12. Soft Tissues – Anatomy: Dentogingival Junction
lassical Periodontal Literature Review
Rapid Search Terms
Study Questions
- What are the various modes of intercellular attachment?
- What is a hemidesmosome? Where are they located in the dentogingival juction? Describe the components of it.
- Is a gingival sulcus necessary and/or desirable?
- What is the “biologic width” and what is its significance?
- What are the dimensions of the dentogingival junction?
- Can you quantify inflamed periodontal tissues?
- What is the turnover rate of the oral epithelia? Draw and label the exfoliation of the cells of the junctional epithelium.
- What is the embryogenesis of the junctional epithelium?
- Define primary and secondary junctional epithelium.
- What are the characteristics of the junctional epithelium, including its structure, function, turnover rate?
- How does the junctional epithelium heal after excision? After incision?
- Can and/or should sulcular epithelium be keratinized? Why?
- Describe the changes that occur in the junctional epithelium at the light and electron microscope level during gingivitis and periodontitis development.
- Describe the pocket epithelium.
- How does a periodontal pocket form?
- What is the role of the epithelial rests of Malassez in the periodontium?
Anatomy and Development
- Kobayashi K, et al. Ultrastructure of the dento-epithelial junction. J. Periodontal Res. 11:313-330, 1976
- Stern IB: Current concepts of the dentogingival junction: the epithelial and connective tissue attachments to the tooth. J. Periodontol. 52:465-476, 1981.
- Ten Cate AR: The dento-gingival junction. An interpretation of the literature. J. Periodontol. 46:475-477, 1975. (Review)
- Pollanen MT., Salonen JI, Uitto VJ. Structure and function of the tooth –epithelial interface in health and disease. Periodontl 2000. 2003; 31:12-31
- Hujoel PP, White BA, Garcia RI, Listgarten MA. The dentogingival epithelial surface area revisited. J Perio Res 36:48-55, 2001.
- 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?
- 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.
- Garguilo, A., et al: Dimensions and relations of the detogingival junction in humans. J Periodontl 32: 261-267, 1961
- Vacek, J.S., et al: The dimensions of the human dentogingival junction. Int J Perio Rest Dent 14: 155 – 165, 1994
- Perez J, Smukler H, Nunn M. Clinical dimensions of the supraosseous gingivae in healthy periodontium. J Periodontol 2008; 79: 2267 – 2272
- 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
- Muller-Glauzer W, Schroeder HE. The pocket epithelium: A light and electron microscopic study. J. Periodontol. 53:133-144, 1982.
Junctional epithelium- structure, function, turnover rate
- 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.
- Bosshardt DD, Lang NP. The junctional epithelium: from health to disease. J Dent Res. 2005 Jan;84(1):9-20. Review.
Wound Healing
- Taylor AC, Campbell MM. Reattachment of gingival epithelium to the tooth. J Periodontol. 43:281-293, 1972.
- Listgarten MA. Ultrastructure of the dento-gingival junction after gingivectomy. J. Periodontal Res. 7:151-160, 1972.
- Braga AM, Squier CA : Ultrastructure of regenerating junctional epithelium in the monkey. J. Periodontol. 51:386-392, 1980.
- 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?
- Caffesse RG et al: The effect of mechanical stimulation on the keratinization of sulcular epithelium. J. Periodontol. 53:89, 1982.
- Squier CA: Keratinization of the sulcular epithelium – a pointless pursuit? J. Periodontol. 52:426-429, 1981.
Epithelial Rests of Malasses
- Grant DA, Bernick S. A possible continuity between epithelial rests and epithelial attachment in miniature swine. J. Periodontol. 40:87-95, 1969.
- Spouge JD. The rests of Malassez and chronic marginal periodontitis. J Clin Periodontol 11: 340-347, 1984.
- 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.
- 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.
- 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.
- 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.
Anatomy and Development of the dentogingival junction
Kobayashi 1976
P: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.
Stern 1981
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
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.
Pollanen 2003
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.
Hujoel 2001
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 cm2 currently 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).
Purpose: To employ a parallel-plate flow cell to measure the attachment strength of epithelial cells and periodontal ligament fibroblasts.
