Jan Lindhe. Clinical Periodontology

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574 • CHAPTER

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CHAPTER

Mucogingival Therapy

Periodontal Plastic Surgery

JAN L. WENNSTROM AND GIOVAN P. PINI PRATO

Gingival augmentation

Interdental papilla reconstruction

Marginal tissue recession

Crown lengthening procedures

Orthodontic therapy

Excessive gingival display

Restorative dentistry

Exposure of sound tooth structure

Procedures

Ectopic tooth eruption

Healing

Root coverage

The deformed edentulous ridge

Clinical outcome

Healing

Mucogingival therapy

is a general term used to describe

non-surgical and surgical treatment procedures for

correction of defects in morphology, position and/or

amount of soft tissue and underlying bone support at

teeth and implants. Accordingly, mucogingival ther-

apy may involve not only traditional periodontal

treatment procedures but also, for example, orthodon

tic therapy.

A more specific term,

mucogingival surgery,

was

introduced in the 1950s by Friedman (1957) and was

defined as "surgical procedures designed to preserve

gingiva, remove aberrant frenulum or muscle attach

ments, and increase the depth of the vestibule". Fre-

quently, however, the term "mucogingival surgery"

was used to describe all surgical procedures which

involved both the gingiva and the alveolar mucosa.

Consequently, not only were techniques designed (1)

to enhance the width of the gingiva and (2) to correct

particular soft tissue defects regarded as mucogingi-

val procedures but (3) certain pocket elimination ap-

proaches were also included in this group of peri-

odontal treatment modalities. According to the

Glos-

sary of Periodontal Terrns

(1992) mucogingival surgery

is defined as "plastic surgical procedures designed to

correct defects in the morphology, position and/or

amount of gingivae surrounding the teeth". Miller

(

1993) proposed thatthe term

periodontal plastic surgery

is more appropriate, since mucogingival surgery has

moved beyond the traditional treatment of problems

associated with the amount of gingivae and recession

type defects to also include correction of ridge form

and soft tissue esthetics.

Periodontal plastic surgery

would accordingly be defined as "surgical procedures

performed to prevent or correct anatomic, develop-

mental, traumatic or disease induced defects of the

gingiva, alveolar mucosa or bone" (Proceedings of the

World Workshop in Periodontics 1996). Among treat

ment procedures that may fall within this definition

are various soft and hard tissue procedures aiming at:

• gingival augmentation

• root coverage

• correction of mucosal defects at implants

• crown lengthening

• gingival preservation at ectopic tooth eruption

• removal of aberrant frenulum

• prevention of ridge collapse associated with tooth

extraction

• augmentation of the edentulous ridge.

This chapter will discuss mainly treatment procedures

for corrections of soft tissue defects in relation to the

tooth and the edentulous ridge, while bone augmen-

tation procedures are covered in Chapters 38 and

39.

MUCOGINGIVAL THERAPY — PERIODONTAL PLASTIC SURGERY • 577

Fig. 27-1. A clinical photograph of a mandibular front

tooth region. The gingiva on the buccal aspect of tooth

41 has a narrow width and shows more pronounced

signs of inflammation than adjacent gingival units

with a wider zone of gingiva.

GINGIVAL AUGMENTATION

A review of the large number of articles published on

surgical, mucogingival therapy reveals that the ration

ale for increasing the width of gingiva as a means to

promote gingival health and to improve attachment

levels has been poorly supported by scientific data.

Usually clinical impressions, case reports and anecdo

tal information have been used as the main reference

to justify surgical intervention. Research performed

during the earlier decades, however, has established

a better understanding of the role played by the

gingiva in the protection of the periodontium proper.

Gingival dimensions and periodontal health

For many years the presence of an "adequate" zone of

gingiva was considered critical for the maintenance of

marginal tissue health and for the prevention of con-

tinuous loss of connective tissue attachment (Nabers

1954, Ochsenbein 1960, Friedman & Levine 1964, Car

ranza & Carraro 1970, Hall 1981, Matter 1982). Clini

cians had the "impression" that sites with a narrow

zone of gingiva (Fig. 27-1) were often inflamed while

the wide zone of gingiva found at neighboring teeth

remained healthy. The prevailing concept was thus

that a narrow zone of gingiva was insufficient (1) to

protect the periodontium from injury caused by fric-

tion forces encountered during mastication and (2) to

dissipate the pull on the gingival margin created by

the muscles of the adjacent alveolar mucosa (Fried-

man 1957, Ochsenbein 1960, Friedman & Levine 1964).

