Introduction To Periodontology And Function Of The Periodontium PDF

YAKINDOĞU ÜNİVERSİTESİ DİŞHEKİMLİĞİ FAKÜLTESİ Assist. Prof. Dr.Ayşe Çaygür Yoran Learning outcomes: 1-Will be able to explain the clinical findings of healthy gingiva. 2- Will be able to define and distinguish hypercementosis radiographically. 3-Will be able to define cement resorption, list its cau...

YAKINDOĞU ÜNİVERSİTESİ DİŞHEKİMLİĞİ FAKÜLTESİ Assist. Prof. Dr.Ayşe Çaygür Yoran Learning outcomes: 1-Will be able to explain the clinical findings of healthy gingiva. 2- Will be able to define and distinguish hypercementosis radiographically. 3-Will be able to define cement resorption, list its causes, define cement repair, define ankylosis, explain its clinical importance. 4- Will be able to describe the periodontal ligament functions, list the physical functions of the periodontal ligament and explain 6the occlusal forces. 5-Will be able to explain the structural functions and clinical importance of the periodontal ligament, list the nutritional and sensory functions of the periodontal ligament. 6-Will be able to describe the anatomical and morphological structure and cells of bone, explain bone formation, remodeling and regulation of remodeling. 7- Will be able to explain remodeling of alveolar bone and define local and systemic factors affecting remodeling. Will be able to define vascularization, venous drainage & lymphatic system and innervation of alveolar bone. INTRODUCTİON TO PERİODONTOLOGY AND FUNCTION OF THE PERİODONTİUM Periodontology” is the branch of science that investigates and treats the diseases, and structures of the periodontium. Periodontium, which provides the necessary support for the teeth to maintain their functions, consists of four main components: gingiva, periodontal ligament, cementum and alveolar bone. To understand periodontal diseases, it is essential to know the anatomy of the periodontium and to define periodontal health. The structures that make up the periodontium were explained in our 1st grade lessons. In this course, the functions and clinical features of the structures that make up the periodontium, periodontal health and disease will be introduced. Periodontal health; can be described as a condition in which there is no inflammatory periodontal disease and no clinical inflammation. The clinical prerequisite in periodontal health is the absence of signs of inflammation associated with gingivitis and periodontitis. Gingivitis; Gingivitis is an inflammatory lesion that is limited only to the gingiva and does not extend to the periodontal attachment (cement, periodontal ligament and alveolar bone) resulting from the interaction between the dental plaque's biofilm and the host's immuneinflammatory response. The main finding is gingival bleeding. Periodontitis; It is characterized by the progressive destruction of the tissues supporting the tooth. Its main findings are periodontal tissue loss manifested as clinical attachment loss and bone loss at radiographs; periodontal pocket and gingival bleeding. GİNGİVA Correlation of Clinical and Microscopic Features An understanding of the normal clinical features of the gingiva requires the ability to interpret them in terms of the microscopic structures that they represent. Color: The color of the attached and marginal gingiva is generally described as “coral pink”; it is produced by the vascular supply, the thickness and degree of keratinization of the epithelium, and the presence of pigment-containing cells. The color varies among different persons and appears to be correlated with the cutaneous pigmentation. It is lighter in blond individuals with fair complexions than in swarthy, dark-haired individuals (Figure 1-25). The attached gingiva is demarcated from the adjacent alveolar mucosa on the buccal aspect by a clearly defined mucogingival line. The alveolar mucosa is red, smooth, and shiny rather than pink and stippled. Physiologic Pigmentation (Melanin): Melanin is a non– hemoglobin-derived brown pigment with the following characteristics: Melanin is responsible for the normal pigmentation of the skin, the gingiva, and the remainder of the oral mucous membrane. Melanin is present in all normal individuals (often not in sufficient quantities to be detected clinically), but it is absent or severely diminished in albinos. Melanin pigmentation in the oral cavity is prominent in black individuals. Ascorbic acid directly downregulates melanin pigmentation in gingival tissue Size: The size of the gingiva corresponds with the sum total of the bulk of cellular and intercellular elements and their vascular supply. Alteration in size is a common feature of gingival disease. Contour. The contour or shape of the gingiva varies considerably and depends on the shape of the teeth and their alignment in the arch, the location and size of the area of proximal contact, and the dimensions of the facial and lingual gingival embrasures. Shape: The shape of the interdental gingiva is governed by the contour of the proximal tooth surfaces and the location and shape of the gingival embrasures. When the proximal surfaces of the crowns are relatively flat faciolingually, the roots are close together, the interdental bone is thin mesiodistally, and the gingival embrasures and interdental gingiva