Methods: Rate and strength of attachment of epithelial cells and PDL fibroblasts were measured. Cells were cultured individually and co-cultured to determine which cell type had 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 hours. 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.
Results: Cells in the effluent were viable. PDL fibroblasts showed a stronger attachment to dentin at 24 hours compared to 2 hours, while epithelial cells attached to dentin equally well at 2 and 24 hours. Epithelial cells were more strongly attached to dentin after 2 hours when compared to PDL fibroblasts, but less strongly attached after 24 hours. When epithelial cells and PDL fibroblasts were seeded together, at different ratios, different results were obtained:
| 1:1 | PDLF were more strongly attached at 2 but not 24 hours |
| 10 (PDL):1 (Epi) | PDLF were more strongly attached at 2 hours and 24 hours |
| 1 (PDL):10 (Epi) | Epi cells more strongly attached at 2 hours, but PDL fibroblasts had stronger attachment at 24 hours. |
Summary of strength of attachment Cultures:
2 hrs PDLF < 2 hrs
Epi
^ =
24 hrs PDLF > 24 hrs
Epi
Discussion: 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. Epithelial cells may release biologic modifiers/growth factors that enhance PDL cells attachment. More force was required to detach PDL cells compared to epithelial cells, so it is suggested that PDL cells have stronger attachment compared to epithelial cells.
Can you quantify inflamed periodontal tissues?
Nesse 2008
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.
Dimensions of the Dentogingival Junction and Biologic Width
Describe the dimensions of the DGJ and the significance of the “biologic width” in dentistry.
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
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
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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
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 & suprabasal cells). Transmigration by neutrophilic granulocytes (mainly between suprabasal cells of epithial ridges).
Conclusion/BL: The mosaic-like structure of the pocket epithelium reflects the heterogeneity of the adjacent plaque. Pocket epithelium permeability>JE>oral epithelium due to absence of membrane-coating granules in the first 2, which provide an efficient intercellular diffusion barrier. Pocket epithelium structurally and functionally differs from JE and oral sulcular epithelium. It is originated from JE, it shows lack of differentiation, no bacterial invasion, high permeability, microulcerations, and reduced thickness.
Pocket epithelium:
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1) Does not attach to the tooth
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2) Forms irregular ridges and, over connective tissue papillae, thin coverings which occasionally ulcerate
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3) Consists of cells only some of which show a tendency to differentiate
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4) Presents a basal lamina complex with discontinuities and multiplications
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5) Is infiltrated by lymphocytes, T and B cells, plasma cells, and is transmigrated by neutrophilic granulocytes
What are the characteristics of the junctional epithelium, including its structure, function, turnover rate?
Purpose: To examine the immunohistochemical localization of the cell adhesion molecules constituting desmosomes and adherens junctions with the oral gingival epithelium, sulcular epithelium and junctional epithelium.
Materials and methods: Samples of the gingival tissues were obtained from adult patients with periodontitis and the samples were examined for proteins associated with desmosomes (desmoglein 1 and 3, catenin) or adherens junction (E- and P- cadherin and a-catenin) and intracellular cytoskeletal actin.
Results: Different patterns of keratin expression were present in the three regions of the gingival epithelium. Desmoglein-1 and 2 were found in the spinous and suprabasal layers of oral and sulcular but not in the JE. Desmoglein-3 was found in all epithelia but not in the uppermost layers of sulcular and oral epithelium. catenin was found in all layers of all samples. Actin was present in all layers of oral and sulcular epithelium and more weakly found in JE.
Conclusion: Tight junction is probably a typical structure in the uppermost layer of oral gingival epithelium, it is equivalent to the stratum granulosum in stratifies epithelium and functions as a barrier.
A few desmosomes are present in JE, comprised of desmoglein-3 (localized in JE) and result in loose connection between cells and wide intercellular spaces.
Introduction: The junctional epithelium is the epithelial component of the dento-gingival unit that is in contact with the tooth surface. It maintains a tight seal against the mineralized tooth surface (a.k.a. epithelial attachment).
