Introduction
Epidemiologic data have consistently shown
a close cotrelation between oral hygiene
states and the severity of periodontal dis-
ease (Schei et al, 1959, Waerhaug 1967), In
1965, Loe, Theilade & Jeasen showed that
individuals with clinically healthy gingiva
developed plaqtie and gingivitis within a few
days after the withdrawal of oral hygiene
measures, and that reinstitution of oral
hygiene resulted in the restoration of gin-
gival health. This study presented evidence
for a cause and effect relationship between
the accumulatioti of plaque on the teeth
and gingival inflamoiatioa. It has also been
demonstrated in dogs that gingival inflann-
mation induced by plaque formation on the
teeth results in deterioration of the peri-
odotital tissues, with the subsequent devel-
opment of periodontitis (Saxe et al, 1967,
Lindhe, Hamp & Loe 1973),
To date, the bulk of experimental evi-
dence suggests that plaque is the primary
catise of periodontal disease. However, both
the extent and the severity of the disease
Bone resorption
As long as inflammation is limited to the
gingival margin the process is considered to
be reversible (Loe et al, 1965), Untreated,
however,, the inflammation may progress
into deeper parts of the periodontium and
cause disintegration of the collagen fibers
lying immediately apical to the epithelial
depend on host resistance and a variety of
local and systemic factors. For example,
faulty dental restorations and poor contact
relationships between the teeth provide for
the retention of dental plaque and thereby
act as secondary etiologic factors (Bjoro,
Bjorn and Grkovic 1969), It has also been
suggested that occlusal forces play an essen-
tial role in the development of periodontal
disease (Glickman and Smulow 1965, 1967),
However, recent experiments in dogs have
shown this to be the case only in the pre-
sence of pre-existing inflammation, of the
gingiva and pathologically deepened pockets
(for review see Svanberg 1974),
Destruction of the periodontium is ustaal-
ly a slow, progressive process, its time course
measured in years. However, in some indi-
viduals a rapid destruction of the periodon-
tal attachment apparatus may take place
(Manson & Lehner 1974), Whether this
rapid destruction is due to differences in
host resistance or variations in the microbial
flora is not known.
attachment. This allows the crevicular epi-
thelitjm to proliferate apically along tbe root
surface resulting in a pathologic, deepened
gingival crevice. This epithelial migration is
followed by resorption of the alveolar bone
supporting the tooth. Regardless of the ex-
tent of bone destruction, 1-2 mm of supra-
 ELLEGAARD
alveolar connective tissue is maintained be-
tween the base of the pocket epithelitim and
the alveolar bone (Waerhaug 1952),
The underlying mechanism responsible
for the resorption of alveolar bone in peri-
odontal disease is unknown.. Certain sys-
temic factors involved in bone metabolism
are present regardless of the gingival status.
For example, parathyroid hormone is known
to stimulate bone resorption and inhibit the
formation of osteoblasts. However, the ab-
solute levels or variation of these systemic
factors in patients with periodontal disease
have not been studied. Working with dogs
Henrikson (1968) observed that the accu-
mulation of calculus and plaque caused
chronic gingivitis, which resulted in loss of
alveolar bone in dogs with indticed hyper-
parathyroidism. On the basis of these find-
ings he stated that the development of peri-
odontitis requires osteopenia caused by nu-
tritional hyperparathyroidism. Svanberg et
al. (1973) demonstrated that by feeding
beagle dogs a diet deficient in calcium but
with excess phosphorus one can induce nu-
tritional hyperparathyroidism and osteopo-
rosis in the jaw bones. However, contrary
to the findings reported by Henrikson, these
authors observed that in areas where plaque
was allowed to accumulate, pathologic
pockets developed and alveolar bone loss
occurred at the same rate in both experi-
mental and control animals.
In periodontitis it has been shown that
plaque bacteria only occasionally invade the
periodontal tissue (Freedman, Listgarten &
Taichman 1968). However, bacterial pro-
ducts such as enzymes, endotoxins and bac-
terial antigens may penetrate into the gin-
giva. Hausmann (1974) has speculated on
the possible mechanisms by which these pro-
ducts can initiate bone resorption. Cells in
the periodontium could be stimulated to
differentiate into osteoclasts; hydrolytic en-
zymes elaborated by plaque bacteria could
destroy alveolar bone through noo cellular
mechanisms by dissolving bone minerals
and hydro!yzing the organic matrix; gin-
gival connective tissue cells, in response to
plaque bacterial products, could release sub-
stances capable of resorbing bone directly;
tnediators could be released which might
catise the formation of osteoclasts (Haus-
mann 1974),
In vitro studies have considered the re-
lationship between plaque bacterial pro-
ducts and the initiation and propagation of
bone resorption,
Utilizitig as a model fetal rat bone in tis-
sue culture, Hausmann, Weinfeld & Miller
(1972) found that endotoxin and Iipotei-
choic acid in dental plaque stimulates bone
resorption and that the effect of endotoxin
was enhanced by the presence of heparin.
