PERIOD1_PM_NOTES-1.pdf

INTRODUCTION TO PERIODONTICS B. Periodontal ligament - Suspends and maintains the tooth in the socket. WHAT IS PERIODONTICS?...

INTRODUCTION TO PERIODONTICS B. Periodontal ligament - Suspends and maintains the tooth in the socket. WHAT IS PERIODONTICS? - Main function is to hold the tooth in place − A branch of dentistry that deals with diseases of the supporting and C. Cementum investing structures of the teeth. - Anchors the ends of the periodontal ligament fibers to the tooth to − Derived from two words: keep it in the socket ▪ Peri – around - One end of the periodontal ligament is attached to the cementum, ▪ Odontos – tooth while the other end is attached to the alveolar bone IMPORTANCE OF KNOWING THE ANATOMY OF D. Alveolar bone PERIODONTIUM - Surrounds and supports the root of the tooth − Normal function of the periodontium 2. NOTE: ▪ Holds teeth in place and to make sure teeth functions properly These parts (gingiva, periodontal ligament, cementum, alveolar bone) of the oral cavity are called periodontium collectively − Disease prevention Each of these components of the periodontium plays an important − The periodontal disease process part in maintaining the function of the oral cavity 1. NOTE: Periodontal disease is preventable, but there are some cases that the TISSUES OF THE PERIODONTIUM patient is immunocompromised, such that the disease of the periodontium is inevitable, but in most instances, it is preventable Periodontal disease usually starts with the accumulation of plaque and from there, the marginal gingiva starts to be infected and inflamed which results to gingivitis. If left untreated, it proceeds to alveolar bone being inflamed and results to periodontitis. THE PERIODONTIUM − Consists of: 3. NOTE: A. Gingiva If the periodontium is healthy, only the gingiva is seen clinically - Provides a tissue seal around the cervical portion of the tooth which prevents bacteria from entering the socket of the tooth and the THE GINGIVA periodontal ligament space THE GINGIVAL TISSUES A. Free Gingiva − The unattached portion of the gingiva that surrounds the tooth in the region of the cementoenamel junction (CEJ) − Not attached but has close proximity to the tooth specially if the tone is firm (healthy). B. Attached Gingiva − Part of the gingiva that is tightly connected to the cementum on the cervical third of the root and to the alveolar bone − Location: lies between the free gingiva and alveolar mucosa − Located apically to the free gingiva and coronally to alveolar mucosa − Color: pale or coral pink or pigmented (light brown to black) − Texture: stippled (Orange peel appearance) Function: − Allows gingival tissue to withstand mechanical forces − Prevents free gingiva from being pulled away from the tooth when tension is applied to the alveolar mucosa NOTE: In some pigmented individuals they could be light brown to black and that is still considered to be healthy because of the pigmentation of the gingiva ▪ There could be increased melanocytes which gives dark color of the gingiva ▪ There could be increased keratinization which makes the attached gingiva darker in color ▪ There could be thickening of the gingiva The texture is stippled because of the connective tissue that holds the gingiva in place Fiber connective tissues causes stippling which is important because it allows gingival tissues to withstand mechanical forces. Attached gingiva does not get separated to alveolar bone easily because of stippling TYPES OF GINGIVA C. Interdental Gingiva (Papilla) and Col  − Portion of the gingiva that fills the area between two adjacent teeth apical to contact area A. Gingival Margin Parts: − Thin rounded edge of the free gingiva a. Interdental Papillae − Coronal boundary or upper edge of the gingiva − Portion of the gingiva that is located on the buccal and on the − Located 1.5 to 2mm coronal to the CEJ after tooth eruption lingual surfaces of the teeth − About 1mm thick if the gingiva is healthy. If there is gingival hyperplasia, gingival growth, or thickening of the gingiva it will be b. Col 2-3mm thick NOTE: − Connects the lingual and facial portion of interdental papilla If there is gingival recession, it is the gingival margin that is moving − Significance: made of non-keratinized tissues which makes it easy apically for bacteria to enter that part and this where initial inflammation usually starts NOTE: B. Alveolar Mucosa Healthy oral cavity has no black triangles − The apical boundary, or lower edge of the gingiva Black triangles: unsightly and unaesthetic appearance of the − Dark red in color with smooth and shiny surface triangle apical to the contact area if the interdental papilla is − Located apical to the attached gingiva diminished NOTE: If a tooth is extracted, the interdental papillae and col is lost − When doing impressions, alveolar mucosa forms the boundary of the impression − When fabricating dentures, make sure that the borders of the D. Gingival Sulcus/Crevice denture do not touch the alveolar mucosa because alveolar mucosa − It is the space between the free gingiva and the tooth surface is mobile. If the border of denture touches this portion, when the − A V-shaped shallow space around the tooth patient speaks or masticates, the denture will get dislodged. − Normal depth is 1-3mm − Base of the sulcus is formed by the junctional epithelium C. Gingival Groove NOTE: − A shallow linear depression that separates the free gingiva and − Space where foods get stuck the attached gingiva − This is the space where plaque usually develops NOTE: − The ideal reading of depth is actually 0, but because of the − This is not always visible presence of bacteria, there is the formation of sulcus which gives − If gingival groove is not visible, it does not automatically indicate rise to 1-2mm depth gingivitis − Some literatures say that gingival groove diminishes over time or − Beyond the normal depth (reads more than 3mm), that will indicate because of aging periodontal disease − Gingival groove is horizontal and simulates the shape of the free − Junctional epithelium starts to attach the gingiva to the cementum gingiva and alveolar bone and this is not seen clinically STRUCTURES OF THE GINGIVA D. Interdental Groove  − The vertical groove, parallel to the long axes of adjacent teeth ▪ Free Gingival Groove − It is found in the interdental area of the attached gingiva ▪ Mucogingival Junction − Separates one root to the other ▪ Alveolar Mucosa ▪ Gingival Margin NOTE: Free Gingival groove − Delineates the free gingiva from the attached gingiva from the alveolar mucosa E. Mucogingival Junction − Clinically visible boundary where the pink attached gingiva meets the red, shiny alveolar mucosa Keyword: Muco – alveolar mucosa Gingival – refers to attached gingiva Festooning − Removal or carving of excess wax to simulate the natural anatomy of gingiva THE PERIODONTAL LIGAMENT Periodontal Ligament − Layer of soft connective tissue