Development of the JE: Shortly before the first contact between the reduced enamel epithelium and the oral gingival epithelium, a slow cell transformation process occurs, the reduced ameloblasts change their morphology from short columnar to flattened cells that are parallel in orientation to the enamel surface. The cells external to the reduced ameloblasts also undergo structural changes, but unlike the reduced ameloblasts, they regain mitotic activity. (the reduced ameloblasts eventually exfoliate). Basal cells originating from the oral gingival epithelium are thought by some to be responsible for de novo formation of the junctional epithelium following gingivectomy. However, basal epithelial cells other than those of gingival origin can also regenerate the junctional epithelium.
Anatomy: In pristine gingiva the junctional epithelium extends from the CEJ to the free gingival margin, in normal gingiva it extends to the base of the sulcus. At least in porcine teeth it appears at frequent intervals to be in continuity with the epithelial rest cells of Malassez. The junctional epithelium is made of non-keratinized stratified squamous cells, 15-30 cell layers coronally and 1-3 layers apically, the epithelium has two distinct layers only, the basal layer and the suprabasal layer. The outer most cells of the suprabasal layer are called DAT cells (directly attached to the tooth). Cells have a large number of lysosomal bodies (containing enzymes that help eradicate bacteria), scarce cytokeratin bundles, large Golgi fields, abundant rough endoplasmic reticulum, and polyribosomes. The cells are interconnected by few desmosomes, and occasional gap junctions. Other cells present include PMN’s, Langerhans and other dendritic cells. The basal layer is well-innervated by sensory nerve fibers.
The external basal lamina separates the junctional epithelium from the connective tissue, whereas the internal basal forms part of the interfacial matrix between the DAT cells and the tooth surface. Basement membranes are thought to play a role in compartmentalization, filtration, cell polarization, migration, adhesion, and differentiation.
The External basement membrane (basal lamina) is common to other basement membranes, contains collagen types IV and VII, laminin, heparan sulfate proteoglycan, fibronectin, entactin, and proteoglycan perlecan.
The Internal basement membrane forms the epithelial attachment, shouldn’t be regarded as a basement membrane in the true sense, it lacks most of the common basement membrane components including collagen types IV and VII. The lamina densa directly faces the enamel, dentin, cementum (fibrillar or afibrillar), or calculus in a bacteria-free environment (Listgarten and Ellegard, 1973). DAT cells attach by hemidesmosomes to the lamina lucida (lamina rara).
Dynamics: High cellular turnover, and in the absence of clinical inflammation, about 30,000 PMNs migrate per minute through the junctional epithelia of all human teeth into the oral cavity.
Molecules: some of the molecules found in the junctional epithelium include Carcino-embryonic Ag-related cell adhesion molecule 1 (CEACAM1) which is thought to play a role in cell adhesion, guidance of PMNs, regulation of cell proliferation, stimulation, and co-regulation of T-cells. ICAM-1 which plays a role in cell-cell interaction in inflammation and guiding PMNs. Integrins which mediate cell-matrix and cell-cell interactions. E-cadherin which is critical in intercellular adhesion and maintaining structural integrity.
Junctional epithelium around implants: unlike the tooth junctional epithelium which is derived from the reduced enamel, the junctional epithelium around implants originate from the oral mucosa. However, structurally and functionally there are many similarities.
Regeneration: clinical probing results in mechanical disruption of the junctional epithelial cells from the tooth, this is completely healed in 5 days, the same time is needed for reestablishment of the junctional epithelium around implants (no permanent injury was ever observed). Flossing also causes injury (Waerhaug, 1981) that starts to heal in 3 days and is complete in 2 weeks. Gingivectomy, which completely removes the junctional epithelium, needs 20 days to heal (Listgarten, 1972).
Pocket formation: The initiation of pocket formation may be attributed to either the detachment of the DAT cells from the tooth surface or the development of an intra-epithelial split. Human studies have shown degenerative changes in the second or third cell layer of the DAT cells in the coronal-most portion of the junctional epithelium face the bacterial biofilm. The disintegration of the junctional epithelium is thought to be mostly due to host factors, including migration of PMNs and mononuclear leukocytes. However, A.a and P.g have been shown to invade the junctional epithelium. P.g produce cysteine proteinases (gingipains) that are known to degrade components of the epithelial cell-to-cell junctional complexes, and also disrupt the ICAM-1-dependent PMNs to epithelial cells adhesion.
