Periodontology Study Manual PDF

PERIODONTOLOGY STUDY GUIDE TIPS  Expect questions where you have to identify if one or both sentences or rationales are true/false and/or related  Be comfortable looking at a periodontal chart and intraoral pictures to assign prognoses and make treatment decisions  Know...

PERIODONTOLOGY STUDY GUIDE TIPS  Expect questions where you have to identify if one or both sentences or rationales are true/false and/or related  Be comfortable looking at a periodontal chart and intraoral pictures to assign prognoses and make treatment decisions  Know all surgical indications/contraindications and flap design principals  Know your implantology  Remember that no matter how hard you study, you’ll never know EVERYTHING and that’s okay! Don’t let random questions shake your confidence during the exam! o EX: Which tooth brushing technique is best suited for removal of interproximal plaque? Modified Charters (why would you ever know this?! You wouldn’t- but neither would anyone else taking the exam and it’s curved- so don’t sweat it!)  Breathe. Smile. You’re almost done!  EPIDEMIOLOGY OF PERIODONTAL DISEASE  Approx 50% of the population has gingivitis (inflammation involving 6 or more teeth)  Approx 30% has Chronic Periodontitis (5 mm attachment loss at one or more sites)  Approx 10 % has advanced periodontitis (Aggressive Periodontitis and Severe Chronic Periodontitis)  Recent evidence suggests that these figures may seriously underestimate the prevalence of periodontitis in the U.S. RISK FACTORS FOR PERIODONTAL DISEASE  Inherited (genetic), Males  Decreased socioeconomic status  Race: African Americans are MORE susceptible to Localized Aggressive Periodontitis than Caucasians  Stress  Presence of pathogenic bacteria  Calculus  Iatrogenic factors (overhanging margins, deficient margins, invasion of biologic width)  Diseases involving neutrophil function, immune status, osteoporosis  TOBACCO USE (esp heavy use) o Smoking is a MAJOR preventable risk factor for PD that cause bone loss & recession even in the absence of PD o # of years of tobacco use= significant risk factor in tooth loss & PD o Tobacco adversely affects the treatment of PD and may decrease the success rate of implants o Tobacco Cessation Drugs:  Nicotine Replacement Therapy Transdermal patches (may cause vivid dreams), gum, lozenges, inhaler, nasal spray (highest potential for abuse)  Bupropion SR Pt continues to smoke first 1-2 weeks and then selects quit date by 2 nd week, helpful in pts with underlying depression  VareniclinePt begins taking this 1 week prior to quit date, eliminated primarily through kidneys (adjust dose for renal impairment), aggressive or suicidal behavior is a side-effect  Combination Therapy CLASSIFICATION OF PERIODONTAL DISEASES AAP/ ADA case types  Case Type I: Gingivitis Version- by S Ashrafi- 11-11-20 updated 1  o No bone loss o Probings between 1-3mm Classifying Chronic & Aggressive  Case Type II: Mild Periodontitis Periodontitis o 10-20% bone loss o Probings between 1-5mm Mild= 1 – 2 mm of clinical attachment loss o 1-2mm attachment loss Moderate= 3 – 4 mm clinical attachment loss  Case Type III: Moderate Periodontitis Severe= > 5 mm clinical attachment loss o 20-40% bone loss o Probings between 1-6mm Localized= 30% of sites o 3-4mm attachment loss  Case Type IV: Severe Periodontitis o >40% bone loss o Probings >6mm o > 5mm attachment loss  Case Type V: Refractory Periodontitis o Pt on maintenance who is still not responding to treatment (not currently being used) 2017 World Workshop on the Classification of Periodontal and Peri-implant Diseases and Conditions 1. Gingivitis associated with plaque 2. Gingival diseases modified by systemic factors 3. Gingival diseases modified by medications  Drugs associated with GINGIVAL OVERGROWTH: i. Phenytoin/Dilantin (antiepileptic) HIGHEST INCIDENCE OF OVERGROWTH ii. Cyclosporine (immunosuppressant) iii. Nifedipine (calcium channel blocker) iv. Diltiazem (calcium channel blocker) v. Verapamil (calcium channel blocker) vi. Sodium valporate vii. Oral contraceptives 4. Gingival diseases modified by malnutrition 5. Non-plaque induced gingival lesions (infections, hereditary, trauma, foreign body reaction)  Example: Hereditary Gingivofibromatosis