that covers the root of the tooth and attaches it to the bone of the tooth socket − Composed mainly of fiber bundles − Width of the periodontal ligament is 0.15mm to 0.38mm NOTE: − In cases where the tooth is ankylosed, or the tooth is directly attached to the alveolar bone, the periodontal ligament is lost ▪ Free Gingiva ▪ Attached Gingiva  DIFFERENT PERIODONTAL LIGAMENTS NAMED AFTER THEIR LOCATION OR Sensory function POSITION − Provides sensory feeling to the tooth, such as pressure, touch, and pain sensations Types of Periodontal Ligament: Gingival Alveolar crest Oblique Nutritive function Trans-septal Horizontal Apical Fibers − Provides nutrients to the cementum and bone − Periodontal ligament attaches tooth to the alveolar bone, and this attachment is cementum of one side and alveolar bone on one side Formative function − Builds and maintains cementum and the alveolar bone of the tooth socket − Functions on the distal portion of the tooth because the area where the tooth came from, that is where new alveolar bone will develop − Provides osteoblast on the distal portion Resorptive function − Can remodel the alveolar bone in response to pressure − More evident in mesial portion of the tooth − Provides osteoclast on the mesial portion NOTE: NOTE: Trans-septal periodontal ligament goes over the septum of the Orthodontic tooth movement is possible because of the formative and alveolar bone resorptive function of the periodontal ligament The connection of the trans-septal periodontal ligament is from the cementum one tooth to the cementum of the other tooth The connection of the Dentino-gingival periodontal ligament is from the dentin of the tooth towards the interdental gingiva Circumferential periodontal ligament goes around the tooth The attachment of Alveolar crest periodontal ligament is from the alveolar crest of the alveolar bone towards the cementum of the tooth FUNCTIONS OF THE PERIODONTAL LIGAMENT Supportive function − Suspends and maintains the tooth in the socket − Main function of the periodontal ligament THE CEMENTUM Cementum − Thin layer of hard, mineralized tissue that covers the surface of the tooth root CHARACTERISTICS OF CEMENTUM − Light yellow in color, but sometimes may be darker yellow − Overlies and is attached to the dentin of the root − Bonelike tissue but is more resistant to resorption than the bone − Does not have their own blood supply or nutrient supply NOTE: In Orthodontic tooth movement, when you move the tooth to a specific position, you want the bone to resorb and not the cementum (cementum is still harder than alveolar bone) The periodontal ligament supplies the nutrients needed by the cementum FUNCTIONS OF THE CEMENTUM Anchors the end of the periodontal ligament fibers to the tooth Protects the underlying dentin Compensates for tooth wear at the occlusal or incisal surface due to attrition NOTE: Without the cementum, the tooth is susceptible to bacterial invasion Once the cementum wears off or abraded, the dentinal tubules are exposed to the oral cavity. The exposed dentinal tubules will become a pathway for bacteria to enter the pulp If there is constant chewing and mastication the incisal and occlusal surfaces of the teeth wear off, which is why as we age, we lose mamelons and the cusp tips of the molars are no longer as sharp, but there is no space between the opposing teeth. This is because teeth continuously erupt to meet the opposing teeth, and the cementum forms cementocytes which forms new cementum on the apical portion of root to maintain the tooth in place THE ALVEOLAR BONE B. Cortical Bone − Layer of compact bone that forms the hard, outside wall of the mandible and maxilla on the facial and lingual aspects Alveolar bone − Thin in the incisor, canine, and premolar regions, thicker in the molar Bone of the upper or lower jaw that surrounds and supports the root regions of the teeth − Not visible in radiographs The existence of the alveolar bone depends on the present of the − Located in the outermost surface of the alveolar process teeth NOTE: NOTE: Sometimes in tooth extraction, when the tooth is ankylosed, or the If the tooth is extracted, the alveolar bone resorbs and is lost over tooth is not properly luxated from the alveolus, it is the cortical bone time that comes off with the tooth because it is thin FUNCTIONS OF THE ALVEOLAR BONE C. Alveolar Crest Forms the bony socket that provide support and protection for the roots of − Most coronal portion of the alveolar process the teeth − Located 1mm-2mm below the cementoenamel junction − From the facial and lingual aspect, the alveolar crest is wavy or scalloped following the cementoenamel junction LAYERS THAT COMPOSE THE ALVEOLAR PROCESS A. Alveolar Bone Proper or Cribriform Plate D. Cancellous bone or Spongy bone − Thin layer of bone that lines the socket to surround the root of a tooth − Latticelike bone that fills the interior portion of the alveolar process − Innermost portion of the alveolar process − Oriented around the tooth to form support for the alveolar bone − Closely located to the root of the tooth proper − Alveolus – the bony socket; cavity in the alveolar process that houses the root of a tooth − The alveolar bone proper has numerous holes that allow blood vessels E. Periosteum from the cancellous bone to connect with the vessels of the − Layer of connective tissue covering the outer surface of the bone periodontal ligament space − Composed of outer layer of collagenous tissue and an inner layer of − The ends of the periodontal ligament fibers are embedded in the elastic fibers alveolar bone proper − Attaches the attached gingiva to the alveolar bone  The Trigeminal Nerve NERVE SUPPLY, BLOOD SUPPLY AND − Responsible for the sensory ability of most of the skin of the front part LYMPHATIC SUPPLY OF THE PERIODONTIUM of the face and head, teeth, oral cavity, maxillary sinus, and nasal cavity − The motor function is responsible for mastication Nerve Supply to the Periodontium − The periodontium is innervated by the branches of the trigeminal nerve Functions of the nerve supply of the periodontium − The trigeminal nerves have sensory, motor, and intermediate roots that attach directly to the brain − Nerve receptors in the gingiva, alveolar bone, and periodontal ligament register pain, touch and pressure NOTE: − Nerves in the periodontal ligament provide information about movement and tooth position The trigeminal nerve provides the sensory and motor innervations to the periodontium NOTE: The mandible is able to move, the teeth feel pain because of the innervation of the trigeminal nerve The tooth and gingiva will not feel hot or cold, it will only feel pain and this is due to the nerve receptors that is innervated by the trigeminal nerve INNERVATION OF THE GINGIVA Maxillary Arch − Superior alveolar nerve (anterior, middle, posterior branches), infraorbital nerve, greater palatine, and nasopalatine nerve − The gingiva is innervated by Superior alveolar