Conclusion: The JE is a unique tissue that functions as an important border in the oral cavity between tooth attachment and bacterial colonies. Despite structurally and functionally well-adapted to control the constant presence of bacteria and their products, this does not preclude the development of inflammatory lesions in the gingiva. The converiosn of the junctional epithelium to pocket epithelium is regarded as a hallmark in the development of periodontitis.
How does wound healing of the DGJ occur after surgery or injury?
P:to determine whether gingival epithelium, after simple separation from the crown can become completely reattached to the tooth by hemidesmosomes (HD) and the time it can occur.
M&M:The attached gingival epithelium in marmosets was separated from the crown enamel of molars and premolars by steel spatula 0.8mm deep. Animals were sacrificed at 0, 1, 2, 3, 5, and 7 days. LM & EM was performed
R:New epithelial attachment by hemidesmosomes is rapidly established within a latent period of one day during which PMNs actively removed dead cells and debris. The new attachment, begins apically and migrates coronaly and is complete by 5 days.
BL:After simple mechanical separation of gingiva from tooth structure, new epithelial attachment, by means of hemidesmosomes, is rapidly reestablished.
Crit: Never said the number of animals used? Said attachment was very weak and could have been broken by careless toothbrushing or flossing or by mastication of hard foods.
P: To investigate earlier stages in the regeneration of the dento-epithelial junction following gingivectomy in monkeys
M&M:2 young monkeys; gingivectomy was carried out in labial and lingual of maxillary and mandibular anterior teeth. At 12 days, 3, 4, and 7 weeks post gingivectomy, 1 upper & 1 lower lateral incisor were extracted “en bloc”.
R/Disc: (1) EM examination revealed epithelium reattachment to enamel and root cementum w/ hemidesmosomes and basal lamina as early as 12 days post-op (completely reestablished). (2) Reattachment appeared to occur against both normal and superficially altered cementum. (3) Hemidesmosomes appeared to form more rapidly than the basal lamina. 4-7 wks post-GV, the internal basement lamina exhibited a lamina densa with only rare interruption. Presence of inflammation did not seem to affect the ultrastructure of the attachment apparatus of the epithelium to the tooth.
BL:JE completely reestablished as early as 12 d post gingivectomy in monkeys.
P: To assess if regeneration of new attachment occurs from gingival oral epithelium, even when portions of the JE remain. As well as, determining the minimum time necessary for a new epithelial attachment to form.
M&M: 3 monkeys had 8 weeks prophylaxis/CHX rinses to establish GI of zero and PI <1. An external bevel incision was used on the B aspect of max 2nd PM and 1st /2nd M to remove all sulcular epi and part of JE. An internal bevel incision was used to completely remove both sulcular and junctional epithelium in the mand teeth on the same side. Biopsies were taken at 5, 10, 15, and 20 days post-op (biopsies of 2 untreated teeth were taken as a control). All samples were prepped for exam w/light microscopy and electron microscopy.
R: Control Group: The oral surface of the gingival epithelium consisted of a well-developed orthokeratinized layer, which became parakeratinized at the gingival crest. The sulcus was lined by Nonkeratinized epithelium. In the external bevel group (maxilla), the residual JE persisted as small cell rests close to the CEJ and did not participate in regeneration of attachment. 5-10 days: Epithelialization of gingival tissue was as early as 5 days w/ ext bevel wound and 10 days w/ int bevel.15 days: Both specimens looked very similar. Cells adjacent to the tooth possessed hemidesmosomes inserted into the basal lamina. 20 days: Both appeared similar to control. Hemidesmosomes were inserted in almost a continuous row. The basal lamina was situated on the dental cuticle or afibrillar cementum. Parakeratinized or Nonkeratinized cells lined the oral sulcular region and keratinization started at the gingival crest.
D: New junctional epithelium originates from the oral epithelium, even when a portion of the original junctional epithelium remains. The rate of formation for this new attachment was rapid, but varied between the two incisions. The difference in rate of epithelialization was attributed to a greater amount of coagulum and cell debris remaining after int bevel, which seemed to hinder epithelial migration. By 20 days, both techniques resembled the control biopsies.