are narrow mesiodistally. Conversely, with proximal surfaces that flare away from the area of contact, the mesiodistal diameter of the interdental gingiva is broad. Consistency: The gingiva is firm and resilient and, with the exception of the movable free margin, tightly bound to the underlying bone. The collagenous nature of the lamina propria and its contiguity with the mucoperiosteum of the alveolar bone determine the firmness of the attached gingiva. The gingival fibers contribute to the firmness of the gingival margin. Position: The position of the gingiva is the level at which the gingival margin is attached to the tooth. When the tooth erupts into the oral cavity, the margin and sulcus are at the tip of the crown; as eruption progresses, they are seen closer to the root. During this eruption process, as described previously, the junctional epithelium, the oral epithelium, and the reduced enamel epithelium undergo extensive alterations and remodeling while maintaining the shallow physiologic depth of the sulcus. Without this remodeling of the epithelia, an abnormal anatomic relationship between the gingiva and the tooth would result. Gingival Antimicrobial Defense Mechanisms The gingiva is exposed to mechanical and bacterial attacks. Gingival antimicrobial defense mechanisms consist of; 1-Gingival epithelium 2- Natural defense systems in the gingival groove 3- Saliva 4-Gingival crevicular fluid CEMENTUM Cementum is the calcified, avascular mesenchymal tissue that forms the outer covering of the anatomic root. It does not physiological resorption and remodeling. The greatest thickness is at the apex. -It is a yellowish color. It is softer than enamel and dentin. Creates an environment for the attachment of collagen fibers that connect the tooth to other tissues. Because it is softer, it causes wear and sensitivity when opened into the mouth. Thickness of Cementum Cementum deposition is a continuous process that proceeds at varying rates throughout life. Cementum formation is most rapid in the apical regions, where it compensates for tooth eruption, which itself compensates for attrition. The thickness of cementum on the coronal half of the root varies from 16 to 60 µm, which is about the thickness of a hair. It attains its greatest thickness (≤150 to 200 µm) in the apical third and in the furcation areas. It is thicker in distal surfaces than in mesial surfaces, probably because of functional stimulation from mesial drift over time. Between the ages of 11 and 70 years, the average thickness of the cementum increases threefold, with the greatest increase seen in the apical region. Average thicknesses of 95 µm at the age of 20 years and of 215 µm at the age of 60 years have been reported. Abnormalities in the thickness of cementum may range from an absence or paucity of cellular cementum (i.e., cemental aplasia or hypoplasia) to an excessive deposition of cementum (i.e., cemental hyperplasia or hypercementosis). The term hypercementosis refers to a prominent thickening of the cementum. It is largely an age-related phenomenon, and it may be localized to one tooth or affect the entire dentition. As a result of considerable physiologic variation in the thickness of cementum among different teeth in the same person and also among different persons, distinguishing between hypercementosis and the physiologic thickening of cementum is sometimes difficult. Nevertheless, the excessive proliferation of cementum may occur with a broad spectrum of neoplastic and nonneoplastic conditions, including benign cementoblastoma, cementifying fibroma, periapical cemental dysplasia, florid cemento-osseous dysplasia, and other benign fibro-osseous lesions. Radiographically, the radiolucent shadow of the periodontal ligament and the radiopaque lamina dura are always seen on the outer border of an area of hypercementosis, enveloping it as it would in normal cementum. On the other hand, from a diagnostic standpoint, periapical cemental dysplasia, condensing osteitis, and focal periapical osteopetrosis may be differentiated from hypercementosis, because all of these entities are located outside of the shadow of the periodontal ligament and the lamina dura. The cause of hypercementosis varies and is not completely understood. The spikelike type of hypercementosis generally results from excessive tension caused by orthodontic appliances or occlusal forces. The generalized type occurs in a variety of circumstances. In teeth without antagonists, hypercementosis is interpreted as an effort to keep pace with excessive tooth eruption. In teeth that are subject to low-grade periapical irritation that arises from pulp disease, it is considered compensation for the destroyed fibrous attachment to the tooth. Hypercementosis itself does not require treatment. It could pose a problem if an affected tooth requires extraction. In a multi-rooted tooth, sectioning of the tooth may be required before extraction. Cementum Resorption and Repair Permanent teeth do not undergo physiologic resorption as primary teeth do. However, the cementum of erupted (as well as unerupted) teeth is subject to resorptive changes that may be of microscopic proportion or sufficiently extensive to present a radiographically detectable alteration in the root contour. Cementum