Short Notes in Periodontics: A Handbook PL Ravishankar, L Chandrasekhar
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Normal PeriodontiumCHAPTER 1

The attached gingiva or functional mucosa extends from the free gingival groove to the mucogingival junction where it meets the alveolar mucosa. The attached gingiva is a mucoperiosteum which is tightly bound to the underlying alveolar bone.
Pale pink
Stippled-like orange peel.
Stippling varies considerably, most prominent on facial surfaces and often disappears in old age. Cause of stippling appears to coincide with epithelial rete pegs.
Width of attached gingiva varies from 0–9 mm.
- Incisor region (3–5 mm)
- Mandibular canines and Premolars
In the past, it was assumed that attached gingiva was necessary to maintain the health of gingival margin by separating the stable margin from mobile alveolar mucosa, but this does not appear to be the case in clean mouth. Thus it has given rise to controversy that any width, even a zero width, is acceptable if the tissue is healthy.
The gingiva is the part of the oral mucosa that covers the alveolar processes of the jaws and surrounds the necks of teeth. Beneath the epithelial integument resides the gingival connective tissue compartment also referred to as the lamina propria. The lamina propria exhibits an exquisitely complex architecture which anticipates its functions. Approximately, 60–65% of the connective tissue compartment of healthy gingiva is occupied by collagen, with the individual fibrils highly organized into discrete and easily discernible fiber bundles.
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Fig. 1.1: Parts of the gingiva and epithelium
3Collectively these fiber bundles have been referred to as the gingival ligament composed of type I collagen. The gingival fibers have the following functions:
  • To brace the marginal gingiva firmly against the tooth.
  • To provide the rigidity necessary to withstand the forces of mastication without being deflected away from the tooth surface.
  • To unite the free marginal gingiva with the cementum of the root and the adjacent attached gingiva.
The gingival fibers constituting the gingival ligament vary in spatial orientation and in size there are 5 principal fiber bundle groups as well as 6 minor groups (Fig. 1.2).
Principal Groups
Secondary Groups
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Fig. 1.2: Gingival fiber groups
The connective tissue of the gingiva is organized to keep the gingival margin tight around the neck of the tooth and to maintain the integrity of the dentogingival attachment.
  • Prevents from occlusal forces.
  • Maintains the position of marginal gingiva.
  • Prevents entry of bacteria
  • Greater resistance to mechanical trauma or muscle pulls than does lining mucosa.
  • Prevents the occurrence of root dehiscence.
The principal cell type of the gingival epithelium, as well as of other stratified squamous epithelia, is the keratinocyte. The main function of the gingival epithelium is to protect the deep structures, while allowing a selective interchange with the oral environment. This is achieved by proliferation and differentiation of the keratinocytes.
  • “Proliferation” of keratinocytes takes place by mitosis in the basal layer and less frequently in the suprabasal layers, where a small proportion of cells remains as a proliferative compartment while a large number begin to migrate to the surface.
  • “Differentiation” involves the process of keratinization, which consists of progressions of biochemical and morphologic events that occur in the cell as they migrate from the basal layer.
Mast cells, which are distributed throughout the body, are numerous in the connective tissue of the oral mucosa and the gingiva. It is a large spherical or elliptical mononuclear cell. Its nucleus is small relative to the size of the cell and in histologic preparations frequently is obscured by the large number of intensely staining granules that occupy its cytoplasm. In human beings the principal contents of the granules are histamine and heparin. They play a role in maintaining normal tissue stability and vascular homeostasis. Histamine is known to be important in initiating the vascular phase of an inflammatory process.
Biological width is defined as the physiologic dimension of the junctional epithelium and connective tissue attachment.
  • Approximately 2 mm.
  • During crown lengthening procedures there should be at least 3 mm between the gingival margin and bone crest.
  • This allows for adequate biological width when the restoration is placed 0.5 mm within the gingival sulcus.
    When the restoration is placed within its zone, it results in–
    • Gingival inflammation
    • Pocket formation
    • Alveolar bone loss
  • Biological width=junctional epithelium (0.97 mm) + connective tissue attachment (1.07 mm)=2.04 mm
The gingiva has a rich blood supply derived from three sources:
  1. Supraperiosteal arterioles: Along the facial and lingual surfaces of the alveolar bone, from which capillaries extend along the sulcular epithelium and between the rete pegs of the external gingival surface.