Also it has been demonstrated in vitro that
parathyroid hormone in the presence of
high concentrations of heparin causes bone
resorption (Goldhaber 1965), On that basis
it has been suggested that a high concen-
tration of heparin released from mast cells
during the inflammatory process in the peri-
odontal tissues may activate bone resorp-
tion factors normally present in an inactive
form within the tissue. In human gingival
tissue Goldhaber (1971) and Jacobsen &
Goldhaber (1973) have demonstrated an un-
defined factor with the potential to resorb
bone in tissue culttire. This factor was found
in healthy as well as in chronically inflam-
med gingiva. In a later investigation Gold-
haber et al, (1973) demonstrated that in
healthy gingiva the action of the bone re-
sorbing factor was inhibited by indometh-
acin, an aspirin like drug which acts by
blocking prostaglandin synthesis. The pro-
staglandins have been shown to stimulate
resorption of fetal bone in tissue culture, an
effect similar to that of parathyroid hor-
mone (Klein & Raisz 1970).
Several other factors, such as immune
complexes and sensitized leukocyte factors,
have been implicated as possible mediators
 BONE GRAFTS IN PERIOOONTAL ATTACHMENT PROCEDURES
of increased bone resorption (Hausmann et
al. 1973, Horton et al, 1972),
Jn vivo studies of germfree rats mono-
infected with oral microorganisms suggest
that cessation of bone formation as well as
bone resorption, is involved in bone loss
seen in periodontal disease (Irving, Socran-
sky & Heeley 1974, Irving et al, 1975),
Kelstrup & Gibbons (1970) observed that
alveolar bone resorption, associated with
hypervascularization of the bone occurred
in rats monoinfected with certain strepto-
coccal strains, while the histologie picture
was different in those infected with other
streptococci. These observations led the au-
thors to suggest that some bacteria initiate
gingival infiammation, while others are re-
sponsible for bone resorption.
On the basis of our present knowledge it
is impossible to assess the relative impor-
tance in periodontal disease of the various
factors which lead to loss of supporting
alveolar bone (for review see Irving 1970,
Hausmann 1974),
Classification of bone resorption
The varying extent of bone resorption in
periodontal disease can be categorized both
clinically and radiographically, Resorption
of alveolar bone which occurs to the same
degree all around the circumference of a
tooth is called horizontal bone resorption.
Vertical bone resorption is defined as re-
sorption which occurs to a different extent
at different points around the circumference
of a tooth. This type of resorption results in
the formation of bony "niches" on one or
more sides of the tooth. Bony defects of
this type have been referred to in the past
as "infrabony defects". It has been sug-
gested, however, that either the term "intra-
bony defect" or "intraosseous pocket"
should be used, since these latter terms indi-
cate that this lesion is within the bone
(World Workshop in Periodontics 1966),
Goldman & Cohen (1958) have suggested
a classification of the lesions caused by
vertical bone resorption according to the
number of osseous walls surrounding the
defect,
1, Three-wall bony pockets, where the de-
fect has three bony walls and where the
tooth constitutes the fourth waH,
2, Two-wall bony pocket, where the defect
is delineated by two bony walls and a root
surface. On the fourth, side, the defect ,is
enclosed by periodontal connective tissue.
If the bony wall between two adjacent
teeth is missing, but the facial atid oral
walls are present, the two-waU pocket
thus formed is denoted an interdental
crater.
3, One-wall bony pockets, where only one
bony wall is involved in the delineation
of the defect.
In most cases, intrabony defects are a com-
bination of these three types.
Histology
The histology of intrabony defects has been
described by Carranza and Glickman (1957)
on the basis of microscopic examination of
twelve intrabony pockets obtained from six
autopsied human jaws. They found that
pathologic changes in intrabony defects are
comparable to those in supraboxiy pockets.
The pocket epithelium extended into the
bony defects with its deepest point placed
about one to two mm from the alveolar bone
in the bottom of the defects. The connective
tissue below the gingival crevice was usually
infiltrated by inflammatory cells. Depend-
ing on the degree of inflammation the fibers
presented varying degrees of degeneration.
Compared to the normal periodontium the
length of the gingival fibers had increased
and the transseptal fibers followed an ob-
lique rather than a horizontal course. In
 ELLEGAARD
interproximal intrabony pockets the col-
lagen fibers extended from the cementtim
beneath the base of epithelial attachment
along the bony surface to the edge of the
bony defect, where they divided into two
groups. One group passed the crest to the
cementum of the adjacent tooth (transsep-
tal fibers) and another group extended into
the gingival papilla (gingival fibers). In de-
fects which were located at the buccal or
lingual aspect of the tooth the fibers ex-
tended over the edge of the defect crest to
the periosteum. The surface of the bone
adjacent to the pocket Vi^all presented a
variety of changes which included osteo-
clastic resorption as well as repair of pre-
viously resorbed areas.
Frequency
The incidence and distribution of alveolar
intrabony defects have been investigated on
anatomical specimens, radiographs and by
clinical registration. On examining the jaws
of 148 skulls from India Saari, Htirt and
Biggs (1968) found that alveolar intrabony
defects occurred most around the third
molar, followed by the first and second
molars. There was no differences in the in-
cidence of defects on the mesial and distal
surfaces.