resorption may be caused by local or systemic factors, or it may occur without apparent etiology (i.e., idiopathic). Local conditions that cause cementum resorption include trauma from occlusion; orthodontic movement; pressure from malaligned erupting teeth, cysts, and tumors; teeth without functional antagonists; embedded teeth; replanted and transplanted teeth3,135; periapical disease; and periodontal disease. Systemic conditions that are cited as predisposing an individual to or inducing cemental resorption include calcium deficiency, hypothyroidism, hereditary fibrous osteodystrophy, and Paget disease. The regeneration of cementum requires cementoblasts, but the origin of the cementoblasts and the molecular factors that regulate their recruitment and differentiation are not fully understood. However, recent research provides a better understanding; for example, the epithelial cell rests of Malassez are the only odontogenic epithelial cells that remain in the periodontium after the eruption of teeth, and they may have some function in cementum repair and regeneration under specific conditions. The rests of Malassez may be related to cementum repair by activating their potential to secrete matrix proteins that have been expressed in tooth development, such as amelogenins, enamelins, and sheath proteins. Several growth factors have been shown to be effective in cementum regeneration, including members of the transforming growth factor superfamily (i.e., bone morphogenetic proteins), platelet-derived growth factor, insulin-like growth factor, and enamel matrix derivatives Ankylosis Fusion of the cementum and the alveolar bone with obliteration of the periodontal ligament is termed ankylosis. Ankylosis occurs in teeth with cemental resorption, which suggests that it may represent a form of abnormal repair. Ankylosis may also develop after chronic periapical inflammation, tooth replantation, and occlusal trauma and around embedded teeth. This condition is relatively uncommon, and it occurs most frequently in the primary dentition. PERİODONTAL LİGAMENT The periodontal ligament is composed of a complex vascular and highly cellular connective tissue that surrounds the tooth root and connects it to the inner wall of the alveolar bone. It is continuous with the connective tissue of the gingiva, and it communicates with the marrow spaces through vascular channels in the bone. Although the average width of the periodontal ligament space is documented to be about 0.2 mm, considerable variation exists. Functions of Periodontal Ligament The functions of the periodontal ligament are categorized as physical, formative and remodeling, nutritional, and sensory. Physical Functions. The physical functions of the periodontal ligament entail the following: 1. Provision of a soft-tissue “casing” to protect the vessels and nerves from injury by mechanical forces 2. Transmission of occlusal forces to the bone 3. Attachment of the teeth to the bone 4. Maintenance of the gingival tissues in their proper relationship to the teeth 5. Resistance to the impact of occlusal forces (i.e., shock absorption) 1.Resistance to Impact of Occlusal Forces (Shock Absorption): Two theories pertaining to the mechanism of tooth support have been considered: the tensional theory and the viscoelastic system theory. The tensional theory of tooth support states that the principal fibers of the periodontal ligament are the major factor in supporting the tooth and transmitting forces to the bone. When a force is applied to the crown, the principal fibers first unfold and straighten, and they then transmit forces to the alveolar bone, thereby causing an elastic deformation of the bony socket. The viscoelastic system theory states that the displacement of the tooth is largely controlled by fluid movements, with fibers having only a secondary role. When forces are transmitted to the tooth, the extracellular fluid passes from the periodontal ligament into the marrow spaces of the bone through the foramina in the cribriform plate. 2. Transmission of Occlusal Forces to Bone: The arrangement of the principal fibers is similar to that of a suspension bridge or a hammock. When an axial force is applied to a tooth, a tendency toward displacement of the root into the alveolus occurs. The oblique fibers alter their wavy, untensed pattern, assume their full length, and sustain the major part of the axial force. When a horizontal or tipping force is applied, two phases of tooth movement occur. The first is within the confines of the periodontal ligament, and the second produces a displacement of the facial and lingual bony plates. The tooth rotates about an axis that may change as the force is increased. The apical portion of the root moves in a direction that is opposite to the coronal portion. In areas of tension, the principal fiber bundles are taut rather than wavy. In areas of pressure, the fibers are compressed, the tooth is displaced, and a corresponding distortion of bone exists in the direction of root movement. 