Intrabony Defects: Diagnosis and Treatment
Studies of periodontal lesions have provided the classification
of periodontal pocket: the suprabony or supracrestal and
the infrabony or subcrestal. The suprabony pocket is defined
as a pathological sulcus where the base of the pocket is
coronal or occlusal to the alveolar crest, while the infrabony
is defined as a pathological sulcus where the bottom of
the pocket is apical to the alveolar crest. Recent publications
has arrived at the correct term for the infrabony pocket
as intrabony pocket. Classification of intrabony pocket
was necessary for academic purposes but also to serve as
a rational basis for the selection of a method of treatment.
According to Henry Goldman ad Walter Cohen, intrabony pocket
is classified base on morphology and is dependent on location
and number of osseous walls remaining about the pocket.
The intrabony pocket can be described as three osseous walls,
of which can be proximal, buccal, and lingual walls; or
buccal, mesial, and distal walls; or lingual, mesial, and
distal walls. The three wall intrabony pockets are usually
observed on the lingual surfaces of the maxillary and mandibular
teeth where the lingual plate is intact as well as both
proximal walls. The four osseous walls defects (buccal,
lingual, mesial, and distal) usually involved circumferential
pocket and involves the four surfaces of the tooth. Two
wall infrabony pockets may be seen in the interdental areas.
Two osseous walls defects usually consists of buccal and
lingual walls; or the buccal and proximal walls, or the
lingual and proximal walls. The two wall infrabony pocket
in which the buccal and lingual walls remain while the proximal
wall is destroyed is referred to as crater. Intrabony pocket
with one osseous wall remaining is also usually seen in
the interdental areas. Here it is most common to observe
the proximal wall with the buccal and lingual walls destroyed.
However, the remaining wall can be a proximal, buccal, or
lingual wall. Goldman and Cohen also stressed the visualization
of the topography of the infrabony pocket is essential for
its clinical management, and also understanding the etiology
is necessary to yield successful result. Etiology of the
intrabony pocket involved tooth anatomy and tooth position.
Tooth anatomy concerns with grooves or crevice or concavity
on the root surface which facilitates accumulation of plaue
and calculus formation, contact areas morphology, and also
type of tooth. Tooth position which contributes to food
impaction, plaque accumulation, angular position or position
of the tooth in respect to the alveolar housing and buccal
bone are the local environmental factors which can initiate
the infrabony pocket process. Another important factor in
the etiology of the intrabony pocket is the occlusal traumatic
lesion. Even though occlusal traumatism cannot cause pocket
formation alone; however, as the pocket formation began
with the local factors (calculus, food impaction), the occlusal
trauma can affect the attachment apparatus. Local factors
and traumatic occlusion will inevitably lead to the formation
of intrabony pocket. Another major cause for intrabony pocket
formation is localized juvenile periodontitis, which predominantly
affect the region of first molars and incisors. Goldman
and Cohen also emphasized the necessity to eliminate causative
factors in the therapy as followed:
1. Tooth anatomy-proximity of roots and width of the interdental
2. Relative position of adjacent marginal ridges, cemento-enamel
junctions and crest morphology.
3. Tilting of the tooth in group relationship.
4. Tilting of solitary tooth.
5. Position of the tooth in respect to alveolar housing
and basal bone.
6. Contact points and resultant food impaction.
7. The occlusal relationships of the tooth.
8. Presence of calculus.
9. Causation by the disease process of Localized Juvenile
Any attempt to treat the infrabony pocket without regard
to the etiologic factor may result in failure. Temporary
splinting of the mobile tooth can be used prior to operation,
making sure that the splint is extended to strongly held
tooth to assure rigid splint and the affected tooth cannot
be moved by the occlusal force. According to Goldman and
Cohen, two major methods of treatment have been developed
for the infrabony pocket. The first consists of curettement
of the portion below the bone crest, then gingivectomy is
carried out for the portion above the alveolus to enhance
the possibility of formation of new cementum, bone, and
periodontal membrane. The second method involved osteoectomy,
which the alveolus is reduced to a point coinciding the
base of the pocket. When the pocket is shallow and not too
much support is lost, osteoectomy is definitely indicated.
