Jan Lindhe. Clinical Periodontology

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DENTAL PLAQUE AND CALCULUS • 93

Fig. 3-27. Thin section of supragingival plaque on a root surface (to the left). The Gram-positive bacteria are ori-

ented in a palisading arrangement. Magnification x 6400. Bar: 1µm. From Listgarten (1976).

trix between them. This outer part of the microbial

accumulation in the periodontal pocket adheres

loosely to the soft-tissue pocket wall (Listgarten 1976)

In cases of juvenile periodontitis (Listgarten 1976,

Westergaard et al. 1978) the bacterial deposits in deep

pockets are much thinner than those found in adult

forms of periodontal disease. Areas of the tooth sur-

face in the periodontal pocket may sometimes even be

devoid of adherent microbial deposits. The cuticular

material has an uneven thickness (Figs. 3-30, 3-31).

The adherent layer of microorganisms varies consid-

erably in thickness and shows considerable variation

in arrangement. It may exhibit a palisaded organiza-

tion of the bacteria (Fig. 3-32). The microorganisms in

this layer are mainly cocci, rods or filamentous bacte-

ria, primarily of the Gram-negative type (Fig. 3-33). A

surface layer with some Gram-positive cocci, fre-

quently associated with filamentous organisms in the

typical corncob configuration, may also be found.

Subgingivally located bacteria appear to have the

capacity to invade dentinal tubules, the openings of

which have become exposed as a consequence of in-

flammatory driven resorptions of the cementum (

Adriaens et al. 1988). Such a habitat might serve as

the source for bacterial recolonization of the subgingi-

val space following treatment of periodontal disease.

The mechanisms involved in such reversed invasion

of the subgingival space are unknown.

The sequential events taking place during the de-

velopment of subgingival plaque have not been stud-

ied in man. However, in dogs, subgingival plaque

may develop in the gingival sulcus within a few days,

if oral hygiene is discontinued (Matsson & Attstrom

1979, Ten Napel et al. 1983). From these studies it has

been established that early dental plaque in the dog

has many structural similarities with that occurring in

man. This applies to the supragingival plaque (Fig. 3-

21a) as well as to the subgingival accumulation (Fig.

3-21b). The deposits may either appear as an apical

continuation of the supragingival plaque, or as dis-

94 • CHAPTER 3

Fig. 3-28. Thin section of subgingival plaque from a deep periodontal pocket. Small microorganisms predominate,

many of which are spirochetes. Magnification x 13 000. Bar: 1 pm. From Listgarten (1976).

Fig. 3-29. Thin section of subgingival plaque from a deep periodontal pocket with many spirochetes (S), which are

recognized by their axial filaments. In the lower part of the figure is a curved organism with flagella at its concave

surface. Magnification x 25 000. Bar: 0.5 gm. From Listgarten (1976).

DENTAL PLAQUE AND CALCULUS • 95

Fig. 3-30. Thin section of deposit in deep pocket of pa-

tient with juvenile periodontitis. The cementum (C) is

covered with cuticular material and cellular remnants.

Magnification x 5500. Bar: 1 pm. From Westergaard et

al. (1978).

Fig. 3-31. Thin section of deposit in deep pocket of pa-

tient with juvenile periodontitis. A cuticle of uneven

thickness is seen to the right on the cementum. A small

colony of degenerating bacteria adheres to the cuticle

in the upper part of the illustration, and below a single

rod-shaped microorganism is partly embedded in the

cuticle. Magnification x 5500. Bar: 1 pm. From Wester-

gaard et al. (1978).

