51. Alveolar Bone: Normal Anatomy, Extraction socket healing, bone loss, osseous defects    

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Discussion Topics

Discuss the gross anatomy of alveolar bone and what occurs during normal deposition and resorption. What is the embryonic origin of bone and the cells involved in bone metabolism? Identify histologically the different types of bone and different cells involved in bone metabolism.

1. Saffar JL: Alveolar bone and the alveolar process: the socket that is never stable. Periodontol 2000. 13:76-90

What are the different types of osseous topography? How common are they in a given patient population? Are all patient populations the same?

2. Elliott JR, Bowers GM: Alveolar dehiscences and fenestrations. Periodontics 1:245-246,1963.

3. Larato DC: Alveolar plate fenestrations and dehiscences of the human skull. Oral Surg. Oral Med. Oral Pathol. 29:816-819, 1970.

4. Abdelmalek RG, Bissada NF: Incidence and distribution of alveolar bony dehiscence and fenestration in dry human Egyptian jaws. J. Periodontol. 44: 586-588, 1973.

5. Edel A: Alveolar bone fenestration and dehiscences in dry Bedouin jaws. J Clin Periodontol.8:491-499, 1981.

6. Rupprecht R, Horning G, Nicoll B, Cohen M. Prevalence of dehiscences and fenestrations in modern American skulls. J Periodontol 72:722-729;2001.

How is the gingival margin or mucogingival junction related to osseous topography? Can tooth shape or form be influenced by alveolar bone morphology?

7. Lost C. Depth of alveolar bone dehiscences in relation to gingival recessions. J Clin Periodontol 11:583-589, 1984.

8. Strahan JD. Relation of mucogingival junction to alveolar bone margin. Acad Rev 13:23-28, 1965.

9. Becker W, Ochsenbein C, Tibbetts L, Becker B: Alveolar bone anatomic profiles as measured from dry skulls. J Clin Periodontol 24:727-731, 1997.

What are the different types of bony outgrowths? Are they a normal occurrence or caused by specific events? Where are they most commonly located and how does that affect periodontal treatment?

10. Glickman I: Buttressing bone formation in the periodontium. J Periodontol 5: 365-70. 1965.

11. Larato DC: Palatal exostoses of the posterior maxillary alveolar process. J Periodontol 43:486-489, 1972.

12. Nery EB, Corn H, Eisenstein IL: Palatal exostosis in the molar region. J. Periodontol. 48:663-666, 1977.

What is the sequence of repair in tooth extraction sockets? How does this affect treatment decisions? Can extraction sockets be utilized as a source of autogenous bone graft?

13. Boyne PJ: Osseous repair of the postextraction alveolus in man. Oral Surg Oral Med Oral Path 21:805-813, 1966.

14. Amler MH: The time sequence of tissue regeneration in human extraction wounds. Oral Surg Oral Med Oral Path 27:309-318, 1969.

15. Soehren SE, van Swol RL: The healing extraction site: a donor area for periodontal grafting material. J. Periodontol. 50:128, 1979.

16. Evian CI, et al: The osteogenic activity of bone removed from healing extraction sockets in humans. J. Periodontol. 53:81, 1982.

17. Halliday DG: The grafting of newly formed bone in the treatment of osseous defects. J. Periodontol. 40:511-514, 1969.

18. Passanezi E, et al. Newly forming bone autografts to treat periodontal infrabony defects: Clinical and histological events. Int. J. Perio Restor. Dent. 9:141-152, 1989.

What can affect socket wound healing? (Age, medications, medical conditions, etc

19. Amler MH. The age factor in human extraction wound healing. J Oral Surg. 35:193-197, 1977

20. Hars E, Massler M: Effects of fluorides, cortico-steroids, and tetracyclines on extraction wound healing in rats. Acta Odont. Scand. 30:511-522, 1972.

21. Teofilo JM, Brentegani LG, Carvalho TL. A histometric study in rats of the effect of the calcium antagonist amlodipine on bone healing after tooth extraction. Arch Oral Biol 46:375-379,2001.

What are some risk factors for bone loss? How are systemic factors able to influence bone metabolism? Are there any specific factors that can inhibit alveolar bone loss?

22. Grossi S, Genco R, Machtei E, Ho A, et al. Assessment of risk for periodontal disease. II. Risk indicators for alveolar bone loss. J Periodontol 66:23-29, 1995.

23. Lesser GV, Krook L: Bone physiology and periodontal disease. Annals of Dent. 33:7-10, 1974.

24. Williams RC, et al. Ibuprofen: An inhibitor of alveolar bone resorption in beagles. J. Periodontal Res. 23:225-229, 1988.

25. Jeffcoat MK, Reddy MS, Haigh S, et al. A comparison of topical ketorolac, systemic flurbiprofen, and placebo for the inhibition of bone loss in adult periodontitis. J Periodontol 66:329-338,1995.

What are the different types of bone loss and bony defects? Are they evenly distributed throughout the mouth? How are bony defects categorized? If these patients are maintained, is there a difference in progression of bone loss between horizontal and vertical defects?

26. Larato DC: Intrabony defects in the dry human skull. J Periodontol 41:496-498, 1970.

27. Manson JD, Nicholson K: The distribution of bone defects in chronic periodontitis. J Periodontol. 45:88-92, 1974.

28. Nielsen IM, Glavind L, Karring T: Interproximal periodontal intrabony defects: Prevalence, localization, and etiologic factors. J. Clin. Periodontol. 7:187-198, 1980.

29. Karn KW, Shockett HP, Moffitt WC, Gray JL: Topographic classification of deformities of the alveolar process. J. Periodontol. 55:336-340, 1984.

30. Vrotsos J, Parashis A, Theofanatos D, Smulow J. Prevalence and distribution of bone defects in moderate and advanced adult periodontitis. J Clin Perio 26:44-48, 1999.

31. Prichard JF. The etiology, diagnosis and treatment of the intrabony defect. J Periodontol 38:455-465,1969.

32. Pontoriero R, Nyman S, Lindhe J: The angular bony defect in the maintenance of the periodontal patient. J. Clin. Periodontol. 15:200-204, 1988

Is there any way to evaluate bony defects prior to surgical access? Is this an accurate estimator of alveolar bone level?

33. Greenburg J, Laster L, Listgarten MA: Transgingival probing as a potential estimator of alveolar bone level. J. Periodontol. 47:514-517, 1976.

34. Ursell MJ: Relationships between alveolar bone levels measured at surgery, estimated by transgingival probing and clinical attachment level measurements. J Clin Periodontol 16:81-86, 1989

Can anatomic factors affect the type of bone loss seen in patients?

35. Heinz PJ, Wieder SM: A histologic study of the width and nature of interradicular spaces in human adult premolars and molars. J. Dent. Res. 65:948-951, 1986.

36. Tal H. Relationship between the interproximal distance of roots and the prevalence of intrabony pockets. J Periodontol 55:604-607, 1984.

37. Heins P, Thomas R, Newton J: The relationship  of interradicular width and alveolar bone loss.J. Periodontol. 59:73-79, 1988.

Discuss the gross anatomy of alveolar bone and what occurs during normal deposition and resorption. What is the embryonic origin of bone and the cells involved in bone metabolism? Identify histologically the different types of bone and different cells involved in bone metabolism.

Saffar 1997                     ARTICLE

P: Review article about dynamic nature of alveolar bone and alveolar process

D: After tooth eruption period, the relationship between the teeth and their supporting structures remains dynamic.

- Alveolar wall is perforated by channels through which blood vessels and nerve fibers connect the marrow spaces to the PDL. The bone lining the socket is known as bundle bone. This layer is thin ranging between 100-200 um in humans. Because of tooth movement, the socket is spatially oriented: the side of the socket in the direction migration is irregular and scalloped by numerous lacunae of various lengths and depths (resorbing side) while the opposite side is regular and smooth (apposition side). Modeling also allows the adaptations to mechanical usage and overloading.