There is a direct relationship between the prognosis of
the therapy and the number of walls intact. Three wall defect
has the best prognosis for new attachment, then the two
walls. One or no wall defect demonstrated poor prognosis.
When osteoectomy is used as part of the treatment, the length
of the root must be considered. Two major procedures for
osteoectomy-osteoplasty consist of 1) raising a flap and
trimming the bone crest and 2) raising a flap and outline
the contour of the bone for removals with small holes, then
united the holes. The crater lesion (two wall defect) is
usually treated by osteoectomy. Thus in short, the one and
two wall lesions are treated with osseous surgery while
the three wall lesions are treated with curettage-gingivectomy
procedures. Inner wall of gingival flap should be debride
prior to replacement. Scaling and root planing of the tooth
surfaces to remove all local factors should be performed
prior to the curettage-gingivectomy operation.
John Prichard outlined the technique for treating infrabony
pocket based on alveolar process morphology. The infrabony
pocket is differ from the suprabony pocket in that the pattern
of bone absorption is vertical rather than horizontal and
the normal arrangement of the gingival and transeptal fibers
of the periodontal ligament is altered. Again John Prichard
stressed the coexistence of local environmental factors
and the occlusal trauma as one of the two etiology of the
intrabony pocket. The second cause is the degeneration of
the periodontium. In Prichard analysis of wound healing
in the intrabony pocket, he described the healing as similar
to the fractured bone repair; healing is from the internal
callus which forms from osteogenic cells that line the interior
of bone and the nearby undifferentiated cells of the marrow.
Cells for the genesis of periodontal ligament, cementum,
and alveolar bone are available in the pocket, in addition
to osteogenic cell from bone and marrow. Prichard stressed
the important of the establishment of blood clot after therapy
since it acts as the biological dressing, which indicates
the absence of infection and greatly enhanced the chance
of success by protecting the osteogenic cells from exposure
and irritation, thus maintaining homeostasis. In described
the anatomical factors, Prichard mentioned that the infrabony
pockets with one osseous walls tend to occur where the dental
arch is narrow as in the mandibular incisor, maxillary incisor,
and the bicuspid regions. Infrabony pocket are most often
found interproximal region. The mandibular molar region
is the most common site of the infrabony pocket with three
osseous walls. Diagnosis of bone topography involved the
use of the periodontal probe, the roentgenogram, and definitive
surgical exploration. Probing is to explored the buccal
and lingual wall, whereas the roentgenogram is valuable
assessing the proximal wall. Three osseous walls are mandatory
for predictable success. Infrabony pocket involving the
furcation area are difficult to treated. For the class II
or class I lesion, regenerative therapy with barrier membrane
are recommended. For class III furcation defects, the osseous
resection as systematized by Schluger is indicated. Prichard
emphasized the careful planing of the root surface and the
complete surgical removal of all soft tissue between the
tooth root and the bone in the intrabony therapy, with second
stage procedure occasionally are necessary to complete the
repair via osteoectomy.
Alan Polson and the Lars Heiji investigated the osseous
repair process in infrabony periodontal defects and published
their result in 1978. Fifteen defects were selected in nine
patients and following the muco-periosteal flap reflection,
the osseous defects were debrided. The flap were replaced
at their original location and optimal plaque control regimen
was instituted. Six to eight month after the therapy, all
areas were reoperated and the osseous defects were remeasured
at the same specific location. All osseous changes are quantitated
in their study. There is the combination of coronal bone
regeneration (mean 77%) and the marginal bone resorption
(mean 18%). Intrabony defect may predictably remodel after
surgical debridement and establishment of optimal plaque
According to William and Burton Becker reports of repair
of intrabony defects by open debridement procedures. 36
three wall or circumferential intrabony defects were treated.