Moreover, it was believed that an "inadequate" zone

gingiva would (1) facilitate subgingival plaque for-

mation because of improper pocket closure resulting

from the movability of the marginal tissue (Friedman

1962) and (2) favor attachment loss and soft tissue

recession because of less tissue resistance to apical

spread of plaque-associated gingival lesions (Stern

1976, Ruben 1979). It was also believed that a narrow

gingiva in combination with a shallow vestibular for-

nix might favor (1) the accumulation of food particles

during mastication and (2) impede proper oral hy-

giene measures (Gottsegen 1954, Rosenberg 1960,

Corn 1962, Carranza & Carraro 1970).

The opinions expressed concerning what could be

regarded as being an "adequate" or "sufficient" di-

mension of the gingiva varied. While some authors

suggested that less than 1 mm of gingiva may be

sufficient (Bowers 1963), others claimed that the api-

cocoronal height of keratinized tissue ought to exceed

mm (Corn 1962). A third category of authors had a

more biologic approach to the question and stated that

an adequate amount of gingiva is any dimension of

gingiva which (1) is compatible with gingival health

(2) prevents retraction of the gingival margin during

movements of the alveolar mucosa (Friedman

1962,

De Trey & Bernimoulin 1980).

One of the first studies in which attempts were

made to evaluate the significance of the gingival zone

for the maintenance of periodontal health was carried

out by Lang & Lbe (1972) on dental students who had

their teeth professionally cleaned once a day for 6

weeks. All buccal and lingual sites were examined for

plaque, gingival conditions and apicocoronal height

of gingiva. The results showed that despite the fact

that the tooth surfaces were free from plaque, all sites

with less than 2 mm of gingiva exhibited persisting

clinical signs of inflammation. Based on this observa-

tion the authors suggested that 2 mm of gingiva is an

adequate width for maintaining gingival health. Find-

ings reported from controlled clinical trials by Mi-

yasato et al. (1977) and Grevers (1977), on the other

hand, failed to support the concept of a required mini

mum dimension of gingiva. In these clinical trials it

was in fact demonstrated that it is possible to maintain

clinically healthy marginal tissue even in areas with

less than 1 mm of keratinized tissue. Furthermore,

when the individuals participating in the study by

Miyasato et al. (1977) ceased oral hygiene for a period

of 25 days, there was no difference in the development

of clinical signs of gingival inflammation between

areas with a minimal (<- 1 mm) and those with an

appreciable (>- 2 mm) width of the gingiva.

The question whether a firmly attached marginal

tissue, i.e. attached gingiva, is critical for the protec-

tion of the periodontium proper was addressed by

Wennstr6m & Lindhe (1983a,b) utilizing the beagle

dog model. In these studies dentogingival units with

578 •

CHAPTER

Fig. 27-2. Two teeth in a dog with varying dimensions of the marginal gingiva. A buccal tooth site with a wide zone

of attached gingiva (a) and a site with an unattached, narrow band of gingiva (b).

Fig. 27-3. The same teeth as in Fig. 27-2a,b after 40 days of plaque accumulation. The clinical signs of inflammation

are more pronounced at the site with the narrow band of gingiva (b) than at the site with the wide zone of attached

gingiva (a).

different clinical characteristics were experimentally

established: (1) units with only a narrow and mobile

zone of keratinized tissue and (2) units with a wide,

firmly attached gingiva (Fig. 27-2). With daily per-

formed mechanical plaque control measures, the gin-

gival units could be maintained free from clinical as

well as histologic signs of inflammation irrespective

the presence or absence of an attached portion of

gingiva. When bacterial plaque was allowed to accu-

mulate (for 40 days), clinical signs of inflammation

(

redness and swelling) developed which were more

pronounced in tooth regions with mobile gingiva (Fig.

27-3b) than in areas with a wide and firmly attached

gingival zone (Fig. 27-3a). However, histologic analy-

sis revealed that the size of the inflammatory cell

infiltrate and its extension in apical direction (an as-

sessment which indirectly may be used as an estimate

of the apical migration of the bacterial plaque) were

similar in the two categories of dentogingival units.

Compared to the gingival units with firmly attached

tissue, it was found that the units lacking attached

gingiva were thinner in the buccolingual dimension

and that the covering oral epithelium had a thinner

keratin layer. Presumably these morphologic differ-

ences in the marginal tissue made the vascular system

more readily visible from the buccal aspect of the

gingiva, and may thus explain why areas with only a

narrow gingival zone clinically appeared more in-

flamed than those with a wide and properly attached

gingiva.