- When the teeth migrate, the bone surrounding them does not migrate, but is re-arranged (deformed) in front of and behind the migrating root. The formation of alveolar wall is achieved through the removal of bone along the resorbing side and the concomitant deposition of bone along the apposition side.

- During resorption, the osteoclasts excavate the layer of bundle bone, pass through the cement line and resorb the supporting bone. They remove all the mineralized material. PDL fiber bundles become detached at their point of insertion in bone. At the end of this phase, the osteoclasts withdraw. Mineralized layer then reform. Fibroblasts secrete thin collagen fibrils. This will restore the continuity of the PDL fiber bundles which become anchored.

- Apposition side is characterized by the presence of a continuous row of osteoblastic cells that lie between the Sharpey’s fibers over a layer of osteoid tissue.

- The deformation of the socket (external architecture) is accompanied by a re-arrangement of the supporting bone (internal architecture). The removal of bone on the resorbing side is compensated by lamellar bone formation of the endosteal aspect of the alveolar wall. On the apposition side, the no longer functional bundle bone is resorbed from the endosteum and replaced by lamellar bone.

What are the different types of osseous topography? How common are they in a given patient population? Are all patient populations the same?

Elliott & Bowers 1963                     ARTICLE

Purpose: To determine incidence of dehiscence & fenestration & to learn the most freq. locations for each.

M & M: 52 skulls, 1153 teeth. Bone loss due to perio dz, periapical rarefaction, or cystic involvement thrown out.

Results: Maxillary 1M (particularly #14) had highest incidence of defect (60%, 53% bilateral), mandibular cuspids next highest (50%, 56% bilateral); Max arch had 3x more fenestrations than dehiscence, whereas mand arch dehiscence was more predominant; maxillary 1M also had most mesial and distal defects.

DISC: Alveolar defects occur in areas with normal thin bone (Orban). When stripped of periosteum during sx, a fenestration could become a dehiscence.

BL 1) Look for fen in max. & deh in mand.; expect bilat involvement when planning Sx.

2. Incidence ranges from 2.4-60.9% with avg of 20.1%

3. Healing associated with fenestrations in MG sx may be uneventful but osseous resorption producing dehiscence may occur resulting in a sx defect.

4. Frequency with anatomic shape.

Larato, 1970                     ARTICLE

P: To study alveolar plate fenestrations and dehiscences of the human skull.

M & M: 108 Mexican Indian skulls studied, 3416 teeth, age early 20 to past 70 y/o; fenestrations, dehiscences, occlusal wear pattern, and root prominence recorded for each tooth

R:

• 7.5% of ALL teeth exhibited fenestrations or dehiscences (4.3% fenestrations, 3.2% dehiscences). Anterior teeth had > number of fenestrations and dehiscences than posterior teeth. : 13.4% exhibited fenestrations or dehiscences of alveolar plate (also (12.5% maxillary, 14.3% mandibular)

• - Maxillary teeth: most common in cuspids and first molars

• - Mandibular teeth: most common in cuspids

• - No fenestration or dehiscence associated w/ either maxillary or mandibular lingual alveolar plates.

• - No correlation b/w # of fenestration & dehiscence w/ age and occlusal trauma

• - 90% of teeth exhibiting alveolar plate fenestration & dehiscences were teeth that had prominent roots in relation to the arch

BL: 7.5% of all examined teeth had fenestration or dehiscences, more in anterior mandibular and maxillary teeth.

Abdelmalek 1973                     ARTICLE

Dehiscence: Denotes the absence of the alveolar cortical plate, in some cases extending more than half of the root length and resulting in a denuded root surface.

Fenestration: A circumscribed defect in the cortical plate which exposes the facial or lingual root surface.

P: To evaluate the incidence and distribution of fenstrations and dehiscences in dry human Egyptian skulls.

M&M: A total of 154 adult jaws (61 maxillary and 93 mandibular) were randomly selected from the museum of the Faculties of Medicine and Denstistry, Cairo University. Each jaw was examined for the presence of fenestration and dehiscence in the alveolar plate.

R: Total # of jaws with one or more bony defects (fenestration and/or dehiscence) was 31/61(50.81%) maxillary and 43/93 (46.23%)mandibular arches. Slightly more defects were found in anterior regions. The mandibular anterior region was the area most affected.The ratio of fenestration to dehiscence in the anterior region of the maxilla was 4.9:1.1 and in the mandible it was 5.3:2.3. In the posterior regions of the maxilla the ratio of fenestration to dehiscence was 5.6:0.56 while in the mandible it was 2.6:2.9. The maxillary first molar showed that highest incidence of bony defects (7.8%) and the mandibular third molar the lowest (0.7%).

BL:

• About half (48.5%) of the maxillary and mandibular jaws examined showed one or more bony defects, with such defects slightly more common in the maxilla than in the mandble.

• The mandibular anterior region showed the highest incidence of these bony defects.

• The maxillary 1^st molar showed the highest incidence (7.8% and the mandibular 3^rd molar the lowest (0.7%).

• Fenestrations were more common than dehiscences in the maxillary arch and in the mandibular anterior region.

• Bony defects were not seen in either the maxillary or mandibular lingual plate.

Edel 1981                     ARTICLE

B: Dehiscence = a deficiency of the alveolar bone margin resulting in a denuded root surface. Fenestration = a circumscribed defect of the alveolar radicular bone exposing the root surface but not involving the alveolar margin.

P: To examine the incidence of fenestrations and dehiscences in Bedouin (Desert-dwelling Arabian ethnic group) skulls

M+M: 87 jaws examined (30 matched pairs, 20 mandibles, 7 maxillae). Dehiscence was a defect in which the crest of the radicular bone was at least 4 mm apical to the crest of the interproximal bone as measured from CEJ (Davies et al, 1974). Probing was made on mesial (in between middle and outer thirds of proximal surface) and midbuccal surfaces. The relationship between the defects and presence or absence of root prominence (root where the total buccal curvature was manifested by a convexity in the external surface of the jaw) was recorded. Faceting of crowns was considered indicative of possible excessive occlusal forces.

R: 14.5% of teeth examined (990 teeth) had fenestration or dehiscence.

Fenestrations

• Maxillary teeth: 17.7% of all teeth. 10.2% of anteriors (canines); 20.4% of posterior teeth (1^st molars).

• Mandibular teeth: 5.4% of all teeth. 10.5% of anterior teeth (lateral incisors+canines). 3.1% of posteriors.

Dehiscence

• Maxillary teeth: 2.1% of all teeth. 0.85% of ant. teeth; 2.6% of post. teeth

• Mandibular teeth: 5.5% of all teeth. 8.77% of ant. teeth (canine); 4.1% of post teeth (1^st premolar)

Association with occlusal facetting:

• 71.6% of teeth with fenestration and 50% of teeth with dehiscence have occlusal wear.

Association with prominent root:

• 37.7% of teeth with fenestration and 35% of teeth with dehiscence have prominent root.

BL: Fenestrations are more prevalent than dehiscences in the maxilla, but they nearly equal to dehiscences in mandible. Fenestration frequency: 1^st max. molar> 2^nd max molar> max canines>mand canines>mand lateral incisor. More involved: distal root of max. molars, mesial root of mand. molars. Dehiscence frequency: Most in mandibular canine and 1^st PM.

Rupprecht 2001                     ARTICLE

P: To examine the prevalence, distribution, and features of alveolar dehiscences and fenestrations in modern American skulls and correlate their presence with attrition, root prominence, and alveolar bone thickness.

