Discussion Topics
A. What are the various modes of intercellular attachment? Draw and label a hemidesmosome.
B. Is a gingival sulcus necessary and/or desirable?
C. What is the “biologic width” and what is its significance?
D. What is the turnover rate of the oral epithelia? Draw and label the exfoliation of the cells of the junctional epithelium.
E. What is the embryogenesis of the junctional epithelium?
F. Define primary and secondary junctional epithelium.
G. How does the junctional epithelium heal after excision? After incision?
H. Can and/or should sulcular epithelium be keratinized? Why?
I. Describe the changes that occur in the junctional epithelium at the light and electron microscope level during gingivitis and periodontitis development.
How does a periodontal pocket form?
Anatomy and Development
1. Kobayashi K, et al. Ultrastructure of the dento-epithelial junction. J. Periodontal Res. 11:313-330, 1976
2. Stern IB: Current concepts of the dentogingival junction: the epithelial and connective tissue attachments to the tooth. J. Periodontol. 52:465-476, 1981.
3.Ten Cate AR: The dento-gingival junction. An interpretation of the literature. J. Periodontol. 46:475-477, 1975. (Review)
4. Pollanen MT., Salonen JI, Uitto VJ. Structure and function of the tooth –epithelial interface in health and disease. Periodontl 2000. 2003; 31:12-31
5. Hujoel PP, White BA, Garcia RI, Listgarten MA. The dentogingival epithelial surface area revisited. J Perio Res 36:48-55, 2001.
6. Messer RL, Davis CM, Lewis JB, Adams Y, Wataha JC. Attachment of human epithelial cells and periodontal ligament fibroblasts to tooth dentin. J Biomed Mater Res A. 2006 Oct;79(1):16-22.
Can you quantify inflamed periodontal tissues?
7. Nesse W, Abbas F, van der Ploeg I, Spijkervet FK, Dijkstra PU, Vissink A. Periodontal inflamed surface area: quantifying inflammatory burden. J Clin Periodontol. 2008 Aug;35(8):668-73. Epub 2008 Jun 28.
Describe the dimensions of the DGJ and the significance of the “biologic width” in dentistry.
8. Garguilo, A., et al: Dimensions and relations of the detogingival junction in humans. J Periodontl 32: 261-267, 1961
9. Vacek, J.S., et al: The dimensions of the human dentogingival junction. Int J Perio Rest Dent 14: 155 – 165, 1994
10. Perez J, Smukler H, Nunn M. Clinical dimensions of the supraosseous gingivae in healthy periodontium. J Periodontol 2008; 79: 2267 – 2272
11. Novak MJ, Albather HM, Close JM. Redefining the biologic width in severe generalized, chronic periodontitis: Implications for therapy. J Periodontol 2008; 79: 1864
Describe the pocket epithelium
12.Muller-Glauzer W, Schroeder HE. The pocket epithelium: A light and electron microscopic study. J. Periodontol. 53:133-144, 1982.
What are the characteristics of the junctional epithelium, including its structure, function, turnover rate?
13. Hatakeyama S, Yaegashi T, Oikawa Y, Fujiwara H, Mikami T, Takeda Y, Satoh M. Expression pattern of adhesion molecules in junctional epithelium differs from that in other gingival epithelia. J Periodontal Res. 2006 Aug;41(4):322-8.
14. Bosshardt DD, Lang NP. The junctional epithelium: from health to disease. J Dent Res. 2005 Jan;84(1):9-20. Review.
Wound Healing
15. Taylor AC, Campbell MM. Reattachment of gingival epithelium to the tooth. J Periodontol. 43:281-293, 1972.
16. Listgarten MA. Ultrastructure of the dento-gingival junction after gingivectomy. J. Periodontal Res. 7:151-160, 1972.
17. Braga AM, Squier CA : Ultrastructure of regenerating junctional epithelium in the monkey. J. Periodontol. 51:386-392, 1980.
18. Tomofuji T, Sakamoto T, Ekuni D, Yamamoto T, Watanabe T. Location of proliferating gingival cells following toothbrushing stimulation. Oral Dis. 2007 Jan;13(1):77-81
What is the significance of keratinization of sulcular epithelium?