  2. Vessels of the periodontal ligament, which extend into the gingiva and anastomose with capillaries in the sulcus area.
  3. Arterioles, which emerge from the crest of the interdental septa and extend parallel to the crest of the bone to anastomose with vessels of the periodontal ligament, with capillaries in the gingival crevicular areas and vessels that run over the alveolar crest.
The interdental gingiva occupies the gingival embrasure which is the interproximal space beneath the area of tooth contact. Interdentally the gingiva adapts its shape to the form, size and the position of adjacent teeth. Therefore in the vestibular/oral dimension, the interdental portion of the gingiva is narrow between the front teeth and broader between premolars and molars.
Between the vestibular and oral papillae, which reach about halfway to the incisal edge the interdental gingival portion forms a concave bridge or col.
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Fig. 1.3: Gingival col
The interdental col increases both in buccolingual width from about 2 to 6 mm and in vertical depth from about 0.3 to 1.5 mm anteroposteriorly. The col is lined by the coronally fused portion of the junctional epithelium that encircles the adjacent teeth. The intervening portion consists of attached gingiva.
If diastema is present, the gingiva is firmly bound over the interdental bone and forms a smooth, rounded surface without interdental papillae.
“Pigmentation” is defined as coloration, either normal or pathologic of the skin or tissues resulting from a deposit of pigment. Color of attached and marginal gingiva is coral pink produced by:
  • Vascular supply
  • Thickness and degree of keratinization
  • Presence of pigment containing cells.
Color varies and correlates with cutaneous pigmentation. Lighter in fair complexions than in swarthy.
Physiologic Pigmentation (Fig. 1.4)
“Melanin”, non-hemoglobin derived brown pigment responsible for oral tissues pigmentation and skin. Present in all and absent or diminished in Albinos. According to ‘Dummett’ distribution of pigmentation.
Gingiva - 60%
Hard palate - 61%
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Fig. 1.4: Melanocyte
7Mucous membrane - 22%
Tongue - 15%
Gingival pigmentation occurs as diffuse, deep purples/irregularly shaped brown patches. Appear in gingiva as early as three hours after birth.
Pathologic Pigmentation
  1. Ingestion of metals in medicinal compounds and through industrial contact result in oral manifestations:
    • Bismuth intoxication: Narrow, bluish black of gingival margin.
    • Lead intoxication: Linear, steel grey (Burtonian line)
    • Mercury intoxication: Linear, results from deposition of mercury sulfide.
  2. Diseases that increase melanin pigmentation:
    • Addison's disease
    • Albright's syndrome
    • von-Recklinghausen's disease
    • HIV infection and Peutz-Jeghers syndrome.
Gingival pigmentation may be due to exogenous or endogenous factors.
Exogenous Factors
  • Atmospheric irritants such as coal and metal dust.
  • Coloring agents in food or lozenges.
  • Tobacco–Causes increase in melanin pigmentation of oral mucosa.
  • Localized bluish black areas of pigment is caused by amalgam implanted in the mucosa.
Endogenous Factors
  • Many systemic diseases may cause color changes in the oral mucosa, including the gingiva.
    Caused by:
    • Melanin
    • Bilirubin
    • Iron
  • Melanin pigmentation is seen in:
    • Addison's disease
    • Peutz-Jeghers syndrome
    • Albright's syndrome
  • 8Bile pigments–Jaundice
    • Oral mucosa acquires yellow color.
  • Iron in hemochromatosis produces blue-gray pigmentation of oral mucosa.
  • Endocrine disturbances
  • Metabolic disturbances
  • Blood dyscrasias, e.g. Anemia, polycythemia and leukemia.
There are three zones of gingival epithelium:
  • Oral epithelium
  • Sulcular (crevicular) epithelium
  • Junctional epithelium
It is a unique anatomic feature concerned with attachment of gingiva to the tooth. Consists of “epithelial and Connective tissue components”.
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Fig. 1.5: Dentogingival unit
Consists of a collar like band of stratified squamous non-keratinizing 9epithelium. It is 3–4 layers thick in early life but the number of layers increases with age to 10–20. It is the only gingival epithelium with two distinct basal laminas, one on each surface.