3.Formative and Remodeling Function: Periodontal ligament and alveolar bone cells are exposed to physical forces in response to mastication, parafunction, speech, and orthodontic tooth movement. Cells of the periodontal ligament participate in the formation and resorption of cementum and bone, which occur during physiologic tooth movement, during the accommodation of the periodontium to occlusal forces, and during the repair of injuries. Radioautographic studies with radioactive thymidine, proline, and glycine indicate a high turnover rate of collagen in the periodontal ligament. The rate of collagen synthesis is twice as fast as that in the gingiva and four times as fast as that in the skin, as established in the rat molar. A rapid turnover of sulfated glycosaminoglycans in the cells and amorphous ground substance of the periodontal ligament also occurs. It should be noted that most of these studies have been performed in rodents and that information about primates and humans is scarce. 4. Nutritional and Sensory Functions: The periodontal ligament supplies nutrients to the cementum, bone, and gingiva by way of the blood vessels, and it also provides lymphatic drainage as discussed later in this chapter. In relation to other ligaments and tendons, the periodontal ligament is highly vascularized tissue; almost 10% of its volume in the rodent molar is blood vessels. This relatively high blood vessel content may provide hydrodynamic damping to applied forces as well as high perfusion rates to the periodontal ligament. Nerve bundles pass into the periodontal ligament from the periapical area and through channels from the alveolar bone that follow the course of the blood vessels. The bundles divide into single myelinated fibers, which ultimately lose their myelin sheaths and end in one of four types of neural termination: (1) Free endings, which have a treelike configuration and carry pain sensation; (2) Ruffini-like mechanoreceptors, which are located primarily in the apical area; (3) Coiled Meissner corpuscles and mechanoreceptors, which are found mainly in the midroot region; (4) Spindlelike pressure and vibration endings, which are surrounded by a fibrous capsule and located mainly in the apex. Regulation of Periodontal Ligament Width: Some of the most interesting features of the periodontal ligament in animals are its adaptability to rapidly changing applied force and its capacity to maintain its width at constant dimensions throughout its lifetime. These are important measures of periodontal ligament homeostasis that provide insight into the function of the biologic mechanisms that tightly regulate the metabolism and spatial locations of the cell populations involved in the formation of bone, cementum, and periodontal ligament fibers. In addition, the ability of periodontal ligament cells to synthesize and secrete a wide range of regulatory molecules is an essential component of tissue remodeling and periodontal ligament homeostasis BONE STRUCTURE A bone is a rigid organ that constitutes part of the vertebrate skeleton. Bones support and protect the various organs of the body, produce red and white blood cells, store minerals, provide structure and support for the body, and enable mobility. Bones come in a variety of shapes and sizes and have a complex internal and external structure. They are lightweight yet strong and hard, and serve multiple functions. Bone tissue is a hard tissue, a type of dense connective tissue. Bone consists of two thirds inorganic matter and one third organic matrix. The inorganic matter is composed principally of the minerals calcium and phosphate, along with hydroxyl, carbonate, citrate, and trace amounts of other ions such as sodium, magnesium, and fluorine. The mineral salts are in the form of hydroxyapatite crystals of ultramicroscopic size and constitute approximately two thirds of the bone structure. The organic matrix consists mainly of collagen type I (90%), with small amounts of noncollagenous proteins such as osteocalcin, osteonectin, bone morphogenetic protein, phosphoproteins, and proteoglycans. Osteopontin and bone sialoprotein are cell-adhesion proteins that appear to be important for the adhesion of both osteoclasts and osteoblasts. In addition, paracrine factors, including cytokines, chemokines, and growth factors, have been implicated in the local control of mesenchymal condensations that occur at the onset of organogenesis. These factors probably play a prominent role in the development of the alveolar processes. Remodeling Remodeling is the major pathway of bony changes in shape, resistance to forces, repair of wounds, and calcium and phosphate homeostasis in the body. Indeed, the coupling of bone resorption with bone formation constitutes one of the fundamental principles by which bone is necessarily remodeled throughout its life. Bone remodeling involves the coordination of activities of cells from two distinct lineages, the osteoblasts and the osteoclasts, which form and resorb the mineralized connective tissues of bone. The bone matrix that is laid down by osteoblasts is nonmineralized osteoid. While new osteoid is being deposited, the older osteoid located below the surface becomes mineralized as the mineralization front advances. Bone resorption is a complex process that is morphologically related to the appearance of eroded bone surfaces (i.e., Howship lacunae) and large, multinucleated cells (osteoclasts). Osteoclasts originate from hematopoietic tissue and are formed by the fusion of mononuclear cells of asynchronous