M&M: 146 American skulls examined, with at least 5 teeth in each jaw for the presence of dehiscences and fenestrations. Dehiscences defined as a defect measuring at least 4mm apical to the crest of the interprox bone. Measurements were done to nearest mm with perio probe. Attrition, alveolar bone thickness, root prominence, and interprox bone loss measured in correlation to dehiscences and fenestrations.

R: Alveolar bone defects assoc with 13% of all teeth. At least one dehiscence was identified in 40.4% of all skulls and dehiscences were assoc with 4.1% of all teeth. At least one fenestration was present in 61.6% of all skulls and assoc with 9% of all teeth. No defects were observed in 30.8% of skulls examined. Females more dehiscences (4.9 vs 3.5) and fenestrations (11.8% vs 6.8%) than males. Dehiscences in mandibular cuspids (12.9%) and maxillary first molars (11.3%). Fenestrations most common at maxillary first molars (37%), maxillary canines (13.9%), and mandibular canines (11.5%). Almost all defects found on buccal alveolar plate (94.5%), and most of the fenestrations were in the apical third. More affected teeth presented no attrition and thin alveolar bone (thin 18% vs thick 9.6%). 23.6% of defects assoc with root prominence. Most fenestrations (72.8%) were located at the apical third of the root. Dehiscences more common in black males and white females, while black females were more likely to have fenestrations.

D: We must be careful comparing prevalence and distribution of dehiscences, because different authors have different definitions of a dehiscence (ej, half the root length, simply a picture of a dehiscence).

BL: The prevalence of these defects is important because they may affect our periodontal surgeries, especially when we extend our incisions multiple teeth.

How is the gingival margin or mucogingival junction related to osseous topography? Can tooth shape or form be influenced by alveolar bone morphology?

Lost 1984                     ARTICLE

P: To assess the depth of the alveolar bony dehiscences in relation to gingival recessions.

M&M: 27 pts. (mean age 25.6 y/o) w/ 50 areas of recession on 113 teeth had flap surgery performed, and both pre-op and intra-op measurements were taken. All recessions met the following criteria: facial surface, intact interdental papillae, no interproximal bone loss, no mobility, no pockets, and minimal gingival inflammation.

R: Mean recession depth was 2.67mm, mean dehiscence depth 5.43mm. Mean PD 1.38mm. Calculated mean distance between (most apical point) recession and dehiscence 2.76mm is almost identical with reported value by Gargiulo (1961) with 2.67mm. (depth of the sulcus + epithelial attachment + CT). 16 teeth had a markedly greater distance b/w the gingival margin and the alveolar crest (4 - 7.5 mm). A correlation b/w dehiscence depth and type of tooth could not be found, but 1/3 of the 16 teeth w/ a distance of 4 mm or more were lower canines.

C: A recession depth of 1 mm is exceeded by an average of 2.8 mm towards the apex by the dehiscence. Each 1 mm increase in recession depth involves an average increase of 0.98 mm in alveolar bone dehiscence.

BL: Since the distance from the FGM to the bone varied from an average of 2.76 to 7.5 mm the authors suggest that a specific correlation can’t be made.

Stranhan 1965                     ARTICLE

Relation of mucogingival junction to alveolar bone margin

Purpose : to study the relationship between the mucogingival junction and bone margin to determine the significance of the MGJ as a surface indicator of bone level

Materials and methods

• -The investigation was made from canine to canine in the mandible.

• -3 methods, histology, radiology (using a radiopaque marquer) and clinical.

• -The margin of the alveolar bone was located by palpation

• -The measurements were from gingival margin to mucogingival junction, from gingival margin to bone margin, and from bone margin to MGJ.

• -The accuracy of these techniques was confirmed in 2 ways. First, it was found by means of a mucogingival flap that a probe previously positioned did, in fact indicate the bone margin. Secondly, by repeating measurements after an interval of one week .

Observations

• -MGJ apical to the alveolar bone margin in the majority of areas examined the gum overlapped the bone margin by up to 3mm marginaly and up to 5 mm interdentally. This is the normal relationship

• -MGJ coronal to the alveolar bone margin the mandibular canine most frequently shows this relationship, as did teeth under occlusal trauma.

• -Localized gingival recession, (incisors) where many times the bony defect was more severe than the gingival recession.

• - The degree of recession did not appear to bare any predictable relationship to the bony crest or the depth of the gingival sulcus.

Becker 1997                     ARTICLE

Purpose: To classify bone anatomy on the maxillary anterior region into alveolar morphotytpes and to relate tooth form to bone anatomy, and to evaluate the presence of dehiscences and fenestrations in the maxillary anterior sextant.

Materials and methods: 111 Caucasian adult human skulls were evaluated. Age and sex of each skull was not ascertained. Each skull should have 6 maxillary anterior teeth in occlusion with the corresponding mandibular teeth. Three examiners evaluated each skull. Skulls were classified as flat, scalloped or pronounced scalloped according to the buccal alveolar anatomy. They were evaluated for dehiscences and fenestrations. 10 skulls from each category were selected for bone height measurements. Teeth dimensions from all skulls were measured. Statistical analysis was performed.

Result/BL: Mean distance from mid – buccal alveolar crest to the interdental bone height was statistically significantly different for the three anatomic morphotypes (flat 2.1mm, scalloped 2.8mm and pronounce scalloped 4.1mm). Differences for fenestrations (0.5/skull for flat and scalloped and 1.2/skull for pronounced scalloped) and dehiscences (average 3.5 per skull) were not significant between groups.

Frequency of fenestrations reported in this and previous (O’Connor 1963) studies indicate that implants placed directly into extraction sockets may have an increased possibility of implant surface exposure.

Serious esthetic changes in bone and mucosal anatomy may result after extractions in patients with thin – scalloped profiles.

Flat bone anatomy had a slight tendency for greater tooth length when compared with the other two groups, and tooth width for the pronounced scalloped group was narrower than the other two groups. CW/L ratio showed a tendency for a decrease in ratios between the flat to pronounced scalloped groups. In this study ratios for canines, lateral and central were 0.80, 0.72 and 0.90 respectively. Measurements were not corrected for incisal wear or attrition.

What are the different types of bony outgrowths? Are they a normal occurrence or caused by specific events? Where are they most commonly located and how does that affect periodontal treatment?

Glickman Smulow 1965                     ARTICLE

P: Discussion article to describe and characterize the formation of "buttressing bone".

D: Description of histological sections cut from 2nd or 3rd molars of 2 Rhesus monkeys. Buttressing bone is formed as a reinforcement of the bone trabeculae weakened by occlusally induced resorption (OIR). If buttressing bone does not keep up with the OIR, an angular bony defect forms next to the root. When the OIR greatly exceeds the bone formation, bone height is reduced. Bone is lost due to excessive occlusal forces without destructive inflammation present. Buttressing bone may be stimulated by occlusal forces not great enough to cause trauma from occlusion. It represents an adaptive mechanism to accommodate to altered occlusal forces. Buttressing bone forms in tension and pressure areas. The alveolar plate is reshaped in the direction of the tension.

BL: Occlusal trauma can cause angular defects and horizontal bone loss without disease present. Buttressing bone is formed to adapt, strengthen, reinforce, and repair problems caused due to excessive forces from occlusion.

Larato 1972                     ARTICLE

Purpose: To find out more information about the anatomy and frequency of occurrence of boney exostoses on the palatal surface of maxillary alveolar process; and to classify these structures by their size, shape, and location.

M&M: Study examined 145 adult dry human skulls. Age of the skulls was determined by suture closure. The skulls were divided into 3 groups: young adult (17-39 y.o.), middle aged adult (40-55 y.o.), and old adult (40-55 y.o.). Each skull had full complement of permanent maxillary molars. Only specimens without bone resorption were observed. The exact location of the exostoses was recorded.