19. Caffesse RG et al: The effect of mechanical stimulation on the keratinization of sulcular epithelium. J. Periodontol. 53:89, 1982.
20. Squier CA: Keratinization of the sulcular epithelium – a pointless pursuit? J. Periodontol. 52:426-429, 1981.
Epithelial Rests
21. Grant DA, Bernick S. A possible continuity between epithelial rests and epithelial attachment in miniature swine. J. Periodontol. 40:87-95, 1969.
22. Spouge JD. The rests of Malassez and chronic marginal periodontitis. J Clin Periodontol 11: 340-347, 1984.
23. MacNeil RL, Thomas HF. Development of the murine periodontium. II. Role of the epithelial root sheath in formation of the periodontal attachment. J Periodontol 1993;64:285-291.
24. Rincon JC, Young WG, Bartold PM. The epithelial cell rests of Malassez–a role in periodontal regeneration? J Periodontal Res. 2006 Aug;41(4):245- 52. Review.
25. Shimonishi M, Hatakeyama J, Sasano Y, Takahashi N, Uchida T, Kikuchi M, Komatsu M. In vitro differentiation of epithelial cells cultured from human periodontal ligament. J Periodontal Res. 2007 Oct;42(5):456-65.
26. Becktor KB, Nolting D, Becktor JP, Kjaer I. Immunohistochemical localization of epithelial rests of Malassez in human periodontal membrane. Eur J Orthod. 2007 Aug;29(4):350-3. Epub 2007 Jul 2.
Topic Overview
:to present new data on the dento-epithelial junction.
The dento-epithelial junctions of 5 Rhesus monkeys were examined by SEM. After making gingival incisions teeth with intact gingiva including the margin of the alveolar bone were excised and examined with electron microscope.
The junctional epithelium contacted the enamel, the afibrillar cementum covering the enamel surface and the root cementum (fibrillar cementum). Multiple hemidesmosomes were easily recognized along the cell membrane facing the tooth surface.
junctional epithelium consists of two basal laminae. Internal lamina towards the tooth and external lamina towards the connective tissue.
Attachment coronal to the CEJ :
Well developed dental cuticles were seen between the afibrillar cementum overlying the enamel and the junctional epithelium. Some areas had no evident dental cuticle. Where the JE apposed the afibrillar cementum without an intervening dental cuticle, there was between the basal lamina and the afibrillar cementum a thin dense line, the linear border.
Junctional epithelium:
Internal Basal lamina: Lamina lucida, lamina densa, sublamina lucida
The lamina lucida occupied the narrow space between the peripheral density and the lamina densa. The lamina densa appeared suspended between the lamina lucida and the clear sublamina lucida. The sublamina lucida lay between the lamina densa and the linear border or the dental cuticle. The border between the dental cuticle and the subjacent afibrillar cementum was highly irregular and unclear. Linear border was not defined in areas where the dental cuticle was well developed. However, the linear border was sharply evident between the enamel and sublamina lucida, between the enamel and the dental cuticle and between the afibrillar cementum and the sub-lamina lucida.
Attachment apical to the CEJ
Basal lamina retained a uniform width. In some cases, the surfaces of the root cementum were covered with a dental cuticle of great thickness variation. The hemidesmosomes were larger than those apposing the basal lamina of the oral epithelium and were sharply outlined along the surfaces of the junctional epithelium. In all specimens the attachment of the lamina densa to the root cementum or the dental cuticle was mediated by a thin clear space, the sub-lamina lucida. The linear border was especially evident in areas devoid of the dental cuticle and where the root cementum lacked collagen fibrils. It was never observed between fibrillar cementum and the basal lamina or dental cuticle. Where the dental cuticle came in contact with afibrillar cementum, this line could not be detected.
Special Considerations of the Denial Cuticle and Hemidesmosomes
Under high-power electron microscopy the dental cuticle may be described as a relatively homogeneous, somewhat granular and electron-dense layer.
Throughout these observations, the hemi-desmosomes were well-preserved regardless of the fixation procedure used. In high- power views of selected areas, details of the hemidesmosomes contained dense pyramidal particles along the inner surface of the peripheral density. Fine filaments extended from the peripheral density into the lamina densa.