The observation that the clinical signs of gingival

inflammation did not correspond with the size of the

inflammatory cell infiltrate illustrates the difficulties

inherent in the interpretation of data from clinical

examinations made in areas with varying width of

gingiva. This should be kept in mind when interpret-

ing the data by Lang & Loe (1972) showing that clini-

cally visible signs of inflammation, such as redness

and swelling, were more frequent in areas with less

than 2 mm of gingiva than in areas with a wider zone

of gingiva.

The necessity for and effectiveness of gingival aug-

mentation in maintaining periodontal attachment

was examined by Dorfman et al. (1980). Ninety-two

patients with bilateral facial tooth surfaces exhibiting

minimal keratinized tissue (i.e. less than 2 mm) had a

free gingival graft placed on one side, while the con-

tralateral side served as the untreated control. Prior to

and after surgery the patients were subjected to scal-

ing and root planing and instruction in oral hygiene

measures. Not surprisingly, the investigators found a

significant increase (approximately 4 mm) in the

MUCOGINGIVAL THERAPY — PERIODONTAL PLASTIC SURGERY •

579

width of keratinized tissue at the grafted sites. This

increased width of gingiva was maintained for a 2-

year follow-up period. The attachment level was also

maintained throughout this time period. In the control

sites the width of gingiva was less than 2 mm and did

not vary significantly during the 2 years of observa-

tion. However, the attachment level was maintained

unchanged also in the non-grafted areas. Thus, a nar

row zone of gingiva apparently has the same resis-

tance to continuous attachment loss as a wider zone

of gingiva. Subsequent 4 and 6-year follow-up reports

of this patient material (Dorfman et al. 1982, Kennedy

et al. 1985) confirmed the 2-year follow-up findings.

Hangorsky & Bissada (1980), who evaluated the

long-term clinical effect of free soft tissue grafts on the

periodontal condition in 34 patients, also failed to

observe any difference between grafted and non-

grafted sites after 1-8 years with regard to gingival

health and pocket depth. They concluded that while

the free gingival graft is an effective means to widen

the zone of the gingiva, there is no indication that this

increase has a direct influence upon periodontal

health. This conclusion is in agreement with the find-

ings of De Trey & Bernimoulin (1980), who examined

the effect of free gingival grafts in 12 patients with less

than 1 mm of attached gingiva on homologous con-

tralateral pairs of mandibular teeth. The authors

found no significant differences in gingival health

when test and control sites were compared longitudi-

nally.

Further support for the conclusion that a certain

quantity of gingiva is not essential for the mainte-

nance of the integrity of the periodontium is found in

a number of longitudinal clinical studies (Lindhe &

Nyman 1980, Kennedy et al. 1985, Schoo & van der

Uelden 1985, Kisch et al. 1986, Salkin et al. 1987,

Wennstr6m 1987, Freedman et al. 1999) showing that

a minimal zone of gingiva may not compromise peri-

odontal health.

Conclusion

Gingival health can be maintained independent of its

dimensions. Furthermore, there is evidence from both

experimental and clinical studies that, in the presence

of plaque, areas with a narrow zone of gingiva possess

the same "resistance" to continuous attachment loss

as teeth with a wide zone of gingiva. Hence, the

traditional dogma of the need of an "adequate" width

(

in millimeters) of gingiva, or attached portion of

gingiva, for prevention of attachment loss, is not sci-

entifically supported.

Marginal tissue recession

Marginal tissue recession, i.e. displacement of the soft

tissue margin apical to the cemento-enamel junction

with exposure of the root surface, is a common feature

in populations with high standards of oral hygiene

(

Sangnes & Gjermo 1976, Murtomaa et al. 1987, Lbe et

al. 1992, Serino et al. 1994), as well as in populations

with poor oral hygiene (Baelum et al. 1986, 1988,

Yoneyama et al. 1988, Loe et al. 1992). In populations

maintaining high standards of oral hygiene, loss of

attachment and marginal tissue recession are pre-

dominantly found at buccal surfaces (Kdllestal et al.

1990, Loe et al. 1992, Serino et al. 1994), and are fre-

quently associated with the presence of a "wedge-

shaped defect in the crevicular area of one or several

teeth" (Sangnes & Gjermo 1976). In contrast, all tooth

surfaces are usually affected with soft tissue recession

in periodontally untreated populations (L6e et al.

