, and is basically an access flap for proper

root debridement.

Technique

• In this procedure incisions were made intracrevicu￾larly through the bottom of the pocket (Fig. 25-13)

on both the labial and the lingual aspects of the

interdental area. The incisions were extended in a

mesial and distal direction.

• The gingiva was retracted labially and lingually to

expose the diseased root surfaces (Fig. 25-14), which

were carefully debrided (Fig. 25-15). Angular bony

defects were curetted.

• Following the elimination of the pocket epithelium

and granulation tissue from the inner surface of the

flaps, these were re-placed to their original position

and secured with interproximal sutures (Fig. 25-16).

Thus, no attempt was made to reduce the preopera￾tive depth of the pockets.

In contrast to the original Widman flap as well as the

Neumann flap, the modified flap operation did not include (

1) extensive sacrifice of non-inflamed tissues and (2)

apical displacement of the gingival margin. Since the

root surfaces were not markedly exposed thereby, the

method could for esthetic reasons be useful in the

anterior regions of the dentition. Another advantage of

the modified flap operation was the potential for bone

regeneration in intrabony defects which, according to

Kirkland (1931), in fact frequently occurred.

The main objectives of the flap procedures so far

described were to:

• facilitate the debridement of the root surfaces as

well as the removal of the pocket epithelium and the

inflamed connective tissue,

• eliminate the deepened pockets (the original Widman

flap and the Neumann flap) and

• cause a minimal amount of trauma to the periodon￾tal tissues and discomfort to the patient.

PERIODONTAL SURGERY: ACCESS THERAPY • 525

The apically repositioned flap

In the 1950s and 1960s new surgical techniquesfor the

removal of soft and, when indicated, hard tissue peri￾odontal pockets were described in the literature. The

importance of maintaining an adequate zone of attached

gingiva after surgery was now emphasized. One of the

first authors to describe a technique for the preserva￾tion of the gingiva following surgery was Nabers (

1954). The surgical technique developed by Nabers

was originally denoted "repositioning of attached

gingiva" and was later modified by Ariaudo & Tyrrell (

1957). In 1962 Friedman proposed the term apically

repositioned flap to more appropriately describe the

surgical technique introduced by Nabers. Friedman

emphasized the fact that, at the end of the surgical

procedure, the entire complex of the soft tissues (

gingiva and alveolar mucosa) rather than the gingiva

alone was displaced in an apical direction. Thus,

rather than excising the amount of gingiva which

would be in excess after osseous surgery (if per￾formed), the whole mucogingival complex was main￾tained and apically repositioned. This surgical tech￾nique was used on buccal surfaces in both maxillas

and mandibles and on lingual surfaces in the mandi￾ble, while an excisional technique had to be used on

the palatal aspect of maxillary teeth.

Technique

According to Friedman (1962) the technique should be

performed in the following way:

• A reverse bevel incision is made using a scalpel with

a Bard-Parker blade (No. 12B or No. 15). How far

from the buccal/lingual gingival margin the inci￾sion should be made is dependent on the pocket

depth as well as the thickness and the width of the

gingiva (Fig. 25-17). If the gingiva preoperatively is

thin and only a narrow zone of keratinized tissue is

present, the incision should be made close to the

tooth. The beveling incision should be given a scal￾loped outline to ensure maximal interproximal cov￾erage of the alveolar bone, when the flap sub￾sequently is repositioned. Vertical releasing inci￾sions extending out into the alveolar mucosa (i.e.

past the mucogingival junction) are made at each of

the end points of the reverse incision, thereby mak￾ing possible the apical repositioning of the flap.

• A full thickness mucoperiosteal flap including buc￾cal/lingual gingiva and alveolar mucosa is raised by

means of a mucoperiosteal elevator. The flap has to

be elevated beyond the mucogingival line in order to

later be able to reposition the soft tissue apically.

The marginal collar of tissue, including pocket

epithelium and granulation tissue, is re-moved with

curettes (Fig. 25-18), and the exposed root surfaces

are carefully scaled and planed.

• The alveolar bone crest is recontoured with the

objective of recapturing the normal form of the

alveolar process but at a more apical level (Fig. 25-

19). The osseous surgery is performed using burs

and/or bone chisels.

• Following careful adjustment, the buccal/lingual

flap is repositioned to the level of the newly recon￾toured alveolar bone crest and secured in this posi￾tion (Fig. 25-20). The incisional and excisional tech￾nique used means that it is not always possible to

obtain proper soft tissue coverage of the denuded

interproximal alveolar bone. A periodontal dressing

should therefore be applied to protect the exposed

bone and to retain the soft tissue at the level of the

bone crest (Fig. 25-21). After healing, an "adequate"

zone of gingiva is preserved and no residual pock￾ets should remain.

To handle periodontal pockets on the palatal aspect of

the teeth, Friedman described a modification of the "

apically repositioned flap", which he termed the bev￾eled flap. Since there is no alveolar mucosa present on

the palatal aspect of the teeth, it is not possible to

reposition the flap in an apical direction.

• In order to prepare the tissue at the gingival margin

to properly follow the outline of the alveolar bone

crest, a conventional mucoperiosteal flap is first

resected (Fig. 25-22).

• The tooth surfaces are debrided and osseous recon￾touring is performed (Fig. 25-23).

• The palatal flap is subsequently replaced and the

gingival margin is prepared and adjusted to the

alveolar bone crest by a secondary scalloped and

beveled incision (Fig. 25-24). The flap is secured in

this position with interproximal sutures (Fig. 25-25).

Among a number of suggested advantages of the

apically repositioned flap procedure, the following have

been emphasized:

• Minimum pocket depth postoperatively.

• If optimal soft tissue coverage of the alveolar bone

is obtained, the postsurgical bone loss is minimal.

• The postoperative position of the gingival margin

may be controlled and the entire mucogingival

complex may be maintained.

The sacrifice of periodontal tissues by bone resection

and the subsequent exposure of root surfaces (which

may cause esthetic and root hypersensitivity prob￾lems) were regarded as the main disadvantages of this

technique.

526 • CHAPTER 25

Fig. 25-17. Apically repositioned flap. Following a vertical

releasing incision, the reverse bevel incision is made

through the gingiva and the periosteum to separate the

inflamed tissue adjacent to the tooth from the flap.

Fig. 25-18. Apically repositioned flap. A mucoperiosteal

flap is raised and the tissue collar remaining around

the teeth, including the pocket epithelium and the in￾flamed connective tissue, is removed with a currette.

Fig. 25-19. Apically repositioned flap. Osseous surgery is performed with the use of a rotating bur (a) to recapture the

physiologic contour of the alveolar bone (b).

Fig. 25-20. Apically repositioned flap. The flaps are reposi￾tioned in an apical direction to the level of the recon￾toured alveolar bone crest and retained in this position

by sutures.

Fig. 25-21. Apically repositioned flap. A periodontal dress￾ing is placed over the surgical area to ensure that the

flaps remain in the correct position during healing.