CONCLUSION: The investigation has once again confirmed the concept that an attachment apparatus consisting of multiple hemidesmosomes and a basal lamina promotes adhesion of the JE to the teeth. This attachment apparatus behaves as a unit which is maintained a short distance from the teeth or dental cuticle by an intervening sub-lamina lucida.
Review article discussing all the history and current concepts of the dentogingival junction (DGJ; the epithelial and CT attachments).
Overall concept is that the DGJ is dynamic rather than static, with a high rate of turnover. Primary junctional epithelium is derived from ameloblasts. During ameloblast histodifferentiation the cells pass through two phases: forming enamel in the first, and primary junctional epithelium in the second. In the ameloblast life cycle, after the enamel matrix secreting and mineralizing stages of amelogenesis, the ameloblasts become smaller, terminate the enamel-forming function, and begin to form the epithelial attachment.
Secondary junctional epithelium is derived from gingival epithelium.
Basal lamina is composed of lamina densa (composed of epithelium and CT interfaces) and lamina lucida (between outer leaflet of epithelial cell membrane and tooth it has important role in epithelial attachment).
Intracellular edema decreases desmosomes and disruption of CT facing basal lamina.
Pocket formation is associated with a loss of cellular continuity in coronal portion of JE.
Healthy JE – no Rete pegs, Diseased – rete pegs, Return to health – Rete pegs remain.
The DGJ shows a capacity to repair/regenerate following plaque elimination and resolution of inflammatory infiltrate.
Ten Cate 1975 No Article
P: To focus attention on the CT component of the DGJ and its possible significance in the etiology of periodontal disease.
D: CT is important in determining the development, structure, and function of epithelium. In embryology, the mesenchyme (embryonic CT) has a key role in determining the epithelial response (Billingham and Silvers;1968 and Slavkin; 1972). All epithelium responds in the same manner to a change in its surrounding CT. Before the tooth erupts, its enamel surface is covered by the reduced dental epithelium, which consists of an inner layer of reduced ameloblasts and an outer layer of polygonal epithelial cells. As tooth erupts and breaks through the oral epithelium there are 2 theories about the origin of the DGJ:
1. Basal epithelial cells, from the pool of epithelial cells over the erupting tooth, migrate apically over the reduced dental epithelium.
2. Reduced dental epithelium becomes JE as a result of epithelial transformation.
This JE is sig different from the gingival epithelium. It is non-keratinized, has a decreased nuclear-cytoplasmic ratio, a higher amount of rough endoplasmic reticulum, and has large extracellular spaces between the cells (18% of the epithelium total volume). JE has a higher rate of cell turnover compared to AG epithelium (Skougaard 1962). The CT supporting JE is different from the CT supporting gingival epithelium. The main difference is in the amount of collagen fibers, which are few in the CT supporting JE and presence of vesiculated fibroblasts. Many investigators have reported that inflammation is always present in CT supporting JE. At the time of eruption, the CT is removed and an acute inflammatory reaction occurs in this CT, therefore, it’s possible that the resultant JE exhibits most of the characteristics of epithelium supported by a disturbed CT. The wide intercellular spaces allow continued ingress of antigen, maintaining a low-grade inflammatory lesion. Attempting to keratinize the sulcular epithelium by repeated stimulation of the epithelial cells has proven to be ineffective. If the ideas proposed in this essay are correct, attention should be paid to modifying the CT, not the epithelium if a keratinized sulcular epithelium is desired.
BL: The CT of the JE dictates the epithelial changes.
Purpose: To review the factors associated with periodontal tissue protection and destruction with special reference to the junctional epithelial cells.
Discussion: Junctional epithelium: Several features that contribute to preventing pathogenic bacterial flora form colonizing the sub-g tooth surface. It is firmly attached to the tooth but allows access of GCF, inflammatory cells and components of the host defense to the gingival margin. It has rapid turnover rate.