Results: 44/145 skulls (30%) had exhibited exostoses, of those, 7/44 had unilateral exostoses. Incidence of these exostoses increased with age, as 26/60 old adult skulls had exostoses, while only 14/50 middle aged adult skulls and 4/35 young adult skulls had them. Most common anatomical type of exostoses were small nodules, followed by sharp ridges, spikes, and combination of all the different kinds. Large nodules were the least commonly observed.

The most common location of the exostoses (39/44) was on the palatal area of the maxillary alveolar process on the tuberosity. The next most common area (29/44) was on the alveolar process lingual to the third molar. 80% of the exostoses began 1-2 mm apical to the alveolar crest and extended 3mm or more apically.

BL: Since 30% of skulls contain exostoses on the palatal surface of posterior maxillary alveolar process, we can conclude that it is a common occurrence and is not apparent in living patient because of the thick gingival tissue on the hard palate.

Incidence increases with age. As a result of their position and prevalence, these exostoses may be a factor in periodontal surgery.

Nery 1977                     ARTICLE

P: to examine the incidence of palatal exostosis (PE) in the molar region, determine whether their presence depends on locality and correlate locality with age and type of exostosis.

M&M: 681 skulls studied, categorized into geographical groups (European, Oceanic-Asiatic, African, Mexican-Peruvian), age groups (17-39, 40-55, 56 or older) and types of exostosis (small nodules, large nodules, sharp ridge, spike-like projection and combination).

R: 40.53% of skulls examined exhibited some form of palatal exostosis. PE were more prevalent in Oceanic-Asiatic sample (47,24%), then in European sample ( 45.54%),and less prevalent in Mexican-Peruvian sample (27.27%) and in African sample (25%). The highest incidence of PE was found in the 40-55 year age group (50.36%). The 56 year age or older category presented incidence 30% and the 17-39 year age group displayed the lower frequency of occurrence (19.57%). Also, the occurrence of exostosis in any age group was dependent upon the locality. The most common type of exostosis was small nodular (27.53%) and the different types of exostosis were influenced by locality.

BL: PE occurrence is dependent upon the locality, influenced by age, in any age group dependent upon locality, dependent upon the type or class of exostosis and in any type influenced by locality.

What is the sequence of repair in tooth extraction sockets? How does this affect treatment decisions? Can extraction sockets be utilized as a source of autogenous bone graft?

Boyne 1966                     ARTICLE

P: To observe osseous repair associated with healing human post-extraction sockets.

M&M: 12 patients (20-45 years) scheduled for extraction of all max teeth had max 1^st premolar removed first. On either side of the 1^st premolar, all teeth scheduled for extraction were allowed to remain during the period of observation of healing of the premolar socket. Each patient received oxy-TTC IM post-op in two consecutive daily doses of 4mg at a predetermined time post-operatively (different time points for different patients). One week following administration of the antibiotic, the remaining teeth were removed and a block section of bone that included the entire socket was taken. Biopsy specimens were taken at 13, 15, 17, 19, 21 and 23 days post-op. Ground undecalcified sections were prepared and evaluated by fluorescence microscopy. Routine hematoxylin and eosin stained decalcified sections were also prepared and correlated with ground specimens.

R: Specimens tagged at 7 and 8 days demonstrated fluorescent new bone in the marrow vascular spaces adjacent to the lamina dura. The first evidence of calcified osseous matrix seen in the healing of the human extraction socket was located outside the alveolus and could be termed a part of extra-alveolar response to the surgical procedure. Bone formation in socket was seen at 9-10 days along lateral wall but not in fundus. At 2 weeks, deposition of bone was seen at the lateral wall and the fundus of the socket. Specimens from 17 and 18 days post-op resembled those taken 2 weeks post-op.

BL: The alveolar bone heals by a series of complex osseous phenomena involving not only the socket but other anatomic areas as well since this bony alveolus does not heal by a simple process of osseous proliferation from the fundus to the crest of the defect. Bone formation in the socket was first observed in specimens 9 and 10 days post-op. The first apposition of new bone was seen along the lateral wall of the socket and not in the fundus. Specimens tagged 2 weeks after extraction demonstrated bone formation along the lateral wall of the socket and in the fundus.

Amler 1969                     ARTICLE

P: To investigate the time sequence of tissue regeneration in human extraction wounds.

M+M: Healthy pts 30-50 years old, 185 biopsy of tissue from ext. sockets were taken up to 50 days post-extractions. Biopsies were stained for histo examination.

R:

Tissue Days after ext.

• Clot formation Same day

• Replacement of clot by granulation tissue 7

• Replacement of granulation tissue by CT 20

• Appearance of osteoid at base of socket 7

• Filling of at least 2/3 of socket fundus by trabeculae 38

• First evidence of epithelization 4

• Fusion of epithelium 24 to 35 and more

BL: At 40 days after extraction the site has epithelium fused, CT and bone filling more than 2/3 of socket.

Soehren 1979                     ARTICLE

P: To discuss collecting bone from extraction sites for use in grafting periodontal defects.

BG: Graft material from a healing extraction site has new marrow spaces filled with young cells producing a collagen-filled connective tissue instead of hemopoietic or fatty marrow.

D: Three cases are presented. When a perio sx is performed that may need grafting and part of the tx plan includes an extraction, the tooth should be extracted 6-14 wks prior to perio sx and become the donor site for the osseous graft. At the time of the perio sx, the post-extraction bone will be harvested with hand instruments (Kirkland 13-back action chisel and Kirkland 14-surgical curette) and placed in the recipient site. Care is exercised not to mix the graft with saliva. The graft should be taken directly to the recipient site (not a dappen dish) to allow for greater retention of cell viability, as the graft material will be located in an area where immediate plasmatic nourishment of the cellular component of the material is possible. If healing of the extraction site appears delayed (ej. infection) it is better to wait 12-14 weeks than to enter the donor site too early. Extracted 3M sites provide more graft material than do tth with previous ALoss. Clinical experience of the authors indicates that the ideal time for re-entry is 8 weeks in the maxilla and 12 weeks in the mandible. Over 10 years involving more than 100 defects the authors have not observed root resorption in any case.

BL: When extractions are included in a comprehensive tx plan, the use of newly formed bone from extraction sites for grafting osseous defects should be considered.

Evian 1982                     ARTICLE

P: To assess the best time for harvesting bone from a healing extraction site for grafting purposes.

M&M: Cores from healing extraction sites were removed with a trephine at 4, 6, 8, 10, 12 and 16 wks and studied histologically.

R:

• 4 wks: abundant fibrous tissue and fibroblasts. Small islands of new bone surrounded by osteoid.

• 6 wks: increase osseous content. Osteogenic cells, Osteoid surrounding new bone.

• 8 wks: fewer osteoblasts, less CT. Bone starts undergoing maturation .

• 10-12 wks: minimum osteoblasts and osteoid, trabeculae of interconnected bone

• 16 wks: masses of mature dense bony trabeculae. Minimal cellular elements.

D: The optimal time seems to be at 8-12 wks when a substantial amount of relatively mature bone is present with some osteoblasts and osteoid. Does the grafted bone act only as a matrix or does it provide osteogenic potential? Is it better to utilize proliferating tissue with osteogenic potential from a 4-8 wk socket or mature tissue to act as scaffolding from a 8-16 wk socket?

BL: There are two distinct phases. Initially there is a proliferation of osteogenic cells and immature bone formation (4-8wks). Then the osteogenesis slows down and the new trabeculae undergo maturation and increase in volume (8-12wks). It may be advantageous to utilize tissue removed from an 8 to 12 wk healing site that possesses both proliferating osteoblastic cells as well as relatively mature bony trabeculae.