nerve Mandibular Arch − The trigeminal nerve branches out into Superior alveolar nerve − Innervated by mental nerve, buccal nerve, and the sublingual branch − The superior alveolar nerve will branch to posterior superior alveolar of the lingual nerve nerve, middle superior alveolar nerve and the anterior superior alveolar nerve − For the mandible, the trigeminal nerve, it branches out buccal nerve, lingual nerve, and inferior alveolar nerve − The inferior alveolar nerve branches out to the mental nerve INNERVATION OF THE TEETH AND PERIODONTAL LIGAMENT BRANCH ARTERIES Maxillary Arch − Superior Alveolar Nerve (anterior, middle, and posterior branch) Mandibular Arch − Inferior Alveolar Nerve BLOOD SUPPLY TO THE PERIODONTIUM − Vessels of the periodontium anastomose to create a complex system of blood vessels that supply blood to the periodontal tissues Function: − Transport oxygen and nutrients to the tissue cells − Detoxification and elimination. Remove carbon dioxide and other waste products from the cells I. Dental Artery − Branch of the Superior Alveolar Artery (SAA) or Inferior Alveolar Artery (IAA) (Supplies the tooth) Blood Supply of Maxillary Gingiva, Periodontal Ligament, and Alveolar Bone − The dental artery is a branch for the inferior alveolar artery of the − Supplied by anterior and superior alveolar arteries mandible and superior alveolar artery of the maxilla, and it supplies − Infraorbital artery the blood towards the tooth − Greater Palatine artery II. Intraseptal Arteries − Enters the tooth socket Blood Supply of Mandibular gingiva, Periodontal Ligament, and Alveolar Bone III. Rami Perforantes − Inferior alveolar artery − Terminal branches of the intraseptal artery − Branches of the inferior alveolar artery: the buccal, facial, mental, − Penetrates the tooth socket and enters the periodontal ligament space and sublingual arteries where they anastomose with the blood vessels from the alveolar bone IV. Supreperiosteal Blood Vessels − Main blood supply of the free gingiva VASCULAR SUPPLY TO THE TEETH AND PERIODONTAL TISSUES A. The Major Arteries V. Subepithelial plexus − Branch of the supraperiosteal blood vessels − Superior Alveolar Arteries – maxillary periodontal tissues − Inferior Alveolar Arteries – mandibular periodontal tissues  VI. Periodontal Ligament vessels − Supplies the periodontal ligaments VII. Dentogingival plexus − Fine-meshed network of blood vessels located in the connective tissue beneath the gingival sulcus − Where blood vessels of different parts in periodontium anastomose or meet − One significance of this is that the gingiva bleeds easily when you manipulate this part, especially if it is inflamed because of the presence of dentogingival plexus NOTE: If the composite restorative materials is contaminated with blood, it compromises the retention of the restorative material THE AGING PERIODONTIUM CLINICAL CHANGES − Compensatory changes occur as a result of aging and disease Functional Changes These changes include: I. Gingival recession and reductions in bone height − Cells of the oral epithelium and periodontal ligament have reduced mitotic activity and metabolic rate leading to decreased healing capacity and rate NOTE: Because of mastication, there is gingival recession: NOTE: There is attrition in incisal areas of anteriors and the occlusal surfaces of the posteriors. Because of attrition, the tooth will supraerupt, this is Over time, the more trauma the periodontal ligament goes through, why there is no space between maxillary and mandibular teeth the lesser its capacity to adapt or heal due to the reduced mitotic despite attrition. The tooth will keep erupting until it meets its activity antagonist This is why periodontitis due to trauma is more prevalent I adults than Somehow, if forces are directed on to the tooth, it deflects towards in young children, because in adults, the periodontal ligament does crestal bone or alveolar bone crest, and this leads to reduction in not heal as fast as young people bone height − Inflammation, when present, develops more rapidly and more severely II. Attrition is a compensatory change that acts as a stabilizer between loss of bony support and excessive leveraging from occlusal forces NOTE: imposed on the teeth In young children, there is such thing as a juvenile periodontitis which is present in teenagers. We also have gingivitis in children, but does not NOTE: develop rapidly. Over time, it heals as long as the patient have When there is an excessive mastication, instead of the periodontal proper oral hygiene, however in adults, because of lesser capacity to ligament getting traumatized or the alveolar bone crest reducing fast. heal, the inflammation may develop to a more severe case. If the It is the incisal or occlusal surfaces that receives the initial brant of patient has gingivitis, it may develop into periodontitis easily (not mastication and this leads to loss of tooth structure of the incisal and always the case) occlusal surfaces of tooth III. Reduction of overjet in anterior teeth - edge to edge bite − Individuals are highly susceptible to viral and fungal infections because of abnormalities in T-cell function NOTE: − Reduce efficiency in mastication In initial migration of tooth, there is proximal surface tooth loss which NOTE: leads to edge-to-edge bite. This is why it is very common in adults to have edge-to-edge bite when initially they have positive overbite. Reduced efficiency of mastication is due to mobility Possible reason is the approximal loss of tooth surface in the posterior Tooth mobility is more common in adults than with children teeth, as well as initial migration of the tooth  IV. Increase in food table - loss of sluiceways NOTE: Possible reason for the migration of the junctional epithelium to a NOTE: more apical position is the supraeruption of the tooth Sluiceways As the tooth supraerupts to compensate for incisal wear, the junctional epithelium which is the attachment or base of the sulcus of the gingiva − Groove or channel through which food may pass from occlusal moves to a more apical position. If initially, the junctional epithelium is surfaces of teeth during masticatory process on the same level as the CEJ, it now moves to a more apical position, and that is closer to the cementum NOTE: Because of the presence of cusps in the posterior teeth, there are grooves. The grooves or spaces where food will pass through during − Gingival recession is not an inevitable process of aging but is a result mastication are sluiceways of cumulative process of trauma and inflammation Sluiceways are lost as we grow old because of the loss of the cusps in adults due to attrition NOTE: Gingival recession happens over time because of trauma and inflammation HISTOLOGICAL CHANGES Trauma when we brush our teeth, ao we are advised to massage our gingiva when we brush, but when we put too much force on the gingiva, gingival recession takes place or the marginal