Flap was raised using vertical relaxing incisions to provide
access for debridement. The intrabony defects were thoroughly
debrided of all visible granulation tissue and the presence
of calculus on the root surfaces was recorded. After debridement,
the defects were bathed in .2% chlorhexidine for three minutes
and were then washed with water. The flaps were then sutured
apically with 4.0 silk or gut sutures; however, an attempt
was made to leave the margins of the flaps open adjacent
to the treated site. Upon reentry at average of 14 month
post operative, there is an average of 2.44 mm clinical
attachment level gain from the initial clinical attachment
level was 7.37 mm. There is also anaverage of 1.62 mm of
recession and the average of .48mm crestal resorption. The
net amount of defect repair was 2.55mm. The defect repaired
by a combination of crestal resorption and fill from the
defect base and surrounding osseous walls. Residual defects
were found on all reentry sites of an average of 1.67mm.
The majority of these defects were reduced with osseous
surgery upon reentry. Compare to the other experiments such
as that of Ellegaard, Karring, and Loe in 1974 which involved
treatment of intrabony defect with autogenous cancellous
bone graft and open debridement were used as control, the
results were almost as favorable for debridement only sites
as they were for the sites that received graft. Altiere,
Reeve, and Sheridan in 1979 compared lyophilized bone allograft
with debridement controls and the result is no difference
between graft sites and control sites. Other studies such
as those of Polson and Heiji and those of Froum et. al.
and Prichard provided supportive evidence that the deeper
the three wall defects, the greater the amount of bone fill
Today, with the advance of guided tissue/bone regeneration
technology, three wall and even two walls defect can be
treated successfully with the used of membrane barrier to
prevent the apical migration of soft tissue and allow true
regeneration of alveolar bone to occur. Carlos Quinones,
Markus Hurzeler, Raul G. Caffesse, Peter Schupbach, and
Edith C. Morrison performed the treatment of interproximal
intrabony defects in monkey with a synthetic bioresorbable
guided tissue regeneration barrier. The control sites did
not receive the barrier. Periodontal lesions were induced
around the mandibular central incisor teeth using the orthodontic
elastic. Resolut material was placed to cover the entire
buccal and lingual extent of the interdental defect. The
animal were sacrificed five month after surgery, and specimen
were stained and sections for histologic and histometric
analyses. Clinical observation of the results revealed uneventful
healing in both experimental and control group with no soft
tissue reaction nor inflammation. Histologic observation
of control sites reveals long junctional epithelium extended
apically along the entire length of the instrumented root
surface, whereas the experimental specimens demonstrated
new cellular cementum extended form the apical termination
of root planing in a coronal direction, new lamellar-like
bone almost completely filled the periodontal defect, and
periodontal ligament attached the newly regenerate cementum
to the bone. No remnants of the bioresorbable regenerative
material were observed. In short, site receiving the bioresorbable
regenerative material exhibit a significantly greater amount
of periodontal regeneration than those sites treated by
flap debridement alone.
Histologic evaluation of new attachment apparatus formation
in humans are also investigated by G. Bowers, B. Chadroff,
R. Carnevale, J. Mellonig, R. Corio, J. Emerson, M.Stevens,
and E. Romberg. In their study, they compared the healing
of intrabony defects with and without the placement of decalcified
freeze-dried bone allograft in a submerged environment.
30 graft defects and 13 nongraft defects were analyzed.
The result indicated that in a submerged environment significantly
more new attachment apparatus and new bone formed in grafted
than the nongrafted sites. Significantly greater loss of
alveolar crest height occurred in nongrafted than graft
defects; and regeneration of new attachment apparatus, new
bone, and new cementum occurred more frequently in grafted
than nongrafted defects. Finally, there was a greater chance
for regeneration of a connective tissue attachment on the
nongraft sites with no root resorption, ankylosis, or pulp
death was observed in both grafted and nongrafted defects.