Halliday 1969                     ARTICLE

The grafting of newly formed autogenous bone in the treatment of osseous Defects

Purpose: To describe a technique to solve the problem of obtaining adequate quantities of autogenous bone by using newly formed bone from a surgically created wound in the mandible.

Methods

-3 subjects with no history or evidence of acute gingival infection

-SRP 6-12 weeks prior to grafting and occlusal adjustment performed

-Each graft in 2 stage surgical procedure

-Initial surgery: mucoperiosteal flap in the mandible (donor site). A hole was made in the mandible with a trephine and the bone that was removed was discarded. 2^nd surgery 6-7 week after, a flap was reflected in the area to be grafted, numerous channels were then made with a round bur through the bone lining the pocket. Donor site was reflected, the tissues within the healing lesion were removed with a trephine and packed firmly into the defect to the coronal height of bone. Flaps were sutured+ dressing.

Discussion

-This method could be applied in almost every instance to an appropriate area in the maxilla or to the second or third molars in the mandible

-One case was considered to be a complete success (5mm reattachment), the other two were partially successful in attaining reattachment 3.5mm and 5mm of new attachment.

Passanezi 1989                     ARTICLE

Purpose: To test the efficacy of newly developing bone as graft. (Immature bone contains an abundance of undifferentiated cells that may have osteogenic potential). Clinical and histologic evidence in dogs and humans are provided.

Materials and methods: Histologic examination: Histologic specimens from six adult dogs. Periodontal osseous defects were created in the furcations of the maxillary first molars. Defects were then filled with soft gutta percha in order to induce inflammatory response. At the same time mandibular molars were extracted. Twelve days later sites were surgically reopened, gutta percha was removed and filled with newly formed bone from the extractions sites. On the control site the defect was allowed to fill with blood clot and the gingiva was sutured to cover the area. Block specimens were obtained at 3,6,9,12,15,18,21,24,30, 36 42 and 75 days.

Clinical studies: Performed in two patients. The first one had a three-wall defect and bone was harvested from a bony defect created 25 days earlier in an edentulous area. The second patient had a one-wall defect, and the donor site was created 30 days ago in an edentulous ridge.

Results: Histologic: Initial phase (3,6,9,12 days): On the experimental side, the collagen fibers between the nonvital grafted bone were degenerating whereas in other areas they exhibited vitality. No other difference between two groups.

Intermediate phase (15, 18, 21, 24, 30 days): On the experimental side new bone forming from the walls and floor of the defect made it difficult to distinguish between the newly forming bone and the graft. Experimental sites exhibited more cementum formation. Overall these phase characterized by newly forming bone, cementum and periodontal ligament.

Advanced phase: Experimental side exhibited newly forming bone with numerous osteoblasts being found. Osteoid tissue was present almost everywhere in the bone. On the control side the general morphology of the surgically created defect was still apparent, and the defect was filled with a mature connective tissue with bone formation being apparent only near the lingual and apical walls of the defect. Ne bone completely covered the bifurcation areas on the experimental sites but only half way up to the middle third of the root on the controls.

Clinical: At the end of two week both control and experimental sides looked essentially the same.

BL: Newly forming bone obtained from prepared sockets can be successfully used as an autologous grafting material. It exhibits good ostegenic potential with no ankylosing or root resorptive properties. It also inhibits epithelial downgrowth and encourages formation of new PDL.

What can affect socket wound healing? (Age, medications, medical conditions, etc

Amler 1977                     ARTICLE

B: Past investigations (Amler 1960, 1964, 1969, 1973) established the following sequence in healing of human extraction wounds: Clot formation the same day, replacement of the clot by granulation tissue by the 7th day, replacement by CT by the 20th day and appearance of bone development w/ 2/3 of socket being filled by the 38th day.

P: To delineate age related differences in the rate of healing after extractions.

M & M: 23 post extraction biopsy specimens from pts <20 yrs old were compared with 62 biopsy specimens from pts >50 yrs old. Specimens were taken at 1, 5, 10, 15, 20, 25, 30, 40 & 45 days post-ext. Different stains were used to distinguish ground substance; glycogen/glycoprotein, CT/collagen, alkaline phosphatase, and reticular fibers in order to show healing.

R: Similar rates of healing and degree of cell proliferation were showed for both groups until 10 days after extraction. At 10 days, the rate of repair of younger tissues continued at an accelerated rate, whereas, in older tissues, a lag phase was noted. A second accelerated growth phase of older tissues did not begin until the 20 day. At 30 days both groups appeared to possess the same degree of healing of CT and bone development.

BL: No difference up to 10 days. Then there is a lag phase in repair of tissues post-extraction in older pts; however, by the 30 day the rates of growth & repair were similar to younger individuals. The authors speculated that the lag phase was due to decreased blood flow in older pts which caused the delay in wound healing.

Hars Massler 1972                     ARTICLE

Purpose: To verify effects of fluorides, corticosteroids and tetracycline upon osteogenesis and the resorptive processes of extraction wounds in rats.

M&M: 137 extraction wound sites on upper jaw of 77 rats. Compounds evaluated: 3 tetracyclines (oxytetracycline 250mg IM or PO, & chlorotetracycline 250mg), 2 corticosteroids (cortisone 50mg IM, prednisolone 50mg IV), 3 fluorides (NaF 2%, SnF 1%, SnF 10%) and penicillin-streptomycin. All medications were agitated 1 min into extraction sites when bleeding had diminished but before clotting could begin. Controls were saline or no treatment. Animals were sacrificed at days 1,2,3,7,10,14,21

Results: Control: Normal healing pattern

Fluorides: 1% and 2% solutions: Inhibited resorption process by day 5, bone formation remained unaffected. 10% solution: Toxic effects upon connective tissue and inhibition of bone resorption.

Corticosteroids: Increase resorptive process with appearance of many osteoclasts. Delayed filling in of the socket with trabecular bone. Effects were no longer evident by day 14^th.

Tetracycline: Acceleration of bone deposition without depressing osteoclastic activity. Stimulant to new bone formation

Pen-Streptomycin: No observable effect

BL: Fluoride had depressing effect upon bone and root resorption. Tetracycline had osteogenic action.

Teofilo 2001                     ARTICLE

Purpose: To investigate whether amlodipine- second-generation calcium antagonist used for tx of HTN and angina, interferes with healing of rat alveolar bone.

M&M: 55 wistar rats received oral doses of an aqueous solution of amlodipine besylate starting 12 days before tooth extraction and continuing until death. Contrls received H2O. On 13^th day of tx, upper right incisors were extracted. Immediate after sx gingiva was sutured. Maxilla dissected out @ 7,14,21,42d post ext.

Results: Various phases of alveolar healing were recognized by histological exam in control and tx rats. End of first week, immature bone trabeculae lined with osteoblasts were found side by side with remnants of coagulum and abundant connective tissue rich in newly formed capillaries (granulation tissue). 2^nd week, the alveolar socket was occupied equally by connective tissue and bone trabeculae. 3^rd week; the socket was occupied by a network of thick trabeculae, surrounding medullary spaces filled with loose connective tissue.

20-30% decrease in bone volume fraction in the alveolus of treated rats, 7-35% higher volume fraction of CT and a tendency toward an increase in the volume fraction of persisting coagulum was reported as compared to controls.

BL: Ca- channel blocker amlodipine in this study showed a delay in alveolar bone healing.

What are some risk factors for bone loss? How are systemic factors able to influence bone metabolism? Are there any specific factors that can inhibit alveolar bone loss?

Grossi 1995                     ARTICLE

P: To identify risk indicators for periodontal disease.