gingiva moves Gingival Epithelium apically − Thinning and decreased keratinization If the tooth is subjected to inflammation as it heals, it will result to − Increased permeability to bacterial antigen gingival recession − Decreased resistance to functional trauma Frenum pull; if the frenum is located more coronally than it should be, normal mastication and speech will lead to the pulling of the gingiva towards a more apical position, this is why we do frenectomy, not NOTE: only for aesthetic purposes, not only for retention of prosthesis, but to As we age, the gingival epithelium thins out and the keratinizarion is avoid gingival recession as well decreased. The implication of this is that it has increased permeability to bacterial antigen, therefore, if there is a presence of bacteria in the oral cavity, it can enter the gingiva easier because of thin gingival epithelium, hence causing inflammation Junctional Epithelium − Migrates to a more apical position on the root surface with accompanying gingival recession − The migration of the JE is caused by the tooth erupting RELATIONSHIP OF THE GINGIVA WITH THE CROWN AND ROOT C. GM moved coronally with the tooth, entire dentogingival SURFACE complex moved with the tooth resulting in increased width of attached gingiva NOTE: There is coronal movement of the tooth and the gingival margin moved with it There is an increase in the width of the attached gingiva because of the movement of the gingival margin with the tooth D. No incisal wear, there is clinical gingival recession, decreased width of attached gingiva NOTE: Possible reason for this is trauma due to toothbrush injury There is a decrease of the width with the attached gingiva A. Normal relationship of gingival margin to CEJ NOTE: Normally, the CEJ is located 2mm apical to the gingival margin The width of the attached gingiva is the same Gingival Connective Tissue − Increasing age results in a denser and coarser GCT NOTE: The gingival connective tissue is denser and coarser which will allow it B. GM remains the same, tooth supra-erupted (gingival to be able to withstand mechanical trauma recession and root exposure is evident, width of attached gingiva is the same) − Increased rate of soluble to insoluble collagen − Increased mechanical strength NOTE: − Increased denaturing temperature Gingival margin is still located in its normal position; however, it looks like there is gingival recession because of the supraeruption of the NOTE: tooth. Possible reason for this is the tooth is compensating for incisal tooth wear All of these changes lead to a more stabilized gingival connective The width of the attached gingiva is the same tissue Periodontal Ligament receiving the forces of multiple opposing teeth, therefore there is an increase width of periodontal ligament of the lone tooth − Decreased number of fibroblasts and more irregular structure Cementum NOTE: − Increased cemental width (5-10 times with increasing age) If there is decreased fibroblasts, there is decreased formation of new − Deposition of cementum continues after tooth eruption periodontal ligament If the patient undergoes periodontal treatment, there is a possibility NOTE: of the tooth not recovering because of the decreased number of the There is continuous deposition in the cementum of the tooth as a result fibroblasts of the tooth supraerupting (tooth supraerupts to compensates for If the patient has periodontitis, it has mobility. It is possible that even incisal tooth wear but the tooth does not become mobile, because if the patient undergoes treatment, the tooth may be stable, but there there is continuous deposition of cementum on the apical area of the is no formation of new periodontal ligament because of the tooth) decreased number of fibroblasts The deposition of cementum happens on the apical area of the tooth, not on the middle third and not on the incisal third of the root of the tooth − Decreased organic matrix production and epithelial rests NOTE: Alveolar Bone − Irregular periodontal surface of bone and less regular insertion of If patient has periodontitis, and the pocket has healed already. Even collagen fibers if the pocket heals, the depth of the pocket does not increase to normal which is 2-3mm because of the decrease in fibroblasts − Osteoporosis — age is a risk factor but is not a causative agent NOTE: − Increased amount of elastic fibers It is possible for adults to undergo osteoporosis, but age is not the − Hypofunction (Unopposed tooth) = decrease width reason Other possible reasons for osteoporosis: lack of calcium and systemic − Hyperfunction= increased width diseases NOTE: If the tooth does not have an opposing tooth, the periodontal − Healing of extracted bone sites is not affected by age ligament decreases in width NOTE: Possible scenario of teeth in hypofunction: maxillary third molars Because there is normal healing of extracted bone sites, even in older erupts and mandibular third molars does not, making it unopposed individuals Possible scenario of teeth in hyperfunction: a lone abutment or teeth- There are older patients (ages 80+) who undergo implant therapy there is no teeth on its mesial or distal. There is only one tooth (implantation of screws to replace tooth that has been extracted), and still have normal regeneration of bone because the patient is healthy Bacterial Plaque − Dentogingival plaque accumulation increases with age Possible reasons: − Increased hard tissue surface area due to gingival recession − Exposed root surface is a substrate for plaque formation NOTE: Initially, in young children, only the enamel is exposed in the oral cavity. That is why if there is plaque build-up, it only happens in the enamel. As we grow old, because of gingival recession, there is the exposure of the cementum, therefore there is an increased area wherein plaque can accumulate The surface of the cementum is rougher than the enamel. The t=rough surface makes it easier for plaque to accumulate COMMON ETIOLOGICAL FACTORS OF TOOTH SURFACE DEPOSITS PERIODONTAL DISEASE ETIOLOGIES OF PERIODONTAL DISEASE I. Bacteria − There are excessive amounts of bacteria in the oral cavity. Although bacteria are always present in the oral cavity, excessive amounts of bacteria and decreased immune system of the patient may result to periodontal disease − If you have good immune system, despite having bacteria in the oral Acquired Pellicle cavity, then you will still have healthy periodontium Calculus Food debris Materia alba II. Systemic Stains − There are systemic diseases or reasons for the presence of Bacterial plaque periodontal disease like diabetes milletus. Diabetes milletus is an endrocrine disorder and it has oral manifestations such as weakening of the periodontal apparatus, bleeding of the gingiva and inflammation of the gingiva − Pregnancy is also a systemic condition and also has oral manifestations similar to puberty III. Local contributing factors − States in the oral