On examination of 337 skulls of Mexican
and European origin, in the age group from
2 to 60 years, Larato (1970) found an in-
crease in the incidence of alveolar intrabony
defects from approximately 3 per cent in
the 2 to 16 year group to approximately 9
per cent in the 17 to 29 year age group.
The incidence of intrabony defects increas-
ed to 40 per cent in the age group between
30 and 60 years. In agreement with the
findings of Saari et al, (1968), the majority
of the defects were found around the first,
second, and third molars.
In an epidemiological investigation in
Boston, GHmore (1970) found intrabony
defects in about 10 per cent of the 795 in-
dividuals examined. He reported that the
number of vertical defects increased with
age, but was independent of race or sex.
The number of intrabony defects was greater
in the mandible than in the maxilla.
Etiology
It is generally accepted that bacterial plaque
is the primary etiologic agent in the devel-
opment of intrabony defects although it has
been suggested that various local factors
play an important role. The evidence which
supports the association of improper dental
restorations and food impaction with for-
mation of vertical defects is meager, but
suggests that such a relationship exists (Pri-
chard 1960).
Gilmore (1970) failed to demonstrate a
relationship between intrabony defects and
overhanging margins as well as poor con-
tact relations of teeth, Bruxism, with and
without the presence of occlusa! interfer-
ences, also did not appear to be related to
vertical defects (Gilmore 1970). This ob-
servation is in agreement with the results
obtained in an experiment in monkeys by
Comar, Kollar & Gargiulo (1969). For the
purpose of assessing a possible relationship
between occlusal interference and vertical
bone loss, they provided teeth with high
crowns. They concluded that no association
could be found between the premature oc-
clusal contacts and the occurrence of intra-
bony defects.
Several authors considered occlusal trau-
ma to be an aggravating factor in the de-
velopment of intrabony defects (Glickman
1963, Glickman & Smulow 1962, 1965,
1967, Svanberg 1974). This opinion is based
upon experiments in monkeys in which an-
gtilar or crater like bony defects developed
adjacent to teeth subjected to excessive oc-
cltisal pressure. Similar!y, data from human
autopsy material have suggested that oc-
 BONE GRAFTS IN PERIODONTAL ATTACHMENT PROCEDURES
clusa] trauma enhances the spread of gin-
gival inflammation to the deeper parts of
the periodontium and results in widening of
the periodontal ligament space. This as-
sumption vyas based on the observation that
teeth with intrabony defects had wear facets
indicating trauma from occlusion (Glick-
Treatment of iotrabony defects
The purpose of periodontal surgery is to
create an anatomical relationship between
the tooth and gingiva which allows the pa-
tient to maintain optimal oral hygiene and
thereby avoid further destruction of the
periodontium. Most periodontists believe
that meeting this requirement involves the
surgical elimination of pathologically deep-
ened periodontal pockets. It is a common
opinion that the contour of the gingiva
depends on the anatomy of the underlying
alveolar bone and that persisting osseous
irregularities may result in residual pockets
following surgery (Schluger 1949, Friedman
1955, Ochsenbein 1958), Therefore, bone
remodelling has been advocated, in order
to remove bony craters and create a proper
anatomical fotindation for the overlying
gingival tissue. However, other authors feel
that bone remodelling is unnecessary since
the alveolar bone spontaneously assumes a
proper architecture when the soft tissue in
the intrabony defects and the deposits on
the teeth are removed (Patur & Giickman
1962, Dontienfeld, Hoag&Weissman 1970),
Elimination of intrabony defects by surgical
bone remodelling implies that the supporting
bone of both the involved tooth and adja-
cent teeth, may be removed. Therefore, in
order to avoid bone recontouring and the
subsequent loss of bony support, various
surgical methods aimed at eliminating the
intrabony defects through regeneration of
man & Smulow 1967), In dogs Svanberg
(1974) demonstrated that trauma produced
by jiggling occlusal forces accelerates loss
of attachment and results in the formation
of angular bony defects in the presence of
experimentally induced periodontitis.
new bone, cementum, and fibrous attach-
ment have been introduced.
The result of this treatment is usually re-
ferred to as reattachment. However, it has
been suggested on World Workshop in Peri-
odontics 1966 that the term reattachment
should be used only if an elevated gingival
flap is replaced and reestablishment of the
fibrous attachment at a level coronal to the
crest of the alveolar bone occttfs through
healing by primary intention. Since the for-
mation of a connective tissue attachment
occurs on a previously exposed root surface
during the regeneration of intrabony de-
fects, it has been proposed that the term
ttew attachment should be used (World
Workshop in Periodontics 1966).
Subgingival curettage
The earliest new attachment experiments
were carried out using sobgingival curet-
tage, i.e, removal of the pocket epithelitun
and planning of the root surfaces with the
aid of ctirettes. This technique was often
combined with the use of various caustic
agents in order to facilitate the removal of
the pocket epithelium.
Observations in humans (Younger 1899,
McCall 1926, 1951, Barkann 1939, Betibe
1947, 1952, Bjomdahl 1948, Orban 1948,
Waerhaug 1952, Schaffer & Zander 1953,
Cross 1956, Rockoff, Rockoff and Sackler