M&M: 1,361 subjects (696F/ 665M), ages 24-75 years were included. All subjects completed demographic-medical-smoking questionnaire and received complete intraoral examination (assessment of soft tissue, dental caries, supra-g plaque, BOP, sub-g calculus, PD, CAL). Radiographic evaluation included 10 intraoral radiographs (4 posterior vertical bitewings, 6 anterior periapicals). Radiographic alveolar bone loss was measured. CEJ-alveolar crest distance was measured. Subjects with a mean distance of <2mm are defined as healthy. According to BL, 4 categories were formed: healthy (0.4-2mm), low (2-3mm), moderate (3-4mm) and severe (4mm). Age was stratified into 5 decades (25-34, 35-44, 45-54, 55-64, and 65-74 years of age), gender (male/female), race (black, white, Native American, Asian or Pacific Islander), smoking (number of packyearsnumber of pack of cigarettes/day number of years smoked). Number of packyears ranged from 1 to 150, stratified into 5 categories (non-smoker, very light or occasional smoker (>0 to 5.2 packyears), light (5.3 to 15 packyears), moderate (15.1 to 30 packyears) and heavy smokers (30.1 to 150 packyears)). Sub-g plaque samples were taken and analyzed with immunofluorescence microscopy.

R: Sample included 51% females, 49% males, 90% whites, 6.5% blacks. All other races represented 2.6% of the study population. Age was positively associated with BL. 77% of the younger individuals were in healthy group compared to 3.2% in the severe BL group. 9.2% of the older subjects were in the healthy group compared to 27% in the severe group. Smoking was significantly associated with severity of alveolar bone loss. 56% of the non-smokers were in healthy group as compared to 7.5% who were in the severe BL group. In contrast, 9.2% of the heavy smokers were in the healthy group compared to 35.2% who were in the severe BL group. There was also a strong positive relationship between BL and amount of smoking. The heavy smoker had an odds ratio of 7.28, more than double that of the light smoker (3.25). Males had higher odds (1.29) for more severe BL than females. Asian, Pacific Islanders or Native Americans had 2.40 times higher odds for exhibiting severe BL compared to Whites. The presence of sub-g P.gingivalis (1.73) or T. forsythia (2.52) was associated with higher odds for more severe BL.

BL: Severity of alveolar bone loss is associated with increasing age, smoking, race and colonization with sub-g T.forsythia or P.gingivalis.

Lesser and Krook 1974                     ARTICLE

P: To offer a new definition: The initial lesion in periodontal disease is due to an excessive resorption of alveolar bone as a localized accentuation of a generalized osteopenia, due primarily, but not exclusively, to a dietary calcium deficiency.

D: Concepts discussed:

1. Osteocytic osteolysis = a major mechanism of bone resorption; maintains calcium homeostasis.

2. Bone flow = hard tissue is constantly being replaced from areas of apposition to areas of resorption.

3. Parathyroid hyperplasia = hyperactivity of parathyroid leading to increase bone resorption.

The initial bone resorption in periodontal disease is a local effect of a generalized osteopenia, due to dietary calcium deficiency. An imbalance between low Ca levels accompanied with high Phosphorus levels. The process will be explained by this sequence: Low Ca Diet  excessive PTH secretion  excessive osteolysis.

Bone loss occurs first in the lamina dura. The loss will be intermittent,of short duration, but over a long period of time.

The bone will be replaced by fibrous tissue, which leads to a rubbing of the tooth against the gingival tissue, leading to irritation and inflammation; irritated gingival tissue leads to gingivitis. Infection, inflammatory osteoclastic resorption, and immune response are secondary to the initial osteolytic lesion in the alveolar bone. The osteolysis continues unless the dietary imbalance is corrected. Calcium-intake treatment has shown to allow and improvement in some patients with perio disease.

BL: Authors believe that periodontal disease is an initial sign of underlying calcium deficiency and that it is secondary to an initial osteolytic lesion in the alveolar bone.

Williams 1988                     ARTICLE

P: To study the effect of ibuprofen as an inhibitor of alveolar bone resorption in beagles.

M&M: Over 13 months, 22 beagles (with naturally occurring moderate to severe periodontal disease) were studied. After a 6 month pre-treatment baseline period, groups were established (so that the mean rate of alveolar bone loss during the pre-tx period was similar for each group): 1) control group -- 6 dogs, placebo; 2) 6 dogs -- 4 mg/Kg ibuprofen; 3) 5 dogs -- 4 mg/Kg sustained release (SR) ibuprofen; 4) 5 dogs -- 0.4 mg/Kg ibuprofen. Standardized x-rays taken at 0, 3 months and 6 months pre-treatment, as well as at 4 months and 7 months during treatment. Bone loss was calculated using a computer digitizer.

R: Pre-treatment bone loss for all dogs was approx. 1%/month. Bone loss for controls showed a 38% increase in the rate of bone loss from baseline. The 4.0 mg/Kg (SR) ibuprofen and 4.0 mg/kg ibuprofen groups showed a 70% and 50% decrease in the rate of bone loss, respectively, compared to baseline. This was SSD. The 0.4 mg/kg ibuprofen group also showed a 50% decrease in rate (all three ibuprofen treated dogs had significantly less bone loss than control).

BL: Ibuprofen administered orally, daily, inhibits alveolar bone loss in beagles. The (SR) ibuprofen inhibits bone loss as well or better than flurbiprofen (NSAID) observed in previous studies (Williams, 1987). The effect of ibuprofen is dose related.

Cr: The numbers are so small it is difficult to measure accurately, even with standardized xrays) to truly find significance (1% bone loss per month for 6 months in pre-tx group).

Jeffcoat 1995                     ARTICLE

P: Compare the progression of alveolar bone loss in a test group of adult periodontitis pts receiving topical NSAID therapy and systemic NSAID therapy.

M&M: Adult periodontitis patients (n = 55) (30 – 50% bone loss, PD 5 – 8mm) were studied in this 6-month randomized, double blind, parallel, placebo and positive-controlled study. Each patient had a least 3 sites at high risk for bone loss as assessed by low dose bone scan. Groups, balanced for gender, were assigned to one of three regimens: bid ketorolac rinse (0.1%) (pyrrolo-pyrolle carboxylic acid class of NSAIDs) with placebo capsule (topical test group); 50 mg bid flurbiprofen capsule (positive control) with placebo rinse; or bid placebo rinse and capsule (negative control group) . Prophylaxes were provided every 3 months. Monthly examinations assessed safety, gingival condition, and gingival crevicular fluid. Standardized radiographs were taken at baseline and at 3 and 6 months for digital subtraction radiography (measured change in alv bone height).

R: A significant loss in bone height was observed during the study period in the placebo group (-0.63 +/- 0.11; P < 0.001), but not in the flurbiprofen (-0.10 +/- 0.12; P = 0.40) or ketorolac rinse (+0.20 +/- 0.11 mm; P = 0.07) groups. ANOVA revealed that ketorolac and flurbiprofen groups had less bone loss (P < 0.01) and reduced gingival crevicular fluid levels (P < 0.03) compared to placebo. ANOVA suggests (P = 0.06) that ketorolac rinse preserved more alveolar bone than systemic flurbiprofen at the dose regimens utilized.

BL: Data indicates that ketorolac rinse may be beneficial in the treatment of adult periodontitis

What are the different types of bone loss and bony defects? Are they evenly distributed throughout the mouth? How are bony defects categorized? If these patients are maintained, is there a difference in progression of bone loss between horizontal and vertical defects?

Larato  1970                   ARTICLE

Intrabony defects in the dry human skull

Purpose: 1.To determine the most common three-walled intrabony lesions, 2. Whether the number of intrabony defects increases with age, 3. Whether intrabony lesions also occur in the jaws of young children.

Material and methods

-337 dry human skull specimens of European and Mexican origin ranging from 2-60 y.o. were examined

-Skulls were divided into 5 age groups: 2-16, 17-29, 30-44, 45-59, 60 and older.