1978, 1992, Miller et al. 1987, Okamoto et al. 1988,

Yoneyama et al. 1988). However, buccal recessions

seem to be more common and more advanced at

single-rooted teeth than at molars (Yoneyama et al.

1988).

Tissue trauma caused by vigorous toothbrushing is

considered to be a dominating causative factor for the

development of recessions, particularly in young in-

dividuals. Traumatizing toothbrushing and tooth

malposition are the factors most frequently found to

be associated with marginal tissue recession (Gorman

1967, Modeer & Odenrick 1980, Vekalahti 1989,

Millestal & Uhlin 1992, Checci et al. 1999). In addition,

Khocht et al. (1993) showed that recessions are related

to the use of hard toothbrushes. Among other factors

that have been associated with marginal tissue reces-

Fig. 27-4a,b. Recessions associated with toothbrushing trauma. The marginal gingiva is clinically healthy and abra

sion defects of various extension can be noted in the exposed roots.

580 • CHAPTER 27

Fig. 27-5. A recession associated with localized plaque

induced inflammatory lesion.

Fig. 27-6. Clinical photographs illustrating the dc elopment of a soft tissue recession as a result of plaque-induced

inflammation in a beagle dog. Note the thin but healthy gingiva (arrow) at the start of the plaque accumulation pe-

riod (a). Pronounced clinical signs of inflammation are seen after 20 days (b), and after 40 days of no toothcleaning,

the gingival margin has receded (c).

sion are (1) alveolar bone dehiscences (Bernimoulin &

Curilivic

1977,

Lost

1984), (2)

inadequate gingival di-

mensions (Maynard

1987), (3)

high muscle attachment

and frenal pull (Trott & Love

1966), (4)

calculus (van

Palenstein Helderman et al.

1998)

and

(5)

iatrogenic

factors related to restorative and periodontal treat-

ment procedures (Gorman

1967,

Lindhe & Nyman

1980,

Valderhaug

1980).

It seems reasonable to suggest that at least three

different types of marginal tissue recessions may exist:

• Recessions associated with mechanical factors, predomi-

nantly toothbrushing trauma

(Fig

27-4).

Recessions

resulting from improper toothbrushing techniques

are often found at sites with clinically healthy

gingiva and where the exposed root has a wedge-

shaped defect, the surface of which is clean, smooth

and polished.

Recessions associated with localized plaque-induced in-

flammatory lesions

(Fig.

27-5).

Such recessions may

be found at teeth that are prominently positioned,

e. the alveolar bone is thin or absent (bone dehis-

cence), and where in addition the gingival tissue is

thin (delicate). An inflammatory lesion that devel-

ops in response to subgingival plaque occupies an

area of the connective tissue adjacent to the den-

togingival epithelium. Measurements made by

Waerhaug

(1952)

suggest that the distance between

the periphery of microbial plaque on the tooth sur-

face and the lateral and apical extension of the

MUCOGINGIVAL THERAPY — PERIODONTAL PLASTIC SURGERY • 581

Fig. 27-7. Recessions associated with generalized forms

of destructive periodontal disease. Recession of the soft

tissue is found not only at the facial aspect of the teeth

but also at proximal sites.

Fig. 27-8. A mandibular tooth segment with multiple

buccal recessions illustrating the association proposed

between recession depth and height of gingiva.

inflammatory cell infiltrate seldom exceeds 1-2 mm.

Thus, if the free gingiva is voluminous the infiltrate

will occupy only a small portion of the connective

tissue. In a thin and delicate gingiva, on the other

hand, the entire connective tissue portion may be

engaged. Proliferation of epithelial cells from the

oral as well as the dento-gingival epithelium into

the thin and degraded connective tissue may bring

about a subsidence of the epithelial surface, which

clinically becomes manifest as recession of the tis-

sue margin (Baker & Seymour 1976) (Fig. 27-6).

Recessions associated with generalized forms of destruc-

tive periodontal disease

(Fig.

27-7). The loss of peri-

odontal support at proximal sites may result in

compensatory remodeling of the support at the buc

cal/lingual aspect of the teeth leading to an apical

shift of the soft tissue margin (Serino et al. 1994).