Fig. 3-32. Thin section of plaque in deep pocket of pa-

tient with juvenile periodontitis. Densely packed Gram-

positive rods grow perpendicular to the cementum to

the right in the illustration. Magnification x 23 000. Bar:

0.5 µm. From Westergaard et al. (1978).

crete aggregates at some distance from the supragingi-

val deposit. Old established subgingival plaque shows

considerable variation in bacterial composition between

dogs: in some, a subgingival microbiota dominated by

spirochetes is seen; in others, colonies of Gram-

negative cocci and rods are found in the

gingival crevice, whereas spirochetes are virtually ab-

sent (Soames & Davies 1975, Theilade & Attstrom

1985). A characteristic feature of subgingival plaque is

the presence of leukocytes interposed between the

surfaces of the bacterial deposit and the gingival sul-

cular epithelium (Fig. 3-34). Some bacteria may be

96 • CHAPTER 3

Fig. 3-33. Thin section of plaque in deep pocket of patient with juvenile periodontitis. The bacterial flora is charac-

terized by cocci, rods or filamentous organisms, primarily of the Gram-negative type. Magnification x 9200. Bar: 1

µm. From Westergaard et al. (1978).

DENTAL PLAQUE AND CALCULUS • 97

Fig. 3-35. Thin section of part of a leukocyte situated between subgingival plaque and the junctional epithelium of

the dog. The large membrane bound compartment of the leukocyte cytoplasm contains a phagocytized Gram-nega-

tive microorganism. Another bacterium is in close apposition to the cytoplasmic membrane of the leukocyte. Mag-

nification x 21 500. Bar: 0.5 km. From Theilade & Attstrom (1985).

Fig. 3-36. Peri-implant infection. (

a) Human explant of an ITI

den-

tal implant affected by a peri-im-

plantitis with an infrabony lesion.

Adhering plaque closely resem-

bles the structure of subgingival

microbiota encountered in ad-

vanced periodontitis. (b) Higher

magnification of plaque adhering

to the implant surface.

found between the epithelial cells. Evidence of phago-

cytosis (by polymorphonuclear leukocytes) is fre-

quently encountered (Fig. 3-35).

Although subgingival plaque formation in the dog

may not develop identically to that in man, the dog may

still serve as a convenient model for investigating the

basic phenomena governing the formation of sub-

gingival plaque (Schroeder & Attstrom 1979).

In summary, there are four distinct subgingival

ecologic niches which are probably different in their

composition:

1. the tooth (or implant) surface

2. the gingival exudate fluid medium

3. the surface of epithelial cells and

4. the superficial portion of the pocket epithelium.

Fig. 3-34. Thin section of old subgingival plaque in a dog with long-standing gingivitis. The most apical colony

consists primarily of spirochetes attached to a dense cuticle and surrounded by migrated leukocytes. Single micro-

organisms are seen between them (arrows). Magnification x 2800. Bar: 1 µm. From Theilade & Attstrom (1985).

98 • CHAPTER 3

Fig. 3-37. Abundance of supragingival calculus deposits. (a) Gross deposits as a result of long-term neglect of oral

hygiene. Two mandibular incisors have been exfoliated. (b) Supragingival plaque usually covering the lingual as-

pect of mandibular incisors. Note the intense inflammatory reaction adjacent to the deposits. (c) Same patient and

region as in Fig. 3-37b following removal of the calculus. The gingival tissues demonstrate healing.

The composition of the bacteria in these niches has still

not been completely investigated. The influence of the

different bacterial compartments on the pathogenesis

of the disease process is generally unknown.

retrieved because of a peri-implant infection may pro-

vide some evidence for the similarity between the

structural image of the submucosal peri-implant mi-

crobiota (Fig. 3-36).

Peri-implant plaque

Biofilms form not only on natural teeth, but also on

artificial surfaces exposed to the oral environment. As

a consequence, the formation of bacterial plaque on

oral implants deserves some attention. Although a

number of studies have characterized the plaque de-

posits of the human peri-implant sulcus or pocket

using either dark field microscopy (Mombelli et al.

1988, Quirynen & Listgarten 1990) or microbiologic

culturing techniques (Rams et al. 1984, Mombelli et al.