-Each skull had at least 28 teeth or 20 decidous teeth in children skulls.

Results

-of 337 skulls, 86 had intrabony lesions

-Of the 86, 191 individual 3 wall defects

Discussion

-The most common location is interproximal bone mesial to a maxillary second molar and a

mandibular third molar.

-The number of skulls with defects increased with age up to 44 years

BL: Intrabony defects ara most commonly found in bone mesial to the second and third permanent molars of the maxilla and mandible. The percentage of skulls exhibiting intrabony defects increases from age 2 to 44. After that the percentage stays the same. Skulls of 60 plus age tend to have on an average more intrabony defects than skulls of younger groups. Children’s skulls (only deciduous teeth) also exhibit intrabony lesions due to periodontal disease.

Manson 1974                     ARTICLE

Purpose: To record the location of bone defects associated with chronic periodontitis in patients undergoing periodontal surgery for pocket elimination.

Materials and methods: 30 patients, 8 males and 22 females b/w 27-65 years. All patients had probings of 4-10mm and generalized alveolar bone loss shown in radiographs. Osseous defects were noted and recorded at the time of flap surgery by one examiner and classified as:

1. Thickened margin

2. Interdental crater

3. Hemiseptum

4. Infrabony defect with 3 osseous walls

5. Infrabony defect with 2 osseous walls (other than crater)

6. Infrabony defect with one wall (other than hemiseptum)

7. Marginal gutter

8. Furcation involvement

9. Irregular bone margin

10. Dehiscence

11. Fenestretion

12. Exostosis

Results/ BL:

• 58 segments were operated and 176 osseous defects investigated. 35 maxillary segments with 111 defects and 24 mandibular segments with 65 defects. (3.2 defects per segment in the maxilla and 2.7 defects per segment in the mandible).

• Bone resorption in an infinite variety of patterns and bone defects do not always conform to the standard shapes under which they are classified. Three main groups of defects are clearly distinguishable (intra – alveolar defects, marginal defects and perforations).

• Furcation involvement is slightly more often in the mandible.

• Interdental crater: was found to represent one – third (35.2%) of all defects recorded, and about two-thirds (62%) of all mandibular defects. It is more common in the posterior areas.

• Intra – alveolar defects other than interdental craters occur almost exclusively in the maxilla.

• Alveolar margin defects were found much more frequently in the maxilla and in the posterior segments. No exostoses were found in this study.

• Three dehiscences found and no fenestrations.

Distribution of the various defects appears to support the idea that they reflect the original bone morphology, although in this study occlusal forces and other factors such as food impaction were not investigated.

Nielsen 1980                     ARTICLE

P: To study the distribution of IP periodontal intrabony defects as related to age, sex and localization, and to examine the relationship between some possible etiological factors and the occurrence of intrabony defects.

M&M: 209 adult patients presenting for dental treatment. The patients were subjected to a questionnaire and were examined clinically and radiographically. All osseous defects in the radiographs were recorded but only those with a depth and width of a least 2 mm were considered periodontal intrabony defects.

R: Only 18% of the participants had one or more periodontal intrabony defects but the prevalence was higher in older than in younger age groups. While defects occurred with the same frequency on the various tooth types, more defects were found on distal than on mesial surfaces and most frequently in the mandible. The presence of periodontal intrabony defects correlated with loss of attachment, increased tooth mobility, a wide interproximal space and open mesio-distal contact relationships between the teeth. NSSD regarding bruxism, smoking habits or food impaction.

BL: The scattered distribution of intrabony defects observed in this study may very well be explained by the establishment of a particular pathogen flora on individual tooth surfaces.

*Note: Manson found more intrabony defects in the max. Gilmore more in the mandible. Larato found more defects on the M surfaces. This study may underestimate presence of intrabony defects because B or L defects may not be detected.

Karn 1984                     ARTICLE

Purpose: To describe a system of nomenclature for alveolar deformities.

Discussion:

1. Crater: Bone loss on only 1 surface of tooth. May be confluent, if they occur on adjacent proximal surfaces (so called 2 surfaces craters).

2. Trench: Bone loss on 2 or 3 surfaces of the same tooth. Described by the surfaces involved.

3. Moat: Bone loss on all 4 surfaces of the tooth.

4. Plane: Alveolar bone & supporting bone lost, such that the margins of the deformity are @ same level (aka Horizontal loss).

5. Ramp: when both alveolar bone & its supporting bone are lost to the same degree in such a manner that the margins of the deformity are @ different levels. They are named for the tooth surface aspect from which the greatest bone loss has occurred.

Vrotsos 1999                     ARTICLE

P: Evaluate prevalence and distribution of different forms of bone defects on pts with moderate-advanced p-itis using direct observation during perio sx.

M&M: 286 pts w/moderate-advanced dz needing flap Sx. 5,476 teeth were examined and osseous defects classified during FTF Sx.

R: Of the 5,476 sites there were 981 bony defects (18% of sites) classified as either 1-,2-,3-,4- wall, hemiseptal or crater type defects. Combination defects were classified as to the dominant type. Of the defects charted, 55% were found in maxilla, 45% in mand; Of the teeth that had defects, 34% were in post mand vs 20% were in post max; NSD in proportion of defects in anterior segments b/w max & mand.

Percent of defects

BL: Craters are most common; majority of defects are found in the posterior sextants with mand posterior having the most defects. Proper classification is important for regeneration purposes.

Prichard 1969                     ARTICLE

P: To discuss the etiology, diagnosis and treatment of the intrabony defect.

D: Defects in interalveolar bone can be classified by their morphology as intrabony defects, hemisepta or craters. A crater is a wide mouthed cup or bowl defect in the interalveolar bone. The side walls of a crater are formed by marginal bone on the vestibular and lingual surfaces. Periodontitis may affect one tooth and destroy septal bone adjacent to that tooth without affecting the adjacent tooth thus leaving a hemiseptum of interalveolar bone. The intrabony defect is surrounded by bony walls on 3 sides with the tooth root forming the 4^th wall. The walls may be at different levels coronally forming combinations with other defects but only the “inside” of the defect, the part that is apically to all 3 bony walls, is “within bone” or intrabony. It is not a circumferential defect, there is an osseous wall or stop on each side of the root. The topography of osseous defects depends on the form of dental arches, the vascular pathways, the nature and severity of the irritant and trauma from occlusion. Where the arch is wide, craters and intrabony defects predominate, but in the narrow arch the margin is destroyed as the defect develops causing an inconsistent margin which may be associated with an IPx crater or a hemiseptum.

Diagnosis: clinical examination (PD), X-rays, (shows vertical bone loss but not width of the alveolar process). Only visual examination during surgery shows exact morphology of the defet.

Therapy: The objective of the therapy for the intrabony defect is reconstitution of the periodontium by new bone, new attachment, PDL and cementum.

• Debridement and removal of all granulation tissue. If calculus is not present on root surface only light scaling is done. It is preferable not to remove the cementum, since it forms on old cementum more readily than on dentin.

• Occlusal adjustment if periodontal traumatism is present. Inclined planes are reduced so occlusal forces will be directed in line with the long axis of the tooth. Consistent marginal ridges are established. Splinting is rarely necessary.

• Therapy for the pulp: if pulpitis is present the canals should be disinfected, but they should not be obturated until several weeks after intrabony surgery. Based on clinical experience.

• Wound protection: after suturing, foil is adapted over the occlusal surface and dressing is applied. Antibiotic should be started the day before surgery to provide a proper blood level before surgical manipulation of tissue in the presence of infection.

Pocket elimination is more certain if the mucogingival flap is sutured snugly against the tooth root and the bone so that it just covers the marginal and interalveolar crest of the bone.

