Junctional epithelium

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The junctional epithelium (JE) is that epithelium which lies at, and in health also defines, the base of the gingival sulcus. The probing depth of the gingival sulcus is measured by a calibrated periodontal probe. In a healthy-case scenario, the probe is gently inserted, slides by the sulcular epithelium (SE), and is stopped by the epithelial attachment (EA). However, the probing depth of the gingival sulcus may be considerably different from the true histological gingival sulcus depth.

Contents

Location

The junctional epithelium, a nonkeratinized stratified squamous epithelium, [1] lies immediately apical to the sulcular epithelium, which lines the gingival sulcus from the base to the free gingival margin, where it interfaces with the epithelium of the oral cavity. The gingival sulcus is bounded by the enamel of the crown of the tooth and the sulcular epithelium. Immediately apical to the base of the pocket, and coronal to the most coronal of the gingival fibers is the junctional epithelium. The JE attaches to the surface of the tooth by way of the EA with hemidesmosomes and is, on average, roughly 1 mm in width in the apico-coronal dimension, constituting about one half of the biologic width. [2] The attachment of the JE to the tooth surface can occur on enamel, cementum, or dentin. The position of the EA on the tooth surface is initially on the cervical half of the anatomical crown when the tooth first becomes functional after tooth eruption. [3] [4]

Origin

Junctional epithelium is derived from the reduced enamel epithelium (REE) during tooth development. [5] Before the eruption of the tooth and after enamel maturation, the ameloblasts secrete a basal lamina on the tooth surface that serves as a part of the primary EA. As the tooth actively erupts, the coronal part of the fused and surrounding epithelium peels back off the crown. The ameloblasts also develop hemidesmosomes for the primary EA and become firmly attached to the enamel surface. However, the cervical part of the fused tissue remains attached to the neck of the tooth by the primary EA. This fused tissue, which remains near the cementoenamel junction (CEJ) after the tooth erupts, serves as the initial JE of the tooth, creating the first tissue attached to the tooth surface. This tissue is later replaced by a definitive JE as the root is formed. [3]

Structure

Cells in the junctional epithelium tend to have wide intercellular spaces and fewer desmosomal junctions, to allow the transmission of white blood cells (WBCs) from lamina propria's blood vessels to the bottom of the gingival sulcus, to help prevent disease. In addition, the JE is also thinner than the sulcular epithelium, ranging coronally from only 15 to 30 cells thick at the floor of the gingival sulcus, and then tapering to a final thickness of 3 to 4 cells at its apical part. The superficial, or suprabasal, cells of the JE serve as part of the EA of the gingiva to the tooth surface. These superficial, or suprabasal, epithelial cells of the JE provide the hemidesmosomes and an internal basal lamina that create the EA, because this is a cell-to-noncellular type of intercellular junction. The structure of the EA is similar to that of the junction between the epithelium and subadjacent connective tissue; the internal basal lamina consists of a lamina lucida and lamina densa. [5]

This internal basal lamina of the EA is continuous with the external basal lamina between the junctional epithelium and the lamina propria at the apical extent of the JE. The EA is very strong in a healthy state, acting as a type of seal between the soft gingival tissue and the hard tooth surface. The deepest layer of the JE, or basal layer, undergoes constant and rapid cell division, or mitosis. This process allows a constant coronal migration as the cells die and are shed into the gingival sulcus. The few layers present in the JE — from its basal layer to the suprabasal, or superficial, layer — does not show any change in cellular appearance related to maturation, unlike other types of gingival tissue. Thus, the JE does not mature like keratinized tissue, such as the marginal gingiva or attached gingiva, which fills its matured superficial cells with keratin.

Nor does JE mature on a lesser level like nonkeratinized tissue of the sulcular gingiva and throughout the rest of the oral cavity, which enlarges its cells as they mature and migrate superficially. The JE cells do not mature and form into a granular layer or intermediate layer. Without a keratinizing superficial layer at the free surface of the JE, there is no physical barrier to microbial attack. Other structural and functional characteristics of the JE must compensate for the absence of this barrier. The JE fulfills this difficult task with its special structural framework and the collaboration of its epithelial and nonepithelial cells that provide very potent antimicrobial mechanisms, such as the white blood cells. However, these defense mechanisms do not preclude the development of extensive inflammatory lesions in the gingival tissue, and, occasionally, the inflammatory lesion may eventually progress to the loss of bone and the connective tissue attachment to the tooth. [6]