Existing JE does not participate in regeneration of JE after incising. New JE originated from oral epithelium. Formation rate is rapid.
PURPOSE: To investigate the location of proliferating cells in gingiva stimulated mechanically by tooth brushing.
METHODS: 2 quadrants from 12 dogs were used over the course of three weeks: 1 quad received daily supragingival curettage and the other curettage and brushing (20s per tooth). A plastic stent was used to ensure position of the tooth brush. Immunostaining: Proliferating cell nuclear antigen (PCNA) was stained immunohistologically and histometrical analysis completed in 12 standard areas in the basal layer of the junctional epithelium (apical to coronal).
RESULTS: PCNA positive cells in the tooth brushing group were 1.8 times that of the plaque removal alone group. A higher density of PCNA positive cells was also seen in CT subjacent to the JE, adjacent to the alveolar bone on the oral epithelial side, and subjacent to the oral epithelium. PCNA positive fibroblasts were also more abundant in the tooth brushing group.
DISCUSSION: Proliferation of basal cells (0.1-1.2 mm from CEJ) in JE was promoted by tooth brushing. The most apical portion of JE showed no change in PCNA positive cells with tooth brushing, suggesting that mechanical stimulation by tooth brushing has no effects on apical migration of JE (pocket formation). Tooth brushing promotes proliferative activity of gingival cells adjacent to cementum alveolar bone of oral epithelial side, and the oral epithelium. However, no change in the density of fibroblasts in CT adjacent to cementum and alveolar bone of the PDL side was observed, suggesting that tooth brushing has no effect on fibroblast stimulation in PDL.
CONCLUSION/BLThe repair of periodontal tissue might be promoted by tooth brushing within the limit of direct mechanical stimulation in cells other than those basal cells in the apical portion of the JE.
What is the significance of keratinization of sulcular epithelium?
P: to evaluate the effect of mechanical stimulation on the keratinization of the sulcular epithelium in four adult Rhesus monkeys.
M&M: the monkeys were divided into 4 groups: (a) daily intravenous tetracycline and rubber cup prophylaxis, (b) daily rubber cup prophylaxis, (c) daily intravenous tetracycline injections; (d) no treatment, as a control. After sacrifice and tissue processing the histologic sections were evaluated for the presence of sulcular keratinization. The keratin width and length were measured, and an Inflammatory Index determined.
R/C: It was found that all treatment modalities reduced inflammation significantly, when compared to the control. Though keratinization occurred in all groups, sulcular keratinization was significantly increased when daily prophylaxes were performed. It was concluded that mechanical stimulation of the sulcular epithelium seemingly plays a role in promoting its keratinization.
Discussion paper on whether trying to achieve keratinization of the oral sulcular epithelium is justifiable.
BG: Efforts have been directed at finding methods for modifying the nonkeratinized sulcular epithelium on the assumption that a keratinized surface may offer a better barrier to antigens and bacterial products present in the gingival sulcus.
D: Non keratinized epithelium is less permeable than keratinized epithelium.
Experiments in vivo have suggested that uninflamed nonkeratinized oral epithelium may be almost as successful as keratinized oral epithelium in resisting the penetration of certain tracer substances.
Keratinization does not always confer superior permeability properties the nonkeratinized epithelium lining the gut and the bladder are highly impermeable to certain substances.
Junctional epithelium forms a seal with enamel which cannot be formed between keratinized epithelium and enamel. Such a seal would be inadequate and not resistant to separation.
Epithelial cells ability to attach appears to be inversely related to the degree of differentiation of cells
Pursuing keratinization of the sulcular epithelium is unjustified as it does not increase the hosts’ resistance. Efforts should better be devoted to mechanical or chemical procedures that minimize or prevent plaque accumulation.
What is the role of the epithelial rests of Malassez in the periodontium?
P: To describe a possible continuum between the network of epithelial cells around the root (epithelial rests of Malassez) and the attached epithelium as seen in microscopic specimens of miniature swine.