Bone grafting materials will enhance regeneration of a new
attachment apparatus with more cementum formation and bone
formation. In their second study, they compared the healing
of intrabony defects with and without the placement of DFDBA
in a nonsubmerged environment. The result is also the same
as before (with submerged environment). Significantly more
new attachement apparatus, new cementum, new bone, new connective
tissue will form in intrabony defects grafted with DFDBA
than in nongrafted defect.
Intrabony defect repair has been always a challenge to the
clinician. Goldman and Cohen classified intrabony defects
according to the number of bony walls surrounding the lesion.
Prichard has presented impressive clinical documentation
on treated three wall intrabony defects. Caranza and Patur
and Glickman have presented the healing response of one,
two, and three wall intrabony defects. Bowers, Schallhorn,
and James Mellonig outlined the treatment of intrabony defect
using DFDBA as the grafting material with regenerative success.
Cafesse et. al. have reported the repair of intrabony defects
using barrier membrane with new regeneration of the periodontal
apparatus. The future is promising for the treatment of
furcation defect using the GTR technology. Regardless of
the treatment modality, understanding the etiology and visualization
of the topography of the defect are the two most important
elements in guarantee the good prognosis of the treatment
therapy. Without elimination the causative factor, the treated
site will fail or intrabony region will inevitably recur.
1. W. Becker, B. Becker, L. Berg, Repair of intrabony defects
as a result of open debridement procedures. Report of 36
treated case, Int Journal of Periodontics and Restorative
Dent, 6: 9, 1986.
2. Caranza, Newman, Textbook of Clinical Periodontology,
W.B. Saunders Company, 1996.
3. H. Goldman, D. Cohen, The infrabony pocket: classification
and treatment, Journal of Periodontology, 29: 272, 1958.
4. Prichard, J., A technique for treating infrabony pockets
based on alveolar process morphology, Dental Clinic of North
America, March 1958.
5. Prichard, J. Regeneration following Periodontal Therapy.
Oral Surg, 10: 247, 1957.
6. Carranza, F.A. A technique for reattachment, J. Periodontology,
7. Prichard, J. The infrabony technique as a predictable
procedure. J. Periodontology, 28: 202, 1957.
8. Stahl, S.S., Froum, S.J., Kushner, L. Periodontal Healing
following open debridement flap procedures, II. Histologic
observation. Journal of Periodontology, 53: 15, 1982.
9. Ellegaard, Karring, T., Loe, H. New periodontal attachment
after treatment of intrabony defects in monkeys, Journal
of Periodontology, 45: 368, 1974.
10. Altiere, E. T., Reeve, C.M., Sheridan, P.J., Lyophilized
bone allografts in periodontal intraosseous defects. Journal
of Periodontology, 50: 510, 1979.
11. Polson, A., Heiji, L.C. Osseous repair in infrabony
periodontal defects, Journal of Clinical Periodontology,
5: 13, 1978.
12. Bowers, G., Chadroff, B., Carnevale, R., Mellonig, J.,
Corio, R., Emerson, J., Stevens, M., Romberg, E. Histologic
evaluation of new attachment apparatus formation in humans.
Part II. Journal of Periodontology, 60:675, 1989.
13. Bowers, G., Chadroff, B., Carnevale, R., Mellonig, J.,
Corio, R., Emerson, J., Stevens, M., Romberg, E. Histologic
evaluation of new attachment apparatus formation in humans.
Part III. Journal of Periodontology, 60:675, 1989.
14. Bowers, G., Schallhorn, R.G., Mellonig, J. Histologic
Evaluation of new attachment in human intrabony defects,
Journal of Periodontology, 53:509, 1982.
15. Quinones, C., Hurzeler, M., Caffesse, R.G., Schupbach,
P., Morrison, E.C. Treatment of interproximal infrabony
defects in monkeys with a synthetic bioresorbable guided
tissue regeneration barrier, University of Texas, Dental