  • External basal lamina
  • Internal basal lamina
In health, the junctional epithelium lies against enamel and extends to cemento-enamel Junction. Its cells are larger than those of oral epithelium and loosely connected together. In adults, it is about 40 cells long from apex to crevicular surface and varies from 0.25–1.35 mm. Listgarten has calculated the rate of cellular exfoliation from a unit surface of junctional epithelium is 50–100 times fast as that of oral gingival epithelium (OGE). In contrast to OGE, junctional epithelium (JE) is relatively permeable and allows two way movement of a variety of substances: From corium into the crevice and vice-versa.
Because of the permeability of junctional epithelium it is inevitable that the tissue defense mechanism should be in a constant state of alertness and this is manifested by an infiltration of inflammatory cells, lymphocytes and plasma cells in the corium.
  • It is a thin, non-keratinized stratified squamous epithelium without rete pegs; lining the gingival sulcus and it extends from coronal limit of the junctional epithelium to the crest of the gingival margin.
  • It contains cells with hydropic degeneration; K4 and K13 (=esophageal type of cytokeratins).
  • It lacks granulosum and corneum strata and K1, K2 and K10 to K12 cytokeratins, Merkel cells.
  1. It acts as semipermeable membrane.
  2. It has potential to keratinize if
    • It is reflected and exposed to the oral cavity.
    • The bacterial flora of the sulcus is totally eliminated.
Composed of four layers:
  • Stratum basale
  • Stratum spinosum (prickle cell layer)
  • 10Stratum granulosum (granular layer)
  • Stratum corneum (cornified layer)
    • It is keratinized/ parakeratinized
    • Keratinization varies in different areas:
      (Palate—most keratinized
      Gingiva; ventral aspect of tongue; cheek—least keratinized)
    • K6, K16—Characteristic of highly proliferative epithelia and K5 and K14—stratification—specific cytokeratins are also present
    • K19—Express parakeratinized areas
Massaging the gingiva with tooth brush/interdental devices produces epithelial thickening, increases keratinization and increases mitotic activity in epithelial connective tissue.
The increased keratinization occurs only on the oral gingiva and not on the areas more vulnerable to microbial attack, the sulcular epithelium and interdental areas where the gingival col is present.
Gingival sulcus is the shallow crevice or space around the tooth, bounded by the surface of the tooth on one side and the epithelium lining the free margin of the gingiva on the other side.
  • Shape – v
  • At absolute normal condition, depth of gingival sulcus – 0 mm or close to 0 mm.
  • Clinically healthy gingiva, depth of sulcus – 1.8 mm (0–6 mm)
Clinical evaluation: By introducing periodontal probe and estimation of the distance it penetrates. Probing depth of clinically normal gingival sulcus – 2 to 3 mm.
Active eruption: It is the movement of teeth in the direction of occlusal plane.
It is coordinated with attrition.
Passive eruption: It is the exposure of teeth by the apical migration of gingiva.
It is now considered as pathologic process.
If the epithelium proliferates along the tooth surface before the cells from other tissues reach the area, the result will be a long junctional epithelium.
  • During periodontitis an anatomic defect occurs, it causes the formation of long junctional epithelium.
Gingival innervations are derived from fibers arising from nerves in the periodontal ligament and from the labial, buccal and palatal nerves.
The following nerve structures are present in the connective tissue:
  1. A meshwork of terminal argyrophilic fibers, some of which extend into the epithelium.
  2. Meissner – type tactile corpuscles
  3. Krause – type end bulbs (temperature receptors)
  4. Encapsulated spindles
The functions of periodontal ligament can be broadly categorized into:
  1. Physical functions
  2. Formative and remodeling
  3. Nutritional and sensory function
Physical Functions
Protection to vessels and nerves: Periodontal ligament provides soft tissue casing in order to protect the vessels and nerves from injury due to mechanical forces.
Transmission of occlusal forces to the bone: When axial forces are applied, oblique fibers of periodontal ligament stretch and transmit the forces to alveolar bone, that encourages bone formation rather than bone resorption. But when horizontal/tipping forces are applied, the tooth rotates around the axis.
Attachment: Periodontal ligament attaches the tooth to the bone with the help of collagen fibers.
Maintenance of gingival relationship: Periodontal ligament maintains the gingival tissues in their proper relationship to teeth.
12Shock absorption: Periodontal ligament resists the impact of occlusal forces.
Two theories have been explained for this mechanism:
  • Tensional theory
  • Viscoelastic theory
According to tensional theory, the principal fibers of periodontal ligament play a major role in supporting the tooth and transmitting forces to the bone.
According to viscoelasticity theory tooth displacement is controlled by fluid movement and fibres play a secondary role.