cavity that may cause periodontal disease such as overhanging restorations, poorly fabricated bridges and crowns, and removable partial denture that is impinged to the alveolar bone. Under this we also have crowding of the teeth. If the teeth is extremely crowded, especially on hard to reach areas such as posterior teeth, food could get retained on the crowded areas and if the patient does not clean that area properly, then it may lead to periodontal disease  A. Acquired Pellicle B. Calculus − An adherent calcified mass that forms on surfaces of teeth or dental appliance − Calculus does not only form on natural teeth, but it can also form on − Thin (0.1 to 0.8μm) protein film that forms immediately on erupted dentures teeth − Its surface is covered by vital tightly adherent non-mineralized − Can be removed by abrasives plaque − Quickly re-forms after being removed TYPES OF CALCULUS NOTE: I. Supragingival Calculus Even if you brush, acquired pellicle will form right away after − They form on the clinical crowns of teeth above the free gingival brushing (around 10 seconds) margin When you brush your teeth, the acquired pellicle is removed or − Also known as Salivary Calculus because it comes from the saliva displaced. The displacement of acquired pellicle through − They are usually whitish in color with a hard clay like consistency, but toothbrushing may be because of the abrasives found on the could be stained dark brown from smoking and pigments from foods toothpaste, or the physical act of toothbrushing itself It is on the acquired pellicle that dental plaque forms NOTE: Supragingival calculus are found coronal to marginal gingiva or the free gingival margin If you remove supragingival calculus through oral prophylaxis, it will come off as pebble-like or stone-like structure Most of the time, supragingival calculus forms on the lingual surface of the mandibular central and lateral incisors or on the buccal surfaces of the maxillary molars because these are where the Bartholin’s duct and Wharton’s duct are located  II. Subgingival Calculus NOTE: Subgingival calculus is always associated with the presence of periodontal pockets If a periodontal pocket is present, there is the loss of clinical attachment, as well as the resorption of alveolar bone, hence the possibility of the formation of subgingival calculus Supragingival calculus are most of the time associated where the salivary ducts are COMPONENTS OF CALCULUS − Calcified material located on the root surfaces below the free gingival margin Inorganic Components − Also known as serumal calculus because they come from salivary Component Dry weight (in percent) exudate Inorganic 70 - 90 − They are greenish or dark brown in color because they get their color Calcium 27 - 29 from the blood pigments located subgingivally Phosphorous 16 - 18 Carbonate 2-3 Sodium 1.5 - 2.5 Magnesium 0.6 – 0.8 SUPRAGINGIVAL CALCULUS VS. SUBGINGIVAL CALCULUS Fluoride 0.003 – 0.04 Crystal forms Hydroxyapatite 58 Supragingival Subgingival Magnesium whitlockite 21 Location Above the gingival Below the gingival Octacalcium phosphate 12 margin margin Brushite 9 Color White, Yellow Greenish black Source Derived from salivary Formed from gingival secretions exudate or gingival Organic Components crevicular fluid Component Dry weight (in percent) Composition More brushite and Less brushite and Mixture of protein, polysaccharide 1.9 – 9.1 octacalcium phosphate, octacalcium phosphate, complexes, desquamated epithelial less magnesium more magnesium cells, leukocytes and various whitlockite whitlockite miroorganisms. Carbohydrate Salivary Proteins Present Absent (consists of glucose, galactose, Sodium Content Lesser Increases with the rhamnose, mannose) depth of the pocket Proteins 5.9 – 8.2 Lipids 0.2 NOTE: Materia Alba Makes up 10% - 30% of the calculus − White matter that lacks the organized structure of dental plaque, easily displaced by water spray NOTE: 4 TYPES OF ATTACHMENT OF CALCULUS TO THE TOOTH SURFACE Clinically, materia alba and plaque looks similar, but their difference is in structure. Materia alba is not as sticky as plaque, and it is not as attached to the tooth surface as compared to plaque, therefore it can be displaced by water syringe Plaque A. Attachment by means of an organic pellicle − Attachment of calculus through an organic pellicle. The presence of an organic pellicle makes it easier for the calculus to attach to the tooth B. Mechanical interlocking into surface irregularities such as resorption lucnae and caries − Because of the presence of these depressions and cavitations, it is easier for the calculus to attach to the tooth. − It is difficult to remove calculus that is attached to the tooth due to caries because caries has uneven surface resulting to a very tight interlocking between the surface of the calculus and caries − A strucutured, resilient yellow-grayish substance that adheres − In this situation, we use ultrasonic scalers to remove the calculus, then tenaciously to the intraoral hard surfaces use manual scalers, and then polished with abrasives to remove the remaining calculus NOTE: Some studies say that plaque is considered to be a biofilm C. Penetration of calculus bacteria into cementum Plaque has an organized structure where there is an interlaced − This theory is not widely accepted as the others because some say aqueous channel which serves as nutritional channels for bacteria that that bacteria cannot penetrate cementum, because cementum is a allows the bacteria to multiply in plaque calcified surface Because of bacterial components of plaque and calcular deposits, it is the main main and usual etiology for periodontial disease D. Close adaptation of calculus under surface depressions to the Plaque is soft compared to calculus. Therefore, they could be easily gently sloping mounds of unaltered cementum surface exposed through disclosing solution TYPES OF DENTAL PLAQUE Subdivisions of Subgingival Plaque I. Supragingival Plaque I. Attached − Found at or above the gingival margin. It is also known as marginal II. Unattached – tooth associated plaque, epithelium associated plaque, plaque when it is in direct contact with the gingival margin connective tissues associated plaque Subdivision of Supragingival Plaque Supragingival Plaque Subgingival Plaque 1. Matrix 50% Matrix Little or no matrix i. Coronal plaque 2. Flora Mostly Gram-positive Mostly Gram-negative − Seen on the tooth surfaces alone 3. Motile bacteria Few Common 4. Anaerobic/Aerobic Aerobic unless thick Highly anaerobic ii. Marginal plaque areas present − Seen on tooth surfaces and gingival margin 5. Metabolism Predominantly Predominantly proteins carbohydrates − Attached and unattached “free floating” NOTE: Matrix is what holds gingival plaque together or it is what forms the II. Subgingival plaque structure of the plaque Gram-negative bacteria are what causes gingival inflammation Subgingival plaque is made up of little matrix, so