populations. When osteoclasts are active rather than resting, they possess an elaborately developed ruffled border from which hydrolytic enzymes are thought to be secreted. These enzymes digest the organic portion of bone. The activity of osteoclasts and the morphology of the ruffled border can be modified and regulated by hormones such as parathyroid hormone (indirectly) and calcitonin, which has receptors on the osteoclast membrane. Another mechanism of bone resorption involves the creation of an acidic environment on the bone surface, thereby leading to the dissolution of the mineral component of bone. This event can be produced by different conditions, including a proton pump through the cell membrane of the osteoclast, bone tumors, and local pressure translated through the secretory activity of the osteoclast. Ten Cate described the sequence of events in the resorptive process as follows: 1. Attachment of osteoclasts to the mineralized surface of bone 2. Creation of a sealed acidic environment through the action of the proton pump, which demineralizes bone and exposes the organic matrix 3. Degradation of the exposed organic matrix to its constituent amino acids via the action of released enzymes (e.g., acid phosphatase, cathepsin) 4. Sequestering of mineral ions and amino acids within the osteoclast. Cells and Intercellular Matrix Osteoblasts, which are the cells that produce the organic matrix of bone, are differentiated from pluripotent follicle cells. Alveolar bone is formed during fetal growth by intramembranous ossification, and it consists of a calcified matrix with osteocytes enclosed within spaces called lacunae. The osteocytes extend processes into canaliculi that radiate from the lacunae. The canaliculi form an anastomosing system through the intercellular matrix of the bone, which brings oxygen and nutrients to the osteocytes through the blood and removes metabolic waste products. Blood vessels branch extensively and travel through the periosteum. The endosteum lies adjacent to the marrow vasculature. Bone growth occurs via the apposition of an organic matrix that is deposited by osteoblasts. Bone Marrow In the embryo and the newborn, the cavities of all bones are occupied by red hematopoietic marrow. The red marrow gradually undergoes a physiologic change to the fatty or yellow inactive type of marrow. In the adult, the marrow of the jaw is normally of the latter type, and red marrow is found only in the ribs, sternum, vertebrae, skull, and humerus. However, foci of the red bone marrow are occasionally seen in the jaws, often accompanied by the resorption of bony trabeculae. Periosteum and Endosteum Layers of differentiated osteogenic connective tissue cover all of the bone surfaces. The tissue that covers the outer surface of bone is termed periosteum, whereas the tissue that lines the internal bone cavities is called endosteum. The periosteum consists of an inner layer composed of osteoblasts surrounded by osteoprogenitor cells, which have the potential to differentiate into osteoblasts, and an outer layer rich in blood vessels and nerves and composed of collagen fibers and fibroblasts. Bundles of periosteal collagen fibers penetrate the bone, thereby binding the periosteum to the bone. The endosteum is composed of a single layer of osteoblasts and sometimes a small amount of connective tissue. The inner layer is the osteogenic layer, and the outer layer is the fibrous layer. Vascularization of the Supporting Structures Structures The blood supply to the supporting structures of the tooth is derived from the inferior and superior alveolar arteries to the mandible and maxilla, and it reaches the periodontal ligament from three sources: apical vessels, penetrating vessels from the alveolar bone, and anastomosing vessels from the gingiva. The branches of the apical vessels supply the apical region of the periodontal ligament before the vessels enter the dental pulp. The transalveolar vessels are branches of the intraseptal vessels that perforate the lamina dura and enter the ligament. The intraseptal vessels continue to vascularize the gingiva; these gingival vessels in turn anastomose with the periodontal ligament vessels of the cervical region. The vessels within the periodontal ligament are contained in the interstitial spaces of loose connective tissue between the principal fibers, and they are connected in a netlike plexus that runs longitudinally and closer to the bone than the cementum. The venous drainage of the periodontal ligament accompanies the arterial supply. Venules receive the blood through the abundant capillary network. In addition, arteriovenous anastomoses bypass the capillaries and are seen more frequently in apical and interradicular regions; their significance is unknown. Lymphatics supplement the venous drainage system. Lymphatic channels that drain the region just beneath the junctional epithelium pass into the periodontal ligament and accompany the blood vessels into the periapical region.From there, they pass through the alveolar bone to the inferior dental canal in the mandible or the infraorbital canal in the maxilla and then go on to the submaxillary ly 1-Newman M, Takei H, Klokkevold P, Carranza F. Newman and Carranza (2019); Clinical Periodontology, 13th Ed., Elsevier.