Formative and Remodeling Functions
  • Cells of PDL have the capacity to control the synthesis and resorption of cementum, periodontal ligament and alveolar bone.
  • Old cells and fibers are broken down and replaced by new ones.
  • This function helps in physiological tooth movement, in the adoption of periodontium to occlusal forces and in repair of injuries.
Nutritional and Sensory Functions
It has a rich vascular supply and provides nutrition to the bone, cementum and gingiva.
It is supplied by nerve fibers that can transmit sensation of touch, pressure and pain to higher centers.
  • Free endings
  • Ruffini
  • Meissners corpuscles and mechanoreceptors.
These are non-keratinocytes of gingival epithelium. These are present in low numbers and are found in basal and suprabasal layers in close contact with adjacent intraepithelial nerve endings. They contain numerous membrane bands dense granules in cytoplasm nearest the nerve endings and over all dendritic sheath. These cells occur in clusters and are identified as tactile receptors.
These cells arise from bone marrow and come to occupy the gingival epithelium. These cells have receptors for immunoglobulins and complement. The presence of surface antigens makes them to have a defensive role against the microoraganisms.
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Fig. 1.6: Langerhans cell
Periodontal ligament contains four types of cells. They are:
  • Connective tissue cells:
    • Fibroblasts
    • Cementoblasts
    • Osteoblasts
    • Odontoclasts and osteoclasts
  • Epithelial rests of malassez
  • Immune system cells:
    • Neutrophils
    • Lymphocytes
    • Macrophages
    • Mast cells.
  • Cells of neurovascular elements:
    • Neuroglial cells
    • Endothelial cells.
Fibroblasts are the most common cells. They are ovoid/elongated cells with pseudopodia like process. Function is to synthesize collagen and degrade old collagen fibers.
The most important elements of the periodontal ligament are the principal fibers, which are collagenous and arranged in bundles and follow a wavy course. Terminal portions of principal fibers that insert into cementum and bone are called Sharpey's fibers. Sharpey's fibers have a central uncalcified core, surrounded by peripheral calcified portion.
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Fig. 1.7: Principal fiber groups of the periodontium
They contain collagen as constituent molecule which is arranged in fibrils with striations. Type of collagen found in principal fibers is type I.
They are arranged in six groups, they are:
  1. Transseptal group: Extend inter-proximally over the alveolar bone crest and embedded in the cementum of adjacent teeth. They can be reconstructed even after alveolar bone destruction. Do not have any osseous attachment.
  2. Alveolar crest group: They extend obliquely from cementum into alveolar crest. Prevent the extrusion of the tooth and also prevent the lateral tooth movement.
  3. Horizontal group: They extend horizontally from cementum to alveolar bone.
  4. Oblique group: They extend from cementum to alveolar bone in a coronal direction. They are largest group of fibers. Bear the vertical forces and transform them into tension on alveolar bone.
  5. Apical group: At the apical region of root, radiate from cementum into alveolar bone. Not present in incompletely formed roots. Prevents tooth tipping and luxation.
  6. Interradicular group: Fan out from cementum to the bone in furcation areas of multi-rooted teeth. Not present is anterior teeth.
The term lamina dura means interdental septum normally presents a thin, radio-opaque border that is adjacent to the periodontal ligament and at the alveolar crest. It is a radiological term used to describe “alveolar bone proper”. Alveolar bone proper is thin, compact bone present immediately surrounding the roots. This appears radiographically as a continuous white line, but in reality it is perforated by numerous small foramina and traversed by blood vessels lymphatics and nerves, which pass between the periodontal ligament and the bone. Even though lamina dura appears radio-opaque, it is not highly calcified as adjacent bone. Increased radioopacity is due to geometrical positioning of bone plate.
Clinical Importance of Lamina Dura
  1. Fuzziness and break in the continuity of lamina dura at the crest of interdental septum is considered as initial radiographic change in periodontitis.
  2. Increased thickness of lamina dura along with vertical bone loss could be seen in trauma from occlusion.
  3. Loss of lamina dura along with ground glass appearance can be seen in hyperparathyroidism.
Double lamina dura: It is a phenomenon seen on the mesial aspect at mesial root of mandibular molars. This is due to inclination of root.
Sharpey's Fibers
Terminal portions of principal fibers that insert into cementum and bone are called Sharpey's fibers. They have a central uncalcified core, surrounded by peripheral calcified portion.