Epithelial attachment apparatus: Hemidesmosomes at the plasma membrane of the cells directly attached to the tooth (DAT cells) and the internal basal lamina on the tooth surface. Internal basement lamina proteins include laminin and Type VIII collagen. Hemidesmosomes may act as specific sites of signal transduction and participate in regulation of gene expression, cell proliferation and cell differentiation. Turnover of the JE cells: JE has two layers. The basal facing the CT and the suprabasal extending to the tooth surface. The turnover rate in nonhuman primates is about 5 days and approximately twice the rate of the oral gingival epithelium. Data show that DAT cells have a more important role in tissue dynamics and reparative capacity of the JE than previously reported. Their phenotype may be affected by the internal basal lamina matrix on the tooth surface. The internal basement lamina appears to be relatively morphologically resistant to external challenges. It”s molecular structures may still be altered leading to changes in DAT cells function. JE in the antimicrobial defense: Although JE cells layers provide a barrier against bacteria, many bacterial substances pass easily though the external basal lamina into the CT. The area covered by the dividing cells in JE, is at least 50 times larger than the area through which the epithelial cells desquamate into the gingival sulcus which create a strong funneling effect. JE cells have been found to contain enzyme-rich lysosomes. The role of these enzymes is not completely studied yet. PMNs comprise probably the most important defense mechanism at the gingival margin. The cell surface carbohydrates expressed by the JE cells are thought to respond to extracellular changes and allow cells to communicate with their environment. JE cells may also secrete antibodies supplementary to system-derived antibodies and antibodies produced locally. Role of GCF: GCF is an exudate and contains components of serum, inflammatory cells, CT epithelium and microbial flora. In the healthy sulcus the amount of GCF is very small, but its constituents participate in the normal maintenance function of the JE. During inflammation, GCF increases and its composition starts to resemble that of an inflammatory exudate. It contributes to host defense by flushing bacterial colonies and their metabolites away from the sulcus. The main route for diffusion is through the external basement membrane and then through the JE in the sulcus. Bacteria and host-derived products found in GCF have been associated with the initiation and progression of periodontal disease. Role of PMNs: When they reach bacteria, they release contents of their granules and may adhere to individual bacteria to phagocytose them. They do not have the ability to remove dental plaque but rather form a protective wall against it. They can also cause tissue damage as a result of the variety of enzymes, oxygen metabolites and other components that are released from their granules. They have two main types of granules: the azurophilic (primary and the specific (secondary) containing different enzymes. Activated PMNs also generate H2O2 and highly reactive oxygen radicals with the potential to destroy bacteria and gingival cells. PMNs are more effective in aerobic conditions close to the gingival margin. Lactoferrin is an important antimicrobial protein present in the secondary granules of PMNs. Role of host proteinases and inflammatory mediators: Different cell types of periodontal tissues produce MMPs, plasminogen activator, cathepsins and elastase in response to bacteria and inflammatory mediators. At the same time, they also contribute to tissue destruction and to apical and lateral proliferation of JE in the CT. Regulation of proteinase activities is a complex process involving activation of latent precursor molecules as well as inhibition of the active enzymes. Cytokines IL-1, IL-6,TNF-and PG-E2 have been strongly associated with periodontal disease. Role of bacterial products: Bacterial substances have a multitude effect on several cell types, ranging from activation of cell functions to cell death. Lipoteichoic acids found mainly in Gram+ bacteria are thought to mediate bacterial adhesion to human cells and teeth. LPS and porin proteins of the walls of Gram- bacteria also cause several host responses. They stimulate leukocyte function, increase cytokine and inflammatory mediator production and activate the complement system. They also stimulate bone resorption, increase epithelial permeability and penetrate healthy gingival sulcular epithelium. Growth and mitotic activity of epithelial cells can be reduced because of lipoteicohoic acids, interfering with the renewal of JE leading to degeneration and detachment.
BGRecent studies implicating p-itis as cause of syst dzs have reported that the surface area of perio pckts exposed to bact biofilm ranges from 50-200 cm2. Since the root surf area of human dentition excluding 3rd M is 75 cm2, this estimate appear to be too large. The dentogingival surface area (DGES) comprise the JE & SE in health, & any pocket epi in dz.
P:To relate linear perio probing measurements to the DGES
M&M:Formulas to estimate the DGES from clinical and radiographic measurements were applied to a representative sample of a US adult pop 1985-86, a sample of 1021 indiv at their initial visit to a periodontist, and the participants of the VA Dental Longitudinal Study.