M&M: Examined 6 miniature swine at 26 & 52 weeks old in block sections (25 – 40 um)
R: 1) There may be a continuity of the root epithelial network (rests) with the reduced enamel epithelium before eruption, and with the attachment epithelium following eruption. This continuum may be persistent or it may be transient. The possible presence of continuity is due to: a) Cords of epithelial cells were seen arising from the reduced enamel epithelium of a non-erupted tooth and projecting apically into the PDL; they seemed to be continuous with the epithelial rest in the upper 1/3 of the root. b) In the erupted tooth, the epithelial rests were found close to cementum, except for near the CEJ. c) The root epithelium formed a lattice network encircling the tooth when viewed in sections cut tangential to the root; in thick longitudinal sections, it was continuous (parallel to cementum) over long lengths of the root.
2) The shape of the rest groups was influenced by the direction and tension of the periodontal fiber bundles.
3) When rest cells were about to be entrapped in cementum, the membrane, which encircled the rest cells, was not demonstrable.
BL: The possible continuity between the epithelial rests and attachment epithelium may contribute to periodontal pocket formation (continuity might become visible because the destruction of fiber bundles in the area of inflammation might make it more apparent and this may be evidence for the participation of attachment and root epithelium in the events of periodontitis)
Purpose: to investigate the structure of the rests of Malassez and the relationship which the bear to the junctional epithelium in the marginal region of pigs’ molars.
Materials and methods: 3-dimensial study of the periodontium of permanent molars of pigs. Specimens from the mandibular teeth of the pigs were prepared to show the structure and relationship of its facial and lingual supporting periodontium and were studied through photomicrographs.
Results/BL: All teeth were diagnosed histologically to suffer from some degree of chronic inflammation. 6 of them had gingivitis with the JE still in contact with the CEJ and the other 2 had periodontitis with the crevice appearing pathologically deepened and loss of crestal bone. The whole JE was situated on the cementum.
In all specimens, it appeared that epithelial rests formed a continuous network. The strands were not evenly distributed but consisted mainly of cords of cells lining in a horizontal spiral around the tooth with occasional strands running vertically to join them together at intervals. The coronal margin of the network was united with the apical border of the JE. Authors believe that epithelial proliferation in diseased sites may start from epithelial rests as a response to inflammation.
Cr: Other studies show the “rests” may possess the capacity to break down collagen so this could be the path for apical pkt migration.
P:To determine the role of epithelial root sheath (ERS) cells in murine (mouse) PDL formation using tissue separation and recombination technique
M&M:Root dentin specimens, w/ and w/o root-associated basement membrane components were recombined w/ dental sac in the presence or absence of ERS. Cultured for 2 wks & histo.
R:Mineralized tissue formed in all tissue recombination. When ERS was included in recombination. B/t dentin specimens and root-associated basement membrane components and dental sac, 25% of recombination formed a PDL w/ fibrous attach of the root specimen to adjacent bone.When basement membrane was present, PDL was formed; but any newly synthesized basement membrane was incapable of initiating or supporting PDL development.
B/L:These results support hypothesis that root and PDL formation is influenced by epithelio-mesenchymal interactions and ERS plays a key role in these processes. In other words, the periodontal attachment formation is dependent upon the presence of both epithelium and root associated basement membrane component.
P: Review of different aspects of the epithelial cell rests of Malassez (ERM), their role in the PDL, and their possible importance in periodontal regeneration.
Hypothesis of the authors is that ERM cells are crucial for successful and predictable perio regeneration: strategic position of these cells in a healthy PDL and ability to secrete matrix molecules are conducive to cementum formation.
ERM are normal structures within the PDL, identified on histological slides as clumps of epithelial cells, closely approximated to the radicular cementum surface and seen as a network of cells surrounding the root (like a fish net).
Embryology: ERM form during root development. As root develops apically, the inner layer of Hertwig’s epithelial root sheath induces dentin formation. When this begins to calcify, the HERS fenestrates to allow for movement of cells that will become cementoblasts towards the root and beginning of cementum deposition. Through these fenestrated areas the collagen fiber bundle attachments become incorporated into both cementum and alveolar bone. The remains of the root sheath become ERM, which are possibly continuous with the reduced enamel epithelium.
