several weeks following surgery. aJE 2.0

aJE

B

1.8

The quality of the connective tissue in the supra-

alveolar compartments at teeth and implants was

Test

Control

observed that the main difference between the mes-

mucosa at both control and test sites contained a 2 mm long

barrier epithelium and a zone of connective tissue that was

about 1.3–1.8 mm high. Bone resorption occurred in order to

accommodate the soft tissue attachment at sites with a thin

mucosa. From Berglundh & Lindhe (1996).

enchymal tissue present at a tooth and at an implant

site was the occurrence of a cementum on the root

surface. From this cementum (Fig. 3-22), coarse

dento-gingival and dento-alveolar collagen fiber

bundles projected in lateral, coronal, and apical

Fig. 3-21 Microphotograph

illustrating the peri-implant mucosa

Test

Control

reduced dimension (right). Note the

periodontal tissues (buccal–lingual section). Note on the tooth

side the presence of an acellular root cementum with

inserting collagen fibers. The fibers are orientated more or

less perpendicular to the root surface.

directions (Fig. 3-13). At the implant site, the collagen

fiber bundles were orientated in an entirely different

manner. Thus, the fibers invested in the periosteum

at the bone crest and projected in directions parallel

with the implant surface (Fig. 3-23). Some of the

fibers became aligned as coarse bundles in areas

distant from the implant (Buser et al. 1992).

The connective tissue in the supra-crestal area at

implants was found to contain more collagen fibers,

but fewer fibroblasts and vascular structures, than

the tissue in the corresponding location at teeth.

Moon et al. (1999), in a dog experiment, reported that

the attachment tissue close to the implant (Fig. 3-24)

contained only few blood vessels but a large number

of fibroblasts that were orientated with their long

axes parallel with the implant surface (Fig. 3-25). In

more lateral compartments, there were fewer fibro-

blasts but more collagen fibers and more vascular

structures. From these and other similar findings it

may be concluded that the connective tissue attach-

ment between the titanium surface and the con-

nective tissue is established and maintained by

fibroblasts.

The vascular supply to the gingiva comes from two

different sources (Fig. 3-26). The first source is repre-

sented by the large supraperiosteal blood vessels, that

put forth branches to form (1) the capillaries of the

connective tissue papillae under the oral epithelium

and (2) the vascular plexus lateral to the junctional

epithelium. The second source is the vascular plexus

in a coronal direction and terminate in the supra-

the bone at the tissue/titanium interface. Note that the

orientation of the collagen fibers is more or less parallel (not

perpendicular) to the titanium surface.

interface of the peri-implant mucosa. A large number of

fibroblasts reside in the tissue next to the implant.


Fig. 3-25 Electron micrograph of the implant–connective

tissue interface. Elongated fibroblasts are interposed between

alveolar portion of the free gingiva. Thus, the blood

supply to the zone of supra-alveolar connective tissue

attachment in the periodontium is derived from two

apparently independent sources (see also Chapter

1).

system of the peri-implant mucosa of dogs (Fig. 3-27)

originated solely from the large supra-periosteal blood

vessel on the outside of the alveolar ridge. This vessel

that gave off branches to the supra-alveolar mucosa

and formed (1) the capillaries beneath the oral epi-

thelium and (2) the vascular plexus located immedi-

Cleared section. The vessels have been filled with carbon.

Note the presence of a supraperiosteal vessel on the outside

of the alveolar bone, the presence of a plexus of vessels

within the periodontal ligament, as well as vascular

structures in the very marginal portion of the gingiva.

ately lateral to the barrier epithelium. The connective

tissue part of the transmucosal attachment to tita-

nium implants contained only few vessels, all of

which could be identified as terminal branches of the

The gingiva at teeth and the mucosa at dental

implants have some characteristics in common, but

differ in the composition of the connective tissue, the

alignment of the collagen fiber bundles, and the dis-

tribution of vascular structures in the compartment

apical of the barrier epithelium.
Probing gingiva and

peri-implant mucosa

It was assumed for many years that the tip of the

probe in a pocket depth measurement identified the

most apical cells of the junctional (pocket) epithelium

or the marginal level of the connective tissue attach-

ment. This assumption was based on findings by, for

example, Waerhaug (1952), who reported that the

“epithelial attachment” (e.g. Gottlieb 1921; Orban

& Köhler 1924) offered no resistance to probing.