R:Individuals w/out periodontitis had a typical DGES of 5 cm2. In p-itis, the mean DGES in the 3 samples ranged from 8 cm2(from1-29 cm2) to 20 cm2 (from 2-44cm2).
D/BL:Depending on the pop studied, p-itis leads to a mean incr of 3-15 cm2 in DGES. The mean DGES among indiv w/p-itis ranges from 8-20 cm2, considerable smaller than the range of 50-200 cm2currently assumed. It needs to be shown whether absolute size of DGES or its incr in p-itis is of sufficient magnitude to represent a clin imp risk factor for syst health (if it’s causally related).
Messer 2006 No Article
P: To measure the rate and strength of attachment of human epithelial cells and periodontal ligaments fibroblasts to tooth dentin.
M&M: Rate and strength of attachment of epithelial cells and PDL fibroblasts were measured. They were cultured individually and co-cultured to dentin surfaces to determine which cell type has a faster attachment rate and greater adhesive strength to human dentin. Longitudinal dentin slices were seeded with either epithelial cells or PDL fibroblasts for 2-24 hrs. The specimens were placed into a parallel plate flow chamber. Effluent fluid was collected and detached cells were counted. Co-cultures of PDL fibroblasts and epithelial cells at 3 seeding ratios (10:1, 1:1, 1:10) were also tested.
R: PDL fibroblasts showed a stronger attachment to dentin at 24 hrs, while epithelial cells attached to dentin equally well at 2 and 24 hrs. Epithelial cells were strongly attached after 2 hrs when compared to PDL fibroblasts, but less strongly attached after 24 hrs. When epithelial cells and PDL fibroblasts were seeded together, at ratios
1) 1:1, PDL fibroblasts appeared to be more strongly attached at 2 but not 24 hrs
2) 10 (PDL) :1 (Epi), PDL fibroblasts appeared to be more strongly attached at 2 and 24 hrs
3) 1 (PDL) : 10 (Epi), Epithelial cells appeared to be more strongly attached at 2 hrs, but PDL fibroblasts showed a trend of stronger attachment at 24 hrs
Cocultures (PDL fibroblasts : Epithelial cells)
|
P > E |
P > E |
E > P |
|
|
24 hrs |
P > E |
P > E |
Summary of strength of attachment
Cultures
|
2 hrs PDLF |
||
|
24 hrs PDLF |
24 hrs |
BL: Epithelial cells attach more quickly to dentin surfaces than PDL fibroblasts, but do not demonstrate increased attachment strength over time. Epithelial cells and PDL fibroblasts do not act independently, because epithelial cells enhanced the attachment rate of PDL fibroblasts.
Can you quantify inflamed periodontal tissues?
To develop a classification of periodontitis (Periodontal Inflamed Surface Area –PISA-) and to evaluate its applicability in quantifying the amount of inflamed periodontal tissue.
A literature search was performed and revealed there were no classification systems that quantified the area of inflamed periodontal tissue. An Excel spreadsheet was developed that calculates PISA based on CAL, recession, and BOP. Population based mean values for both root surface area and root length are used in the Excel formula. Results reflect the surface area of bleeding pocket epithelium in square millimeters. Calculating PISA using Hujoel et al’s spreadsheet for ALSA;
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1-ALSA (attachment loss surface area) was calculated.
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2-RSA (recession SA) was calculated.
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3-ALSA-RSA=PESA (periodontal SA)
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4-BOP tested on six sites per tooth
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5-PESA multiplied by the BOP sites per each tooth = PISA (periodontal inflamed SA) e.g. if 3 surfaces are BOP+ then PISA for each tooth= PESA multiplied by 3/6)
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6- PISA for the whole mouth is the sum of PISAs of individual teeth.
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Then the system was applied to 3 pts; with healthy periodontium, local periodontitis and sever generalized periodontitis.
PISA measures the surface area of bleeding pocket epithelium in square millimeters. But it is not a precise tool because:
-PISA is subject to operator errors associated with measuring CAL and BOP.
– Actual patients are likely to differ from the population means used in the formula.
-Only quantifies in two dimensions and is less accurate when gingival overgrowth or pseudo pockets are present.