Cross-sectional studies showing that a correlation ex-

ists between the presence of recession defects and the

height (width) of the gingiva (e.g. Stoner &

Mazdyasna

1980, Tenenbaum 1982) have often been

interpreted

as evidence that a narrow zone of gingiva

is a

contributing factor in the development of soft tissue

recessions (Fig. 27-8). It should be realized,

however,

that data derived from cross-sectional stud

ies can

neither prove nor disprove a cause-effect rela-

tionship. Consequently, the data reported from such

studies may equally well be interpreted to demon-

strate that the formation of a recession defect results

in a reduced height of the gingiva. Fig. 27-1 illustrates

a mandibular incisor tooth region with a localized

gingival recession at the buccal aspect of tooth 41. The

gingiva apical to the recession defect is narrow –

insufficient" – while at neighboring teeth the gingi

val

height may be considered "adequate". It is reason-

able to assume that the gingiva at tooth 41,

before the

recession defect developed,

had a height that was similar

to that found at tooth 31 and tooth 42. In other words,

the narrow zone of gingiva found at tooth 41 may be

the result of loss

of gingival tissue during the period of

recession development,

rather than being the cause of the

formation of the defect. If this interpretation is valid,

the rationale for increasing the height of the gingiva

in an area

apical to the existing defect

as a means of

preventing further recession may appear somewhat

obscure. In fact, data obtained from prospective, lon-

gitudinal studies of patients showing areas with only

a minimal zone of gingiva favor the conclusion that a

certain quantity of gingiva is not essential for the

preclusion of soft tissue recessions. Lindhe & Nyman

(1980) examined the alterations of the position of the

gingival margin following periodontal surgery in 43

patients with advanced periodontal breakdown. Fol-

lowing active treatment, all patients were recalled

once every 3-6 months for maintenance care. The po-

sition of the soft tissue margin in relation to the ce-

mento-enamel junction was assessed on the facial as

pect of all teeth after initial healing and after 10-11

years of maintenance. The presence or absence of

keratinized tissue after surgical treatment was also

determined. The results showed that in areas both

with and without visible keratinized tissue after heal-

ing, a small coronal regrowth (-- 1 mm) of the soft

tissue margin had occurred during the period of main

tenance. In other words, no recession was observed in

this group of patients maintained on a careful prophy

laxis program.

Dorfman et al. (1982) reported a 4-year follow-up

study including 22 patients with bilateral tooth areas

exhibiting gingival recession and lack of firmly at-

tached marginal soft tissue. In conjunction with scal-

ing and root planing a free gingival graft was placed

on one side, while the contralateral control side was

treated by scaling and root planing only. All patients

were recalled for prophylaxis once every 3-6 months

during a 4-year period. The data obtained from the

examinations of the non-grafted control areas re-

vealed that no further recession of the soft tissue mar

gin or loss of probing attachment had occurred despite

the lack of attached marginal tissue. In fact, there was

a slight gain of probing attachment. The authors con-

582 • CHAPTER 27

Fig. 27-9. Clinical photographs of a canine and a first

premolar in the mandible with < 1 mm of attached por

tion of gingiva 6 months after surgical treatment (a).

Note the increase of the width of the gingiva at the fa

cial aspect of the teeth and the more coronally posi-

tioned gingival margin 5 yrs later (b).

Fig. 27-10. A mandibular canine and first premolar

tooth region showing a very narrow zone of gingiva 6

months following surgical therapy (a). No major

change in the position of the soft tissue margin has oc

curred during a 5-year period despite the lack of at-

tached gingiva (b).

Fig. 27-11. Clinical photographs of the right mandibular canine-premolar tooth region in the patient showing sev

eral sites with apical displacement of the soft tissue margin during the 5 years of observation. At the initial exami

nation the two premolars had < 1 mm and the canine > 1 mm of attached portion of gingiva (a). After 5 years (b) re

cession and loss of keratinized tissue can be seen on the buccal aspect of the canine, which initially had a broad

zone of gingiva (black arrow). The second premolar also showed further apical displacement of the soft tissue mar

gin.

cluded that recession sites with lack of attached

gingiva will not develop further attachment loss and

recession if the inflammation is controlled, a conclu-

sion which was also valid in their 6-year report on the

same patient material (Kennedy et al. 1985). The latter

report also included data on 10 patients who had not

participated in the maintenance phase of treatment for

period of 5 years. In these patients plaque and clini

cal

signs of inflammation as well as some further

recession were noted at the 5-year examination as

compared with the data obtained after termination of

active treatment. However, except for the clinical signs

of inflammation, which were more pronounced in

non-

grafted sites, no differences were observed between

control sites with < 1 mm or complete lack of

attached

gingiva and grafted sites.