Immunohistochemistry/protein expression: epithelial phenotype (cytokeratins), extracellular matrix and cell surface proteins (amelogenin, enamelin, GAGs, hyaluronic acid, dermatan sulphate, chondroitin sulphate and type IV collagen, fibronectin, laminin). Cell surface markers: growth factors receptors, growth factors and some BMPs, cytokines (IL-1α,6,8), prostaglandins E and F and others. Has the ability to degrade collagen: secretes collagenase, gelatinase and TIMP (tissue inhibitor metalloprotheinases). Can also induce/produce MMPs.
Although the functional role of ERM is unknown, it is known that they can express factors important for formation of bone and cementum, and therefore hypothesized that they could be important for periodontal regeneration
ERMs major functions that might be useful for perio regeneration:
Maintenance of PDL space. Absence of ERM after regenerative studies showed narrow PDL; always present in vital areas of replanted teeth.
Osteopontin synthesis: acts as an aid for cementum repair & mineralization. Reported to inhibit apoptotic events, such as those associated with inflammation
Bone Sialoprotein (BSP) : acts as an adhesion molecule. Initiates mineralization on the root surface (found regularly during cementogenesis and bone formation)
Absence of these cells in regenerated tissues may account for some lack of predictable functional outcomes. These cells can be successfully isolated & cultured, so future studies might evaluate their use in periodontal regeneration. Possible that in current PDL regeneration studies, the environment is not conducive to ERM migration and proliferation.
BL: ERM play an important role in the development of the periodontal apparatus. Their presence during &/or after periodontal regenerative therapies should be studied further.
Alkaline phosphatase and noncollagenous bone proteins are produced prior to cementum formation. It has been suggested that epi rests of Malassez are involved in cementum formation.
To determine whether the epithelial rests of Malassez cells cultured from human PDL can produce alkaline phosphatase and noncollagenous bone proteins such as osteopontin, osteocalcin, and bone sialoprotein to support their involvement in the formation of cementum.
PDL explants attached to the mid-third of each root of fresh extracted 3rd molars of 36 patients (17-25 yrs) were carefully removed and cultured. Epithelial rests of Malassez cells were produced from the PDL explants. Human gingival epithelial cells and PDL fibroblasts were used as controls. Expression levels of amelogenin, alkaline phosphatase, and non-collagenase bone proteins were assessed.
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-Epi rests of Malassez stained + for cytokeratin which indicates their epithelial origin.
- -Amelogenin, alkaline phosphatase and osteopontin proteins and their corresponding mRNAs were detected in high levels in epi rests of Malassez.
- -Osteocalcin and bone sialoprotein were not expressed.
- -noncollagenous bone proteins were seen in PDL fibroblasts, but not in gingival epithelial cells.
- -Epi rests of Malassez and fibroblasts were + for alkaline phosphatase activity but gingival epi cells were not.
BL: Epithelial rests of Malassez cells cultured alone do not transform into maturing cells to form the cementum, but may play a role in mineralization process.
P: To describe the localization and extension of epithelial rests of Malassez in the periodontal membrane in normal erupting human third molars.
M&M: 24 normal human third molars surgically removed from patients (age range15-27 yrs; 6 females and 6 males). The extracted teeth were fixed in 10% neutral-buffered formalin; decalcified in ethylene diamine tetra acetic acid. The tissue was paraffin embedded and cut sagittaly in 5 µm serial sections. Immunohistochemistry was performed using wide-spectrum screening, and the EnVision + dual link system. The results were based on the visual comparison of WSS in the tissue sections using a light microscope.
R: The epithelial rests of Malassez cells were distributed in the periodontal membrane in a network-shaped manner along the root surface and in the furcation region. The distribution of ERM was more prominent in teeth with incomplete root formation.
BL: During root maturation, disintegration of Hertwig’s epithelial root sheath takes place leaving epithelial rests of Malassez in the periodontal membrane. Epithelial rests of Malassez may play a significant role in maintaining periodontal ligament space thereby preventing ankylosis.
Steven Spindler DDS, LLC updated 2020.7.1