-Does not take into account type of inflammation or flora and therefore cannot be used to predict the diseases that inflammation might cause
PISA is a classification system with some short comings. However, it is more accurate than any other classification systems currently used for quantifying inflammation. May serve as a method of classification for associating periodontitis as a risk factor for other diseases.
Describe the dimensions of the DGJ and the significance of the “biologic width” in dentistry.
Garguilo 1961 No Article
To evaluate the measurements of the dentogingival junction during four phases of passive eruption.
: 30 jaws of human autopsies. A total of 287 teeth were measured. Measured surfaces: M, D, vestibular and oral. 6 measurements were made for each: 1) Depth of sulcus, 2) Length of attached epi, 3) Most apical point of epi attachment from the CEJ,
4) Distance from base of sulcus to CEJ, 5) Distance of CEJ from alveolar bone,
6) Distance from most apical point of epithelial attachment to alveolar bone (CT)
All surfaces were placed in one average value for the given measurement. They evaluated these measurements at four different phases of passive eruption. The following values were found:
|
Phase |
Avg. Age |
Length of dentogingival junction (mm) |
|
Phase I |
24.5yrs |
3.23mm |
|
Phase II |
31.4yrs |
3.06mm |
|
Phase III |
32.3yrs |
2.41mm |
|
Phase IV |
39.7yrs |
2.53mm |
The dentogingival junction is a functional unit with 2 components: 1) CT fibrous attachment and 2) epithelial attachment. As we age the total measurement of the DGJ decreases. During passive eruption the epithelial attachment diminishes. In correlating the epithelial attachment with age it is seen that there was less epithelial attachment with an increase in age; however, the CT component appeared to stay constant through all stages of passive eruption. The following table is the total average magnitude of 3 of the measurements taken:
|
Sulcus Depth |
0.69 mm |
|
Attached epithelium |
0.97 mm |
|
Connective Tissue |
1.07 mm |
Vacek 1994 No Article
PURPOSE: To provide information on the dimensions of the dentingingival junction (biologic width) and related structures.
METHODS: 10 preserved jaws from cadavers (age 54-78) were used to prepare 7 block segments of 2-3 teeth each. Block segments were sectioned first in a M-D direction along the long axis and contacts of the teeth. The remaining F-L portions were then sectioned B-L along the long axis of teeth. Sections were stained with Masson’s trichrome and eosin stain and histomorphologically measured with Zeiss interactive digital analysis system. Measurements recorded were sulcus depth (SUL), epithelial attachment (EA), connective tissue attachment (CTA), and loss of attachment (LOA).
RESULTS: There were no mean differences between measurements for the tooth surfaces (BLMD) for SUL, LOA, EA, or CTA. LOA did not affect the CTA, or biologic width. Molars showed a significantly greater biologic width than anterior teeth. Tooth surfaces with subG restorations had sig longer EA, but no other sig differences. Mean measurements: SD- 1.34mm, EA-1.14mm, CTA-0.77 mm, LOA- 2.92mm.
DISCUSSION: The CTA varied in width, but with a more narrow range and variance than EA, SUL, or LOA. SubG restored teeth showed a longer EA. No correlation could be found between LOA and width of biologic width (CTA). LOA should not be used as a guide to determine requirements for reestablishment of EA and CTA.. Biologic width was slightly wider in molars than anterior teeth, therefore these teeth may require a greater length of biologic width when restoring these teeth.
CONCLUSION/BL: No correlation was found between LOA and length of biologic width. Of the dimensions measured, CTA (biologic width) had the least amount of variance.
P: To provide and compare the clinical Supra Osseous Gingivae (SOG) dimensions around molar, premolar, canine, incisor teeth in the maxillary and mandibular arches as measured by trans-sulcular probing (TSP) in patients without a history of periodontitis.
M&M: 23 patients (mean age of 35 years), 8 males and 15 females were included in the study. SOG dimensions were evaluated around incisor and canine (zone 1), premolars (zone 2), molars (zone 3). Inclusion criteria: free of gingival hyperplasia and overt signs of inflammation, adequate plaque control, absence of altered passive eruption, no attachment loss or history of periodontitis. Clinical parameters (PI, GI, BOP, PD) were measured to establish gingival health. TSP was done using standardized periodontal probes, with marking-width differences <0.2mm. Calibration exercises to achieve >90% intraexaminer reproducibility of measurements were conducted before the study started. ANOVA was used for statistical analysis.