it could be easily displaced, however, it is made up mostly of gram- negative bacteria and anaerobic bacteria, which means that it is the subgingival plaque that causes inflammation more than the supragingival plaque CONSTITUENTS OF PLAQUE a. Colonized organisms b. Epithelial cells − It is found below the gingival margin, between the tooth and the c. White blood cells, leukocytes and PMNs gingival pocket epithelium d. Erythrocytes NOTE: e. Protozoa. Entamoeba and Trichomonas This type of plaque is thin, is contained within the gingival sulcus or periodontal pocket, and it could not be clinically observed f. Food particles Its presence could be detected by running a probe through the gingival margin or you can use manual scalers or explorers g. Miscellaneous components MICROORGANISMS OF PLAQUE BACTERIA ASSOCIATED WITH HEALTH AND DISEASE 1 – 2 days: A. Healthy gingiva: − Gram-positive and some gram-negative cocci and rods in an − 100 – 1000 bacteria amorphous mucopolysaccharide pellicle; − 75% - 80% gram-positive and nonmotile − Less than 1μm; − Attached to the enamel, cementum or dentin B. Gingivitis NOTE: − 1000 – 100000 Since it is primarily made up of gram-positive bacteria, then 1 – 2 − Equal proportion of gram-positive and gram negative days old plaque is not as detrimental to the gingiva as compared to older plaques 2 – 4 days − Increased number of gram-negative cocci and rods C. Periodontitis − Fusiform bacilli − 100000 – 100000000 − Filamentous organisms − High proportion of gram-negative and motile bacteria NOTE: Becomes more detrimental to the gingiva as it causes more inflammation more than the 1 – 2-day old bacteria 4 – 9 days − Same bacterial population as in 2 – 4 days − Plus increasing number of motile bacteria like spirilla and spirochetes  b. Contours and overhanging dental restorations LOCAL AND SYSTEMIC CAUSES OF PERIODONTAL DISEASE NOTE: - Factors that are caused by the dental practitioner Contours We are referring to the convexity of the tooth 1. Faulty dental restorations When we make jacket crowns, we don’t want the buccal portion or the lingual portion of the crown to be over contoured or overly a. Margins of restoration convexed, because if the crown is overly contoured, the plaque will retain on the marginal area of the tooth causing gingivitis − Bone loss can be seen in the radiograph. Bone loss is due to the margin of the was jacket crown encroaching on to the biological width of the tooth Overhanging restoration seen on radiograph. This is an example of a − That is why it is best that the margins of restoration is placed Class II with overhanging restoration on mesial part. And this area will equigingivally or supragingivally in non-aesthetic zones so that it will become an area for plaque retention not encroach on the biological width − Studies have proven that restorations encroaching on the biological width will cause periodontal pockets c. Occlusion − When you bite and the occlusion is not restored properly (ex: newly NOTE: restored tooth is higher than other teeth), it will cause trauma on the periodontal ligament on the tooth that has been restored, causing Biological width periodontal disease Attached portion of the gingiva beneath the cementoenamel junction d. Dental materials − Dental materials do not have direct relationship with the occurrence of periodontal disease, but only when the dental materials used are not polished properly or when there is a presence of voids on the margins, then it will become an area for plaque, causing periodontal disease  e. Design of removable partial dentures placed too apically and it encroaches on the gingival sulcus, then it − If the metal framework encroaches on the gingiva, then that will cause will favor plaque retention periodontal disease In orthodontic treatment, we want the tooth to move, but if we put too − If the clasps of the removable partial dentures impinge on the much force on the tooth, then it will cause necrosis on the tooth marginal gingiva, then that will cause periodontal disease f. Restorative materials DIETARY AND NUTRITIONAL ASPECT OF PERIODONTAL DISEASE − When we do composite restorations, we use etchant. Etchants are The consistency of Diet made of phosphoric acid, and if it has long contact with the tissues of the gingiva, then it will burn the gingiva, causing periodontal disease − Firm and fibrous diet is more beneficial than an intake of soft and more loosely textured food − Other materials that may cause periodontal disease are phenolic compounds. Phenolic compounds are used as medicaments in − Fibrous diet tent to impart natural cleansing action on the teeth endodontic treatment NOTE: Orthodontic Therapy The vitality of the periodontal tissue (gingiva, periodontal ligament, alveolar bone) depends on the essential nutrients Research shows that nutritional deficiency produces changes on the oral cavity, however there are no nutritional deficiencies that causes gingivitis or periodontal pockets by themselves only. Lack of vitamins will go in conjunction with other factors such as plaque retention or overhanging restorations, and hormonal imbalances PROTEIN DEFICIENCY AND PERIODONTAL DISEASE − Studies indicate that protein deprivation causes pathologic changes in − Orthodontic therapy favors plaque retention the periodontium − Overextended bands may directly injure the gingiva − Marked degradation of periodontal support − Unnecessary forces may cause necrosis NOTE: NOTE: Protein is a constituent of the organic matrix of dental tissues like the Orthodontic therapy in layman’s term in braces alveolar bone, therefore lack in protein may result to alveolar bone Orthodontic appliance is connected to a molar band. Molar bands loss are placed on the first molars. When we cement our molar bands, we The integrity of the periodontal ligament is also dependent upon want it placed equigingivally or subgingivally, but when the band is proteins, specifically the amino acids  In protein deficiency, there is degradation or loss of periodontal POSSIBLE ETIOLOGIC RELATIONSHIPS BETWEEN ASCORBIC ACID support, mainly on the periodontal ligament and alveolar bone AND PERIODONTAL DISEASE VITAMINS AND PERIODONTAL DISEASE 1. Low levels of Ascorbic acid influences the metabolism of collagen within the periodontium, thereby affecting the ability of the tissue to regenerate and I. Vitamin C repair by itself − Deficiency may result in scurvy 2. It interferes with bone formation leading to the loss of the alveolar bone 3. Increases the permeability of oral mucosa to tritiated endotoxin and inulin NOTE: These endotoxins may come from the bacteria found in plaque If the mucosa has increased permeability to endotoxins from bacteria, then inflammation will take place 4. Increased levels of Ascorbic acid enhances both the chemotactic and migratory action of leukocytes without influencing phagocytic activity Clinical Manifestations: 5. Optimal level of Ascorbic acid is required to maintain