Oxytalan Fibers
Periodontal ligament other than collagen fibers contains two immature forms of elastin fibers. They are:
  • Elaunin fibers.
  • Oxytalan fibers.
Elastic meshwork composed of elastin lamellae with peripheral oxytalan fibers and elaunin fibers are present in periodontal ligament. Oxytalan fibers resemble pre-elastic fibers.
16Orientation: Run parallel to the root surface in vertical direction and bend to attach to cementum, in cervical third of root.
  1. To regulate the vascular flow.
  2. They are responsible for elastic properties of periodontal ligament (PL) along with principal fibers, those fibers develop in regenerated PL.
  3. Have a role in tooth support.
Dental cementum–The dynamic tissue covering of the root.
Acellular Cementum
It is also called primary cementum which forms during root formation. It is the first formed cementum present in cervical one-third of root, formed before tooth reaches the occlusion, hence called acellular, because it doesn't contain cementocytes.
: Thin surface layer
: Sharpey's fibers, intrinsic collagen fibers.
: 30–230 µm
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Fig. 1.8: Cementum
17It does not contain cementocytes within its substance but as cementoblasts populate its surface, the term “Acellular” may not be wholly appropriate. Incremental lines of salter are present, which represent the rest periods in cementum formation.
Cellular Cementum
It is also called secondary cementum which forms after the eruption of the tooth and responds to functional demands formed after the tooth reaches the occlusal plane.
Components: Less number of Sharpey's fibers, cementocytes in lacunae, which like osteocytes in bone, communicate with each other through a network of canaliculi.
Primary function of cementum is to furnish a medium for the attachment of collagen fibers that bind the tooth to alveolar bone.
  • Cementum is responsible for connective tissue attachment to the tooth.
  • Functional age of the tooth is represented by repeated apposition of cemental layers.
  • Cementum serves as major reparative tissue for root surfaces.
  • Damage to roots such as fractures and resorption can be repaired by deposition of new cementum.
Cementum: Calcified avascular mesenchymal tissue that forms the outer covering of the anatomic root.
Enamel: Calcified avascular mesenchymal tissue that forms the outer covering of the anatomic crown.
Three types of relationships involving the cementum may exist at the CEJ:
  1. Cementum overlapping the enamel
    It is seen in 60–65% of cases.
  2. Edge to edge joint of cementum and enamel also called “Butt Joint”.
    It is seen in 30% of cases.
  3. Cementum doesn't meet enamel.
    It is seen in 5–10%. In this case, dentin will be exposed to oral environment resulting in hypersensitivity.
Fenestrations: Isolated/Circumscribed areas in the alveolar bone in which the root is denuded of bone and marginal bone is intact.
Dehiscence: Denuded areas of the root which extend through the marginal bone. In these areas root surface is covered only by periosteum and overlying gingiva.
Etiology: Due to A. Prominent root contours, B.Tooth malpositions, C. Thin bony plates.
  • More common on facial surfaces of the anterior teeth and frequently bilateral.
  • It is seen in 20% of teeth.
Clinical Importance
May complicate periodontal surgery while reflecting the periodontal flaps. Hence, partial thickness flaps have to be elevated. Progression of periodontal diseases will be more rapid in these cases.
  • Thinning and decreased keratinization of the gingival epithelium occurs.
    zoom view
    Fig. 1.9: Fenestration and Dehiscences
  • 19This causes increase in epithelial permeability to bacterial antigens and decreased resistance to functional trauma.
  • This influences long-term periodontal outcomes.
  • There will be flattening of rete pegs and altered cell density.
  • The junctional epithelium will migrate from its normal position (i.e. on enamel) to more apical position on the root surface with gingival recession.
  • The width of attached gingival increases.
Connective Tissue
  • The width of attached gingiva increases.
  • Gingival connective tissue becomes coarser and denser.
  • Collagen synthesis decreases with age but has greater collagen content and increased collagen stabilization.
  • Increased conversion of soluble to insoluble collagen.
  • Increased mechanical strength.
  • Increased denaturing temperature.
  1. Periods of exacerbation/periods of activity – bone and connective tissue attachments are lost as pocket deepens. Clinically active periods show bleeding, either spotaneously or with probing and greater amounts of attachment loss, presence of exudating or pus.
  2. Periods of remission/quiescence/inactivity–reduced inflammatory response, little or no loss of bone and connective tissue attachment.