1987, 1988,

Apse et al. 1989, Leonhardt et al. 1992), no

studies have attempted to document the structure of

the supramucosal or the peri-implant (submucosal)

microbiota. However, the similarities between peri-

implant and subgingival microbial deposits have

clearly been demonstrated in cross-sectional (Mom-

belli et al. 1987, 1995) and longitudinal studies (Mom-

belli et al. 1988, Pontoriero et al. 1994), and it may be

anticipated that the structure of peri-implant plaque

deposits may resemble that encountered in the sub-

gingival environment. Micrographs from an implant

DENTAL CALCULUS

Although calculus formation has been reported to

occur in germ-free animals as a result of calcification

of salivary proteins, dental calculus or tartar usually

represents mineralized bacterial plaque.

Clinical appearance, distribution and clinical

diagnosis

Supragingivally, calculus can be recognized as a

creamy-whitish to dark yellow or even brownish mass

of moderate hardness (Fig. 3-37). The degree of calcu-

lus formation is not only dependent on the amount of

bacterial plaque present but also on the secretion of

the salivary glands. Hence, supragingival calculus is

predominantly found adjacent to the excretion ducts

of the major salivary glands, such as the lingual aspect

of the mandibular anterior teeth and the buccal aspect

of the maxillary first molars, where the parotid gland

DENTAL PLAQUE AND CALCULUS • 99

Fig. 3-39. Subgingival calculus presents as a black-brownish hard mass if the gingival margin is retracted or re-

flected during a surgical procedure (a). Healing of the site following removal of all hard deposits (b).

Fig. 3-40. Plaque- and calculus-free zone coronal to the

epithelial attachment. SP: Subgingival plaque bacteria.

PFZ: Plaque-free zone. EA: Remnants of junctional epi-

thelium.

ducts open into the oral vestibule. The duct openings

of the submandibular glands are located in the former

region. It should be noted that calculus continually

harbors a viable bacterial plaque (Zander et al. 1960,

Theilade 1964, Schroeder 1969).

Subgingivally, calculus may be found by tactile

exploration only, since its formation occurs apical to

the gingival margin and, hence, is usually not visible

to the naked eye. Occasionally, subgingival calculus

may be visible in dental radiographs provided that the

deposits present an adequate mass (Fig. 3-38). Small

deposits or residual deposits following root instru-

mentation may barely be visualized radiographically.

If the gingival margin is pushed open by a blast of air

or retracted by a dental instrument, a brownish to

black calcified hard mass with a rough surface may

become visible (Fig. 3-39). Again, this mineralized

mass reflects predominantly bacterial accumulations

mixed with products from gingival crevicular fluid and

blood. Consequently, subgingival calculus is found in

most periodontal pockets, usually extending from the

cemento-enamel junction and reaching close

Fig. 3-38. Subgingival calculus may be visible (arrows)

on radiographs if abundant deposits are present.

100 • CHAPTER 3

Fig. 3-41. Seven-day-old calcified plaque. Observe the

isolated calcification centers indicated by the black ar

eas (van Kossa stain).

to the bottom of the pocket. However, a band of ap-

proximately 0.5 mm is usually found coronal to the

apical extension of the periodontal pocket (Fig. 3-40).

This zone appears to be free from mineralized deposits

owing to the fact that gingival crevicular fluid is

exudating from the periodontal soft tissues and acting

as a gradient against the microbial accumulation. Like

supragingival calculus, subgingival calculus also pro-

vides an ideal environment for bacterial adhesion (

Zander et al. 1960, Schroeder 1969).

Plaque mineralization varies greatly between and

within individuals and — as indicated above — also

within the different regions of the oral cavity. Not only

the formation rate for bacterial plaque (amount of

bacterial plaque per time and tooth surface), but also

the formation rate for dental calculus (time period

during which newly deposited supragingival plaque

with an ash weight of 5-10% becomes calcified and

yields an ash weight of approximately 80%) is subject

to great variability In some subjects, the time required

for the formation of supragingival calculus is 2 weeks,

at which time the deposit may already contain ap-

proximately 80% of the inorganic material found in

mature calculus (Fig. 3-41) (Miihlemann & Schneider

1959, Mandel 1963, Muhlemann & Schroeder 1964). In

fact, evidence of mineralization may already be pre-

sent after a few days (Theilade 1964). Nevertheless, the

formation of dental calculus with the mature crystal-

line composition of old calculus may require months

to years (Schroeder & Baumbauer 1966). Supragingi-

val plaque becomes mineralized saliva and subgingi-

val plaque in the presence of the inflammatory

exudate in the pocket. It is, therefore, evident that

subgingival calculus represents a secondary product

of infection and not a primary cause of periodontitis.