the integrity of the a. Increased susceptibility to infections periodontal microvasculature as well as the vascular response to bacterial irritation and wound healing b. Impaired wound healing c. Bleeding and swollen gingiva NOTE: This refers to the defense mechanism of the body, where in the d. Mobile teeth presence of bacteria, leukocytes will act on them. If the patient has optimum levels of vitamins, the patient may be able to fight bacterial NOTE: invasion Vitamin C is important in collagen production 6. Depletion of vitamin C may interfere with the ecologic equilibrium of In healing of oral tissues, collagen production is important. If there is bacteria in plaque and increases its pathogenicity vitamin c deficiency then there will be a decrease in collagen production PERIODONTAL FEATURES OF SCURVY NOTE: Vitamin D is important for the absorption of calcium from the GIT and the maintenance of the calcium, phosphorous homeostasis If the patient has vitamin D deficiency, then the patient will not be able to absorb calcium from the GIT, and may result to alveolar bone destruction Loss of trabeculae Increased radiolucency of the trabecular interstices Increased prominence of the remaining trabeculae Vitamin A Deficiency 1. Chronic gingivitis involving the free gingiva, attached gingiva, and − Essential for normal functions of the retina, for growth, differentiation, alveolar mucosa and maintenance of epithelial tissues, for bone growth, and 2. Gingiva is bright red, tender, and swollen embryonic development 3. The spongy tissues are hyperemic and bleeds spontaneously 4. In long standing cases, gingiva becomes dark blue or purple in color. NOTE: Alveolar bone resorption and increased tooth mobility may also occur Vitamin A is also important for immune response of the body Oral mucosa is made up of keratinized and non-keratinized epithelium. If the non-keratinized epithelium is compromised, because of vitamin a deficiency, then there will be a susceptibility to bacterial invasion because of its increased permeability Vitamin D Deficiency Vitamin B Complex Deficiency − B Complex deficiency may result to gingivitis, glossitis, glossodynia, angular cheilitis, and inflammation of the entire mucosa NOTE: Glossitis − Inflammation of the tongue Glossodynia − Radiographically, there is partial to generalized complete − Pain in the tongue disappearance of the lamina dura and reduced density of supporting bone Angular Cheilitis − Wound on labial commissures  There is no specific vitamin b deficiency that may lead to these MILD HYPERKERATOSIS TO SEVERE BURNS, MAY RESULT FROM diseases, however extreme deficiency in all kinds of vitamin b may EXPOSURE TO: lead to these diseases - Aspirin - Phenolic compounds Protein Deficiency − Necrotizing lesions of the gingiva and other oral tissues and with - Volatile oils, anesthetics increased gingival inflammation and periodontal bone loss - Fluoride preparations, and - Astringents, DRUGS AND PERIODONTIUM - Hydrogen peroxide mouth rinses METABOLIC AND ENDOCRINE DISORDERS I. Diabetes Mellitus − Drugs induced xerostomia: increases plaque and calculus accumulation Diuretics, antipsychotics, antihypertensives, and antidepressants − Patient is more susceptible to periodontal breakdown characterized by extensive bone loss, increased tooth mobility, widening of periodontal ligament space, suppuration, and abscess formation NOTE: Xerostomia NOTE: − Decreased salivary secretions Endocrine glands produce hormones, they control metabolism and Xerostomia will lead to plaque and calculus accumulation, because maintain homeostasis they are not washed off by the saliva Clinical manifestation: Even if we treat the patient properly, with scaling and root planning, or even if the patient undergoes oral prophylaxis every 6 months,  brushes their teeth properly, if the problem is that the patient has diabetes mellitus, then the periodontal disease will not resolve 4. Changes in Plaque Microflora − Hyaluronidase activity is lower in patients with diabetes mellitus PATHOGENESIS OF PERIODONTAL DISEASE OF PATIENTS WITH NOTE: DIABETES MELLITUS Hyaluronidase − Responsible for the breakdown of Hyaluronic acid If hyaluronic acid is not broken down properly, the integrity of the epithelium is also compromised, leading to increased permeability to bacteria Hyperpituitarism − Causes enlarged lips 1. Vascular changes − Localized areas of hyperpigmentation along the nasolabial folds − This results from the thickening of the vascular walls that may impair (Freckle-like accumulation on nasolabial folds) or impede transport of oxygen, white blood cells, immune factors, − Also associated with food impaction and hypercementosis and waste products which will lead to impaired tissue repair and − Hypopituitarism leads to crowding and malposition of teeth function − One of reasons why patients with diabetes mellitus have increased susceptibility to infection in the oral cavity Parathyroid Glands 2. PMNL’s function − Parathyroid hypersecretion produces generalized demineralization of − Polymorphonuclear cells function skeleton − Reduced phagocytosis and intracellular killing which results to poor − Oral changes include malocclusion, tooth mobility, radiographic ability of the oral cavity to fight against bacterial invasion evidence of alveolar osteoporosis, widening of the periodontal space, and absence of lamina dura 3. Biochemistry of Crevicular Fluid − In patients with diabetes milletus, there is reduced cyclic AMP − Cyclic AMP is involved in the regulation of glycogen, sugar and lipid metabolism. Therefore, if there is increase in sugar or glycogen in the crevicular fluid, the bacteria will live off of this sugar causing their number to increase, and then the patient have decreased ability to fight off bacteria, there will be an increased infection and inflammation  − Gingiva bleeds easily − Bleeding is persistent presence of linear gingival lesions which may be Sex Hormones and Pregnancy localized (one area only) or generalized (whole oral cavity) − Erythematous gingivitis may be limited to marginal tissue (punctuate), may be diffused erythema, or extend into the alveolar mucosa Image: Pyogenic Granuloma − Puberty and pregnancy or intake of oral contraceptives- gingival inflammatory hyperplasia − Sex hormone alters capillary permeability and increased tissue fluids, resulting in edematous, hemorrhagic, hyperplastic gingivitis in response to dental plaque NOTE: Pyogenic Granuloma disappears on its own after pregnancy If, however, the pyogenic granuloma does not disappear, then it can be excised Antibody Deficiency − Acquired Immunodeficiency Disorder − Caused by persistent HIV virus and is characterized by destruction of lymphocytes which makes the patient susceptible to infection Clinical Manifestations: HIV Gingivitis PATHOGENESIS AND DEVELOPMENT OF NOTE: PERIODONTAL DISEASE The tissue that is most directly challenged by the pathologic bacteria is the junctional