In a controlled animal study Gould et al. (1992)

evaluated whether placing a gingival graft to augment

the apicocoronal height of keratinized tissue would

prevent development of recession. Despite an almost

6 mm mean increase of the gingival height at grafted

sites, recession continued to develop to a similar de-

gree as in non-grafted contralateral control sites. The

authors concluded that augmenting the width of

gingiva does not prevent or retard naturally occurring

recession.

The lack of relationship between the height of

gingiva and the development of soft tissue recession

further validated by results from longitudinal clini

cal

studies reported by Schoo & van der Velden (1985),

Kisch et al. (1986), Salkin et al. (1987), Wennstr6m

(

1987) and Freedman et al. (1999). The study by

Wennstr6m (1987) reports observations made at 26

buccal sites surgically deprived of all keratinized tis-

sue. Abaseline examination carried out 6 months after

treatment revealed that these sites had regained a zone

of gingiva which was, however, not attached or had

only a minimal (< 1 mm) portion attached to the

underlying hard tissues (Figs. 27-9a and 27-10a). Ad-

jacent teeth with a broad zone of attached gingiva

MUCOGINGIVAL THERAPY — PERIODONTAL PLASTIC SURGERY • 583

were also included in the examinations. In most sites

the position of the soft tissue margin had been main-

tained unchanged over the 5 years of follow-up (Figs.

27-9b and 27-10b). Afurther apical displacement of the

soft tissue margin had occurred at two out of 26 sites

with no/minimal attached gingiva and at three out of

12 adjacent control sites with a wide attached zone of

gingiva. Since four of these five sites were found in

one

patient (Fig. 27-11), and all sites were free from

clinical

signs of inflammation, excessive toothbrush

ing was

considered to be the causative factor, and

following

correction of the brushing technique no

further

progression was observed. Furthermore, the

development of soft tissue recession at the control sites

resulted in a decreased height of the gingiva, an ob-

servation that supports the concept that a narrow zone

of gingiva apical to a localized recession is a conse-

quence rather than a cause of the recession.

Conclusion

Marginal soft tissue recession is a common feature in

populations with good as well as poor standards of oral

hygiene. There is evidence to suggest that the

predominant cause for localized recessions in young

individuals is toothbrushing trauma, while periodon

tal

disease may be the primary cause in older adults.

Evidence from prospective longitudinal studies

shows

that the gingival height is not a critical factor

for the

prevention of marginal tissue recession, but

that the

development of a recession will result in loss

gingival height.

Marginal tissue recession and orthodontic

treatment

Results from clinical and experimental research have

documented that most forms of orthodontic therapy

are innocuous to the periodontium (see Chapter 31).

The clinician may experience, however, that some

patients respond to frontal movements of incisors and

Fig. 27-12. Soft tissue recession at tooth 11 observed

during the course of active orthodontic treatment.

lateral movements of posterior teeth by gingival reces-

sion and loss of attachment (Pearson 1968, Maynard

& Ochsenbein 1975, Coatoam et al. 1981, Foushee et

al. 1985) (Fig. 27-12). Based on the clinical observation

that recession may occur during orthodontic therapy

involving sites which have an "insufficient" zone of

gingiva, it has been suggested that a grafting proce-

dure to increase the gingival dimensions should pre-

cede the initiation of orthodontic therapy in such areas

(Boyd 1978, Hall 1981, Maynard 1987).

As discussed previously, the presence of an alveolar

bone dehiscence is considered to be a prerequisite for

the development of a marginal tissue recession, i.e. a

root dehiscence may establish an environment which,

for one reason or another, is conducive to loss of

gingival tissue. With respect to orthodontic therapy,

this would imply that as long as a tooth is moved

exclusively within the alveolar bone, soft tissue reces-

sion will not develop (Wennstr6m et al. 1987). On the

other hand, "predisposing" alveolar bone dehiscences

may be induced by uncontrolled facial expansion of

teeth through the cortical plate, thereby rendering the

teeth liable to development of soft tissue recession. In

this context it is interesting to note that experimental

Fig. 27-13. Schematic drawing il-

lustrating alterations occurring in

the marginal periodontal tissues

following lingual movement of a

tooth prominently positioned in

the arch and having a bone dehis-

cence (a). An increase in bone

height and gingival height will be

seen as well as a coronal migra-

tion of the soft tissue margin fol-

lowing lingual positioning of the

tooth (b).