Attachment to tooth surfaces and implants

Dental calculus generally adheres tenaciously to tooth

surfaces. Hence, the removal of subgingival calculus

may be expected to be rather difficult. The reason for

this firm attachment to the tooth surface is the fact that

the pellicle beneath the bacterial plaque also calcifies.

This, in turn, results in an intimate contact with

enamel (Fig. 3-42), cementum (Fig. 3-43) or dentin

crystals (Fig. 3-44) (Kopczyk & Conroy 1968, Selvig

1970). In addition, the surface irregularities are also

penetrated by calculus crystals and, hence, calculus is

virtually locked to the tooth. This is particularly the

case on exposed root cementum, where small pits and

irregularities occur at the sites of the previous inser-

tion of Sharpey's fibers (Bercy & Frank 1980). Uneven

root surfaces may be the result of carious lesions and

small areas of cementum may have been lost due to

resorption, when the periodontal ligament was still

invested into the root surface (Moskow 1969). Under

such conditions it may become extremely difficult to

remove all calculus deposits without sacrificing some

hard tissues of the root.

Although some irregularities may also be encoun-

tered on oral implant surfaces, the attachment to com-

mercially pure titanium generally is less intimate than

to root surface structures. This in turn, would mean

that calculus may be chipped off from oral implants (

Fig. 3-45) without detriment to the implant surface (

Matarasso et al. 1996).

Fig. 3-42. Thin section of enamel surface (E) with overlying calculus. The enamel and calculus crystals are in inti

mate contact, and the latter extends into the minute irregularities of the enamel. Magnification x 37 500.

Bar:

0.1 µm. From Selvig (1970).

DENTAL PLAQUE AND CALCULUS • 101

Fig. 3-43. Thin section of cementum surface (C) with

overlying calculus. The calculus is closely adapted to

the irregular cementum and is more electron-dense and

therefore harder than the adjacent cementum. To the

right in the illustration, part of an uncalcified micro-

organism. Magnification x 32 000. Bar: 0.1 µ.m. From

Selvig (1970).

Mineralization, composition and structure

The mineralization starts in centers which arise in-

tracellularly in bacterial colonies (Fig. 3-46) or ex-

tracellularly from matrix with crystallization nuclei (

Fig. 3-47). Recent and old calculus consists of four

different crystals of calcium phosphate (for review see

Schroeder 1969):

1. CaH (PO4) x 2 H

O = Brushite (B)

2. Ca4H (PO4)3 X 2 H2O = Octa calcium phosphate

(

OCP)

3. Ca5 (PO4)3 X OH = Hydroxyapatite (HA)

4. a-Ca3 (PO4)2 = Whitlockite (W)

Supragingival calculus is clearly built up in layers and

yields a great heterogeneity from one layer to another

with regard to mineral content. On average, the min-

eral content is 37%, but ranges from 16% to 51%, with

Fig. 3-44. Thin section of dentin (D) surface with overly-

ing calculus. The interface between the calculus and

dentin cannot be precisely determined because the cal-

culus crystals fill the irregularities of the dentin sur-

face, which is devoid of cementum as a result of a pre-

vious scaling of the root surface. The circular profiles in

the calculus completely surround calcified bacteria.

Magnification x 19 000. Bar: 1 gm. From Selvig (1970).

Fig. 3-45. Calculus deposit on an oral implant in a pa-

tient without regular maintenance care.

some layers yielding a maximal density of minerals of

up to 80% exceptionally (Kani et al. 1983, Friskopp &

Isacsson 1984). The predominant mineral in exterior

layers is

OCP,

while HA is dominant in inner layers of

old calculus. W is only found in small proportions (

Sundberg & Friskopp 1985). B is identified in recent

calculus, not older than 2 weeks, and appears to form

the basis for supragingival calculus formation. The

appearance of the crystals is characteristic for

OCP

forming platelet-like crystals, for HA as forming

sandgrain or rod-like crystals, while W presents with

hexagonal (cuboidal, rhomboidal) crystals (Kodaka et

al. 1988).