epithelium − Onset of periodontal disease and how it comes about, how it is Because of the subgingival presence of bacteria, the junctional maintained, and how it progresses epithelium gets inflamed due to butyric acid and propionic acid (metabolic wastes of the bacteria) that the bacteria releases. These metabolic wastes cause damage to collagen fibers, periodontal ligaments and alveolar bone. The damage is permanent and PATHOGENESIS OF PERIODONTAL DISEASE irreversible To put it into context, gingivitis is reversible, the inflammation is 1. Direct Effect contained in the gingiva, if the patient is practicing good oral hygiene − Bacterial invasion, production of exotoxins, role of cell constituents, and goes oral prophylaxis, then the gingiva heals and will go back to and production of various enzymes its healthy state. If the inflammation reaches the alveolar bone and periodontal ligament, then the destruction becomes irreversible, even NOTE: if with good oral hygiene and oral prophylaxis, the progression of The direct exposure of the periodontium to the bacteria can affect inflammation will stop, the periodontium may go back to its healthy the fibroblast which are connective tissue forming cells state, but whatever alveolar bone is lost through bone resorption, It may also affect the epithelial cells, endothelial cells, and whatever periodontal ligament is destroyed, it won’t go back inflammatory cells which are found on the junctional epithelium anymore Some studies say that there is minimal growth of alveolar bone after healing, but is not enough to bring back the alveolar bone to its 2. Indirect Effect original height − Evasion of immunologic host response NOTE: NOTE: The bacteria release butyric acid and propionic acid, that alone is The main thought is that the body is able to fight off the bacteria already is already toxic to periodontal tissue. On the other hand, the because of its immune response, but sometimes the immune response keratinocytes that are found on junctional epithelium will fight off the has negative effects on the periodontium which is destructive and bacteria by releasing cytokines and inflammatory mediators which irreversible are damaging to the periodontal tissue Cytokines and inflammatory mediators are ways of the body to fight off bacteria, but these are damaging to the gingiva, periodontal ligament, and alveolar bone Junctional Epithelium − Bacteria releases large quantities of metabolic (butyric acid and propionic acid) ROLE OF BACTERIAL INVASION − The keratinocytes respond by releasing cytokines and inflammatory mediators  − Virulence factors - the properties that enable bacteria to cause disease − Bacteria in sulcus must attach to available surfaces to avoid displacement − Root of the tooth, the tissue, plaque mass − Bacteria attach to the acquired pellicle through the fimbriae NOTE: − Bacteria may attach to existing plaque through coaggregation Gingivitis and periodontitis are caused by bacteria that colonizes the − Bacteria may enter through ulceration in the pocket epithelium gingival crevice or the gingival sulcus Small amounts of bacteria are tolerated by the body NOTE: Only when the bacteria increase beyond threshold of the host or his/her ability to fight off the bacteria, then there is a shift of health Small structures on the outer surface of the bacteria that allows them to disease to attach to the tooth. They attach to the acquired pellicle Bacteria is partially responsible for tissue degradation, but most of If there is already inflammation on the gingival margin, the pocket the tissue degradation comes from the host’s immune response epithelium is ulcerated. It is no longer a healthy barrier to ward off bacteria Bacterial Attachment How does Plaque Bacteria Cause Tissue Damage? − They produce metabolic waste products that directly contribute to tissue damage − They include ammonia, hydrogen sulfide, butyric acid, and propionic acid NOTE: Bacteria produce butyric acid and propionic acid which are short chained fatty acids that causes tissue destruction. They also produce  nutrient supply for the bacteria through the bleeding of the The production of leukotoxin by Aggregatibacter periodontal pockets which allows the bacteria to multiply and grow in actinomycetemcomitans allows for this bacterium to evade the host’s number defense or immune system Butyric acid and Propionic acid are detectable in the gingival Leukotoxin is not only toxic to Polymorphonuclear cells, but it also crevicular fluid in more severely advanced periodontal diseases releases proteins that degrade the host’s immune factors − Plaque bacteria produces proteases which are capable of breaking ROLE OF CELL CONSTITUENTS down structural proteins in the periodontium such as collagen, elastin, and fibronectin a. Endotoxin or lipooligosaccharide (or lipopolysaccharide) − Found on the outer membrane of all gram-negative bacteria NOTE: − The role of endotoxin in periodontal disease is their ability to If there is breakdown of collagen in the gingival margin or attached produce leukopenia gingiva, it will no longer function as it should. The function of gingival margin is to protect the pocket or sulcus from NOTE: plaque formation because it is closely attached to the tooth. If there is Gram-negative bacteria are those that are found subgingivally collagen breakdown of the gingival margin, it will become flabby, it Gram-positive bacteria are seen coronal to the gingiva. These are is no longer closely attached to the tooth and will become susceptible also called aerobic bacteria to plaque accumulation, and as well as gingival recession Gram-positive bacteria are more dominant in healthy gingiva, as well If there is breakdown of proteins, the interdental papilla loses its as aerobic bacteria integrity, creating black triangles on the patient Gram-negative bacteria and non-aerobic bacteria are more Black triangles are spaces apical to the contact point of the teeth dominant in periodontium undergoing disease In healthy gingiva, the apical portion of the contact points of the teeth are covered by interdental papilla. If the interdental papilla is NOTE: compromised, and the collagen is broken down, it will start to sag or degrade and there will be recession causing black triangles. Black Leukopenia is the condition of the body where there is not enough triangles are not only unesthetic, but it also creates a space for more disease fighting leukocytes in the blood plaque accumulation b. Bacterial surface components c. Capsular components ROLE OF EXOTOXINS Aggregatibacter actinomycetemcomitans ROLE OF CYTOKINES − Produces an exotoxin called leukotoxin (because of its toxic effects on the human Polymorphonuclear neutrophils) Cytokines NOTE: − Are cell proteins that transmit information from one cell to another  − They act on fibroblasts, macrophages, keratinocytes, and PMNL’s to release matrix metalloproteinases (MMPs) that degrade connective tissue ma