Pontoriero Nyman Lindhe 1988                     ARTICLE

P: To evaluate long-term alterations of the alveolar bone level at periodontal sites with angular (vertical) or even patterns (horizontal) of bone loss in patients following treatment for advanced periodontal disease.

M+M: Retrospective study. 48 pts (26-66 yrs old) treated for periodontitis were placed on recall interval of 3-6 months for a period of 5-16 yrs. 100 teeth from these patients had radiographic vertical defects associated after treatment (test sites). Contralateral or neighboring teeth with horizontal bone loss were used as controls to assess alveolar bone level changes. Radiographs were compared from immediately after treatment to follow up exam 5-16 yrs later. Lens with 2x magnification and the Bjorn technique.

R: Found only minor, NSSD bone level alterations during the 5-16 yr period. Any loss of bone was the same for angular and horizontal defects.

BL: Same amount of bone loss in horizontal as vertical defects with 3-6 month maintenance. Angular defects are not particularly susceptible to further bone loss if patient periodontal disease is treated and is well maintained.

Is there any way to evaluate bony defects prior to surgical access? Is this an accurate estimator of alveolar bone level?

Greenberg 1976                     ARTICLE

P: To determine whether bone sounding is valid for localizing the most coronal level of supporting bone at selected points along the dental arch.

M&M: 32 pts scheduled for flap Sx. Michigan probes were used on buccal surfaces only of “easily accessible teeth”. A rubber stop was fixed to the probe and a measurement was realized from the occlusal edge to the gingival crest (FGM). The stop was then removed and a measurement was made from ging crest to bone. These two measurements were added. After flap reflection and wound debridement, the distance from the occlusal edge to the bone crest was taken. Cusp tips and/or buccal grooves were utilized to aid in duplicating the position of the probe pre- and post-op.

R: The match-up of transgingival sounding and flap measurements was extremely close (max difference of about 0.25mm), NSD between the two. Even the presence of dehiscences did not affect the accuracy of the bone sounding.

D: The utilization of this technique may potentially replace re-entry to evaluate sx procedures, especially when grafting was performed.

BL: Bone sounding is an accurate way to evaluate the position of the alveolar crest without exposing the bone surgically.

Cr: Only buccal surfaces probed. Authors infer that this applies to other tooth surfaces.

Ursell 1989                 ARTICLE

P: To investigate the relationship between measurements of alveolar bone levels obtained by transgingival probing and at surgery on a wide range of tooth types and sites with varying degrees of inflammation and to investigate the relationships between the above measurements and clinical attachment level measurement using forces of 30 g and 60 g at the same sites.

M & M: 9 periodontal patients aged 20-59 years (2 male and 7 female). All had received OH instructions, and SRP prior to the study; 178 sites were studied (59 situated on incisor and canine teeth, 70 on premolar and 49 on molar) and 6 measurements were made on incisor, canine and premolar, and 8 for molar area. Acrylic stent was used to provide maximum guide for the sensitive probe. Probe markings were at 3-10mm at 1mm intervals, and at 13, 14 and 15mm. PDs were recorded initially with load of 30g, and 60g was used with local anesthesia, and then switched off load sensitive circuit and advanced through the tissues until bone was felt.

R: There was a SSD of 0.52 +/- 1.21mm (p<0.001) between PD measured using loads of 30g and 60g. The differences between transgingival and surgical measurements of alveolar bone height were not SSD. Transgingival probing was found to be most accurate estimator of alveolar bone levels. The correlation coefficients between transgingival and surgical measurements of bone levels were similar for different tooth types, as were those between attachment levels and bone levels measured at surgery. Reproducibility was found of 93.25%, of measurements being within 1mm.

BL: From this study, transgingival probing measurements of crestal bone levels showed to give an accurate indication of bone levels measured at surgery.

Can anatomic factors affect the type of bone loss seen in patients?

Heins 1986                 ARTICLE

A histologic study of the width and nature of inter-radicular spaces in human adult premolars and molars

Purpose: to investigate the histologic nature and relative incidence of various interproximal widths in a human population

Material and methods

- Location of the site along the root surfaces where adjacent roots were nearest each other, dimensions of this inter-root distance, & the consequence of variable inter-root distances upon the bony septum and PDL at these sites.

-Dentulous posterior maxillae and mandibles of adult humans.

-Blocks containing 2-3 teeth were removed postmortem

-Interproximal sites from 29 individuals 26-65 YO

-116 second premolar/molar and first molar/second molar interproximal spaces

Results

-Inter-radicular bone and periodontal ligament observations

-With 3 exceptions all root surfaces of adjacent teeth were separated by bone and periodontal ligaments (lamina dura and cancellous bone)

-Cancellous bone was observed between the laminae dura separating adjacent teeth in instances where the roots were greater than 0.5mm apart, but not observed between the adjacent lamiae dura where the inter-root distance was less than this dimension, instead the single lamina dura appeared to be thicker than normal

-3 areas showed no bone between them. This occurred where the interradicular distance was less than 0.3 mm

-The mean widths of the periodontal ligaments were 0.23mm in the coronal third, 0.12 mm in the middle third and 0.17 mm in the apical third.

Discussion

-Cancellous bone and lamina dura appears to be present between adjacent roots when the inter-root distance is 0.5mm or greater

-Further reduction of the inter-root distance to less than 0.3 mm appears to preclude the existence of any bone, instead, adjacent root surfaces are connected by a periodontal ligament

-At these sites, the inter-root dimensions were approximately twice the width of a typical periodontal ligament

-Fenestration appears to be a function of inter-root distance.

Tal 1984             ARTICLE

Purpose: To investigate possible correlations between interproximal distances of adjacent roots and the frequency of intrabony pockets facing these roots.

Materials and methods: 81 patients (43 males and 38 females) scheduled for periodontal surgery at NYU dental school. Age 24-69 years. 58 surgeries on the maxilla and 56 on the mandible. 374 interproximal distances between two adjacent root surfaces were measured and presence of 117 intrabony pockets in relation to the root surfaces with which they were associated was recorded. Statistical analysis was performed.

Results: Percentage of OBP increased with increasing interproximal distance with a positive and significant correlation between the two. When interdental distances greater than 2.1m and less than 4.1mm were considered separately, the slope was steep and correlation high and significant. Correlation was negative and non significant when distances greater than 4.6mm were considered.

IBP in both adjacent roots ranged between 2.7 to 25% and never occurred when their distance was less than 3.1mm.

In the maxilla IBP were more associated with 1^st premolars followed by canines, molars and central incisors. In the mandible canines and lateral incisors were most commonly associated with IBP followed by molars, premolars and lastly by central incisors.

Discussion/BL: Complete (horizontal) destruction of interdental septae appeared to be negatively related to their thickness (less than 5% IBP associated with distances less than 1.6mm).

Greater distances were associated with increased frequency of intrabony defects and the correlation is not significant for distances greater than 4.6mm

Heins, 1988             ARTICLE

P: To examine the relationship between interradicular width and the extent of bone loss using a continuous scale of measurement.

M&M: Radiographs of 114 adult patients with evidence of bone loss consistent with periodontitis were examined. Measurements of interradicular width and the location of the bone margin from the CEJ were made at 811 interproximal sites using an optical digitizer at 3X magnification. The relationship between bone loss and interradicular width was investigated.

R: The results indicate that as the interradicular width increases, the interproximal bone margin tends to be in a more apical location. When the data were separated into various tooth group combinations, they showed the positive correlations were localized primarily to the anterior and premolar and premolar tooth group. Site-by-site analysis showed no positive or negative correlations. No findings supported the contention that bone in a narrow interradicular space is at greater risk in patients who have had periodontitis.

BL: Narrow interproximal spaces do not experience greater bone loss than do wider spaces.

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