R: All clinical parameters were indicative of the absence of gingival inflammation. The overall mean of SOG was 3.75mm (vs. Gargiulo 1961, 2.73mm).
For the maxillary teeth, a statistically significant difference was found among SOG measurements by tooth type for mean overall and lingual dimensions. For mean facial SOG measures, the difference between SOG measures by tooth type approached statistical significance. When comparing site level measures of SOG by tooth type, statistical significance was found for mid-facial, disto-facial, mesio-lingual, mid- lingual, and disto-lingual measures.
For mandibular teeth, statistical significance was found among mean overall and mean lingual SOG measurements but not among mean SOG facial measurements when comparing by tooth type. When comparing site- level measures of SOG by tooth type, statistical significance was found for the disto-facial and the mesial-, mid-, and distal-lingual SOG measurements but not for the mesial- and mid-facial measurements.
For both arches there was a SSD for mean overall and mean lingual dimensions. SOG increased from anterior to posterior.
BL: The average 3mm figure used to estimate the amount of sound structure needed after crown lengthening to accommodate the restorative and SOG dimension should be considered to be pre-empted by the SOG dimensions of the particular tooth.
To determine whether previously observed norms in the biological width (BW) apply in a previously untreated population with severe generalized chronic periodontitis. The importance of understanding the variations in BW that may occur with periodontal pathology may impact our approach to surgical intervention in conserving the existing periodontal attachment is a clinical priority.
28 patients (29-45 years old) with severe generalized chronic periodontitis. Clinical and radiographic measurements (not standardized) were taken by calibrated examiners. BW was determined from most coronal level of clinical attachment to the crest of the alveolar bone for interproximal surfaces only and compared to the histological BW previously reported.
The clinical BW in subjects with severe generalized periodontitis was significantly greater than previously reported. The mean clinical BW was 3.95mm vs. mean histological width of 2.04mm. The greatest clinical BW was seen with pockets < 2mm with 5.02 mm BW. As PD increased, the associated mean BW tended to de-crease
|
Mean clinical BW in subjects with severe chronic periodontitis seemed to be significantly greater than the histologic BW previously reported for subjects not demonstrating significant periodontal pathology.
Describe the pocket epithelium
Muller-Glauser & Schroeder 1982 No Article
P: To examine the pocket epithelium: a Light microscope and Electron microscope study
M&M: 8 Beagle dogs with experimental periodontitis for periods of 4 to 21 days or up to 5 months were studied. Block biopsies of the 4th premolar buccal gingiva were excised and processed for LM and EM exam.
R: Pocket epithelium was displaced from the teeth by deep subgingival plaque, which was close to the apical termination of the pocket. The pocket epithelium had very irregular shape with rete pegs (RP) penetrating more than half of the infiltrated CT. Occasionally, rete pegs branched to form irregular network, (some portions of 2 cells only). Subepithilial CT was collagen poor, highly vascularized and infiltrated by leukocytes (mainly plasma cells).
Variable thickness of epithelium: at coronal and mid-pocket regions—thin and occasionally ulcerated. It was thicker apically.
Epithelial cells: pocket epithelium was non-keratinized. Atypical stratification.
Basal cells: cuboidal to cylindrical with characteristic flat processes along the basal lamina. Hemidesmosomes at the basal side, but mainly microvilli and gap junction laterally.
Suprabasal cells: Polygonal or elongated, more basophilic.
Superficial cells: Variably basophilic & electron dense. Numerous filament bundles. Low-density cells were seen only at the very surface, (often lacking cytoplasm. membrane). Microorganisms occasionally adhered to those cells.
Intercellular spaces: Mostly dilated spaces with infiltrated leukocytes, PMNs, lysosomes and cell fragments. Microorganisms in the superficial intercellular spaces with openings to the pocket space.
Basal complex: Consisted of Lamina Lucida, Lamina densa, and anchoring fibrils. Cytoplasmic projections from epithelial cells in areas of basal lamina discontinuity.
Infiltrations: Mainly by Lymphocytes T and B, and plasma cells (basal & suprabasa