Waerhaug (1952) inserted, “with the greatest caution”,

thin blades of steel or acrylic in the gingival pocket

of various teeth of100 young subjects without signs

of periodontal pathology. In several sites the blades

were placed in approximal pockets, “in which posi-

tion radiograms were taken of them”. It was

concluded that the insertion of the blades could be

performed without a resulting bleeding and that the

device consistently reached to the cemento-enamel

junction (Fig. 3.28). Thus, the epithelium or the

epithelial attachment offered no resistance to the

insertion of the device.

Fig. 3-27 (a) A buccal–lingual cleared

section of a beagle dog mucosa facing

an implant (the implant was positioned

to the right). Note the presence of a

supraperiosteal vessel on the outside

of the alveolar bone, but also that there

is no vasculature that corresponds to

the periodontal ligament plexus. (b)

Higher magnification (of a) of the

peri-implant soft tissue and the bone

implant interface. Note the presence

of a vascular plexus lateral to the

junctional epithelium, but the absence

of vessels in the more apical portions

of the soft tissue facing the implant

2 mm

In subsequent studies it was observed, however,

that the tip of a periodontal probe in a pocket depth

measurement only identified the base of the dento-

gingival epithelium by chance. In the absence of an

inflammatory lesion the probe frequently failed to

reach the apical part of the junctional epithelium (e.g.

Armitage et al. 1977; Magnusson & Listgarten 1980).

If an inflammatory lesion, rich in leukocytes and poor

in collagen, was present in the gingival connective

tissue, however, the probe penetrated beyond the

epithelium to reach the apical–lateral border of

the infiltrate.

The outcome of probing depth measurements at

Ericsson and Lindhe (1993) used the model by Berg-

lundh et al. (1991) referred to above and, hence, had

both teeth and implants available for examination.

The gingiva at mandibular premolars and the mucosa

at correspondingly positioned implants (Brånemark

System®) were, after extended periods of plaque

control, considered clinically healthy. A probe with

a tip diameter of 0.5 mm was inserted into the buccal

“pocket” using a standardized force of 0.5 N. The

probe was anchored to the tooth or to the implant

and biopsies from the various sites were performed.

The histologic examination of the biopsy material

revealed that probing the dento-gingival interface

had resulted in a slight compression of the gingival

tissue. The tip of the probe was located coronal to

the apical cells of the junctional epithelium. At the

implant sites, probing caused both compression and

a lateral dislocation of the peri-implant mucosa, and

the average “histologic” probing depth was mark-

edly deeper than at the tooth site: 2.0 mm versus

0.7 mm. The tip of the probe was consistently

positioned deep in the connective tissue/abutment

interface and apical of the barrier epithelium. The

distance between the probe tip and the bone crest

at the tooth sites was about 1.2 mm. The correspond-

ing distance at the implant site was 0.2 mm. The

findings presented by Ericsson and Lindhe (1993)

regarding the difference in probe penetration in

healthy gingiva and peri-implant mucosa are not in

agreement with data reported in subsequent animal

experiments.

Lang et al. (1994) used beagle dogs and prepared

the implant (Straumann® Dental Implant System)

sites in such a way that at probing some regions were

healthy, a few sites exhibited signs of mucositis, and

some sites exhibited peri-implantitis. Probes with dif-

ferent geometry were inserted into the pockets using

a standardized probing procedure and a force of only

0.2 N. The probes were anchored and block biopsy

specimens were harvested. The probe locations were

studied in histologic ground sections. The authors