The JE cells have many organelles in their cytoplasm, such as rough endoplasmic reticulum, Golgi complex, and mitochondria, indicating a high metabolic activity. However, the JE cells remain immature or undifferentiated until they die and are shed or lost in the gingival sulcus. Lysosomes are also found in large numbers in JE epithelial cells; enzymes contained within these lysosomes participate in the destruction of bacteria contained in dental biofilm. [3]

Pathology

The increased permeability of the JE that allows emigration of the PMN type of WBC also allows microorganisms from the dental biofilm (especially noted is P. gingivalis, and associated toxins from the exposed tooth surface) to enter this tissue from the deeper lamina propria, setting up the possibility of infection to occur. [7] Damage to the junctional epithelium results in it being irregular in texture, rather than smooth, at its surface. Most importantly is the formation of pocket epithelium within the periodontal pocket, which is a histopathological characteristic of periodontal disease, having the true apical migration of the EA. [8] [9] In addition, there is the presence of ulceration with gingival hyperplasia, including the formation of rete ridges and connective tissue papillae at the one smooth interface of the JE with the lamina propria. Further, there is increased levels of exfoliation of epithelial cells, WBC migration, and bacterial internalization, as well as internalization-induced programmed epithelial cell death. [10]

See also

Related Research Articles

Cementum

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Gums

The gums or gingiva consist of the mucosal tissue that lies over the mandible and maxilla inside the mouth. Gum health and disease can have an effect on general health.

Periodontal fiber

The periodontal ligament, commonly abbreviated as the PDL, is a group of specialized connective tissue fibers that essentially attach a tooth to the alveolar bone within which it sits. It inserts into root cementum one side and onto alveolar bone on the other.

Human tooth development

Tooth development or odontogenesis is the complex process by which teeth form from embryonic cells, grow, and erupt into the mouth. For human teeth to have a healthy oral environment, all parts of the tooth must develop during appropriate stages of fetal development. Primary (baby) teeth start to form between the sixth and eighth week of prenatal development, and permanent teeth begin to form in the twentieth week. If teeth do not start to develop at or near these times, they will not develop at all, resulting in hypodontia or anodontia.

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Periodontal probe

A periodontal probe is an instrument in dentistry commonly used in the dental armamentarium. It is usually long, thin, and blunted at the end. The primary purpose of a periodontal probe is to measure pocket depths around a tooth in order to establish the state of health of the periodontium. There are markings inscribed onto the head of the instrument for accuracy and readability.

The vestibular lamina is responsible for the formation of the vestibule and arises from a group of cells called the primary epithelial band. This band is created at about 37 days of development in utero. The vestibular lamina forms shortly after the dental lamina and is positioned right in front of it. The vestibule is formed by the proliferation of the vestibular lamina into the ectomesenchyme. The vestibular lamina is usually contrasted with the dental lamina, which develops concurrently and is involved with developing teeth. Both the vestibular lamina and the dental lamina arise from a group of epithelial cells, called the primary epithelial band.

Cementogenesis is the formation of cementum, one of the three mineralized substances of a tooth. Cementum covers the roots of teeth and serves to anchor gingival and periodontal fibers of the periodontal ligament by the fibers to the alveolar bone.

Gingival sulcus

The gingival sulcus is an area of potential space between a tooth and the surrounding gingival tissue and is lined by sulcular epithelium. The depth of the sulcus is bounded by two entities: apically by the gingival fibers of the connective tissue attachment and coronally by the free gingival margin. A healthy sulcular depth is three millimeters or less, which is readily self-cleansable with a properly used toothbrush or the supplemental use of other oral hygiene aids.

Gingival and periodontal pocket

Gingival and periodontal pockets are dental terms indicating the presence of an abnormal depth of the gingival sulcus near the point at which the gingival tissue contacts the tooth.

Bleeding on probing (BoP) which is also known as bleeding gums or gingival bleeding is a term used by dentists and dental hygienists when referring to bleeding that is induced by gentle manipulation of the tissue at the depth of the gingival sulcus, or interface between the gingiva and a tooth. BoP is a sign of periodontal inflammation and indicates some sort of destruction and erosion to the lining of the sulcus or the ulceration of sulcular epithelium. The blood comes from lamina propria after the ulceration of the lining. BoP seems to be correlated with Periodontal Inflamed Surface Area (PISA).