Subgingival calculus appears somewhat more ho-

mogeneous since it is built up in layers with an equally

high density of minerals. On average the density is

58% and ranges from 32% to 78%. Maximal values of

60-80% have been found (Kani et al. 1983, Friskopp &

Isacsson 1984). The predominant mineral is always W,

102 • CHAPTER 3

Fig. 3-46. Thin section of old plaque. A degenerating or

ganism is surrounded by intermicrobial matrix in

which initial mineralization has started by the deposi-

tion of small needle-shaped electron-dense apatite crys

tals. Magnification x 26 500. Bar: 0.5 gm. From

Zander et al. (1960).

although HA has been found (Sundberg & Friskopp

1985). W contains small proportions (3%) of magnesia

(McDougall 1985).

In the presence of a relatively low plaque-pH and a

concomitant high Ca/P-ratio in saliva, B is formed

which may later on develop into

and W. When

supragingival plaque mineralizes, OCP forms and is

gradually changed into

HA.

In the presence of alkaline

and anaerobic conditions and concomitant presence

of magnesia (or Zn and CO

), large amounts of W are

formed, which are a stable form of mineralization.

Clinical implications

Although strong associations between calculus de-

posits and periodontitis have been demonstrated in

experimental (Wrhaug 1952, 1955) and epidemiol-

ogic studies (Lovdal et al. 1958), it has to be realized

that calculus is always covered by an unmineralized

layer of viable bacterial plaque. It has been debated

whether or not calculus may exert a detrimental effect

on the soft tissues owing to its rough surface. How-

ever, it has clearly been established that surface rough

ness alone does not initiate gingivitis (Wa?rhaug

1956). On the contrary, in monkeys a normal epithelial

attachment with the junctional epithelial cells forming

hemidesmosomes and a basement membrane on cal-

culus could be established (Listgarten & Ellegaard

1973) if the calculus surface had been disinfected us-

ing chlorhexidine (Fig. 3-48). Furthermore, it has been

demonstrated that autoclaved calculus may be encap-

sulated in connective tissue without inducing marked

Fig. 3-47. Thin section of old mineralizing plaque. The

intermicrobial matrix is totally calcified, and many mi

croorganisms show intracellular crystal deposition.

Magnification x 9500. Bar: 1 gm. From Theilade (1964).

inflammation or abscess formation (Allen & Kerr

1965).

These studies clearly exclude the possibility of

dental calculus being a primary cause of periodontal

diseases. The effect of calculus seems to be secondary

by providing an ideal surface configuration condu-

cive to further plaque accumulation and subsequent

mineralization.

Nevertheless, calculus deposits may have devel-

oped in areas with difficult access for oral hygiene or

may – by the size of the deposits – jeopardize proper

oral hygiene practices. Calculus may also amplify the

effects of bacterial plaque by keeping the bacterial

deposits in close contact with the tissue surface,

thereby influencing both bacterial ecology and tissue

response (Friskopp & Hammarstrom 1980).

Well-controlled animal (Nyman et al. 1986) and

clinical (Nyman et al. 1988, Mombelli et al. 1995) stud-

ies have shown that the removal of subgingival plaque

on top of subgingival calculus will result in healing of

periodontal lesions and the maintenance of healthy

gingival and periodontal tissues, provided that the

supragingival deposits are meticulously removed on a

regular basis. One of these studies (Mombelli et al.

1995) clearly demonstrated that the diligent and com-

plete removal of subgingival plaque on top of miner-

alized deposits after chipping off gross amounts of

calculus showed almost identical results in the com-

position of the microbiota and the clinical parameters

to those obtained with routine removal of subgingival

calculus by root surface instrumentation. Again, it has

to be realized that meticulous supragingival plaque

control guarantees the depletion of the supragingival