Gingival margin

The free gingival margin is the interface between the sulcular epithelium and the epithelium of the oral cavity. This interface exists at the most coronal point of the gingiva, otherwise known as the crest of the marginal gingiva.

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The gingival fibers are the connective tissue fibers that inhabit the gingival tissue adjacent to teeth and help hold the tissue firmly against the teeth. They are primarily composed of type I collagen, although type III fibers are also involved.

The interdental papilla, also known as the interdental gingiva, is the part of the gums (gingiva) that exists coronal to the free gingival margin on the buccal and lingual surfaces of the teeth. The interdental papillae fill in the area between the teeth apical to their contact areas to prevent food impaction; they assume a conical shape for the anterior teeth and a blunted shape buccolingually for the posterior teeth.

Debridement (dental)

In dentistry, debridement refers to the removal by dental cleaning of accumulations of plaque and calculus (tartar) in order to maintain dental health. Debridement may be performed using ultrasonic instruments, which fracture the calculus, thereby facilitating its removal, as well as hand tools, including periodontal scaler and curettes, or through the use of chemicals such as hydrogen peroxide.

Clinical attachment loss (CAL) is the predominant clinical manifestation and determinant of periodontal disease.

Tissue engineering of oral mucosa combines cells, materials and engineering to produce a three-dimensional reconstruction of oral mucosa. It is meant to simulate the real anatomical structure and function of oral mucosa. Tissue engineered oral mucosa shows promise for clinical use, such as the replacement of soft tissue defects in the oral cavity. These defects can be divided into two major categories: the gingival recessions which are tooth-related defects, and the non tooth-related defects. Non tooth-related defects can be the result of trauma, chronic infection or defects caused by tumor resection or ablation. Common approaches for replacing damaged oral mucosa are the use of autologous grafts and cultured epithelial sheets.

Gingival grafting

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References

This article incorporates text in the public domain from the 20th edition of Gray's Anatomy (1918)

  1. ↑ AAP 2010 In-Service Exam, question A-20
  2. ↑ Newman MG, Takei HH, Carranza FA (2002). Carranza's Clinical Periodontology (9th ed.). W.B. Saunders. p. 23. ISBN   978-0-7216-8331-7.
  3. 1 2 3 Bath-Balogh M, Fehrenbach MJ (2011). Illustrated Dental Embryology, Histology, and Anatomy. Elsevier. p. 127. ISBN   978-1-4377-1730-3.
  4. ↑ Naci A (2013). Ten Cate's Oral Histology. Elsevier. p. 351. ISBN   978-0-323-07846-7.
  5. 1 2 Shimono M, Ishikawa T, Enokiya Y, Muramatsu T, Matsuzaka K, Inoue T, Abiko Y, Yamaza T, Kido MA, Tanaka T, Hashimoto S (2003). "Biological characteristics of the junctional epithelium". Journal of Electron Microscopy. 52 (6): 627–39. doi:10.1093/jmicro/52.6.627. PMID   14756251.
  6. ↑ Listgarten MA. "University of Pennsylvania and Temple University".
  7. ↑ Sandros J, Papapanou PN, Nannmark U, Dahlén G (January 1994). "Porphyromonas gingivalis invades human pocket epithelium in vitro". Journal of Periodontal Research. 29 (1): 62–9. doi:10.1111/j.1600-0765.1994.tb01092.x. PMID   8113953.
  8. ↑ Bosshardt DD, Lang NP (January 2005). "The junctional epithelium: from health to disease". Journal of Dental Research. 84 (1): 9–20. doi:10.1177/154405910508400102. PMID   15615869. S2CID   12115399.
  9. ↑ Nanci A, Bosshardt DD (2006). "Structure of periodontal tissues in health and disease". Periodontology 2000. 40: 11–28. doi:10.1111/j.1600-0757.2005.00141.x. PMID   16398683.
  10. ↑ Vitkov L, Krautgartner WD, Hannig M (2005). "Surface morphology of pocket epithelium". Ultrastructural Pathology. 29 (2): 121–7. doi:10.1080/01913120590916832. PMID   16028668. S2CID   27306243.
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