is a genetic disease that is a progressive proliferation of the gingiva (especially the collagenous elements) characterized by a lack of inflammatory cells, proliferating capillaries, and vascular engorgement commonly seen with gingivitis  Example: Desquamative Gingivitis is a painful condition where the outer gingival layer peels away exposing an acutely red surface that occurs most commonly in post-menopausal females (40-70 yoa) and is associated with erosive lichen planus, pemphigoid, or pemphigus. Treated via steroids. A. Periodontal Health: can be on an intact periodontium and reduced periodontium B. Gingivitis- dental biofilm induced can be on an intact periodontium and reduced periodontium (Reduced periodontium due to causes other than periodontitis, eg. crown lengthening surgery and recession related to tooth brush trauma). 1. Gingivitis associated with plaque Note: Diagnosis of Dental biofilm induced gingivitis is identified based on extent and severity of patient’s BOP score (%)  Extent: BOP sites and expressed in % - Few sites ( 5 mm (Stages III and IV) Radiographic Bone loss  < 15% (Stage I)  15%-33% (Stage II)  Bone loss extending to middle third of the root and beyond (Stages III and IV) Tooth loss  No tooth loss (Stages I and II)  < 4 teeth(Stage III)  >5 teeth (Stage IV) Complexity  Probing depth  Bone loss (horizontal vs. vertical)  Tooth mobility- Degree 1, 2, 3  Furcation involvements-Class I, II, III Version- by S Ashrafi- 11-11-20 updated 3   Moderate/severe ridge defects  Masticatory dysfunctions  Secondary Occlusal trauma  Bite collapse, drifting and flaring to teeth Extent/distribution  Localized (< 30% of sites involved)  Generalized (> 30% of sites involved)  Molar/incisor pattern Periodontitis Staging Stage I: Initial periodontitis Interdental CAL 1-2mm at site of greatest loss Radiographic bone loss< 15% in the coronal third of root Horizontal bone loss Probing depths- 3-4mm Stage II: Moderate periodontitis Interdental CAL 3-4 mm at site of greatest loss Radiographic bone loss 15% -33% in the coronal third of root Horizontal bone loss Probing depths- 4-5mm Stage III: Severe periodontitis with potential for additional tooth loss Encompasses all stage 2 with additional features Interdental CAL > 5mm extending to middle third Radiographic bone loss, extending to the middle third of root Vertical defects >3mm Probing depths > 6mm Furcation involvement degree II and III Moderate ridge defect Periodontal tooth loss < 4 teeth Stage IV: Severe periodontitis with potential for loss of dentition Encompasses all stage 3 with additional features Interdental CAL > 5mm Radiographic bone loss, extending to the middle third of root and beyond Probing depths > 6mm Furcation involvement degree II and III Masticatory dysfunction-need for complex rehabilitation Secondary occlusal trauma, mobility > 2 Bite collapse Less than 20 teeth remaining Severe ridge defect Periodontal tooth loss > 5 teeth Grading (A, B, C)-when grading a patient, general health status and other exposures like smoking or level of metabolic control in diabetes needs to be taken into account to allow comprehensive patient management. How to determine Grading? Direct evidence of progression-radiographic bone loss or CAL  Slow rate- no loss over five year  Moderate rate- 2mm over 5 years Indirect evidence of progression- % bone loss /age  1.0 Case phenotype Version- by S Ashrafi- 11-11-20 updated 4   Heavy biofilm deposits with low levels of destruction  Destruction commensurate with biofilm deposits  Destruction exceeds expectations given biofilm deposits; specific clinical patterns suggestive of periods of rapid progression and or early onset disease Periodontitis Grading Grade A: Slow rate of progression Grade B: Moderate rate of progression Grade C: Rapid rate of progression 5. Other Conditions Affecting the Periodontium a) Systemic diseases or conditions affecting periodontal supporting tissues b) Periodontal Abscesses c) Endodontic –Periodontal Lesions d) Mucogingival Deformities e) Traumatic Occlusal Forces f) Tooth and Prosthesis Related Factors a. Periodontitis as a manifestation of systemic diseases  Diabetes (15x risk of PD) uncontrolled DM impairs chemotaxis & adherence & decreases phagocytosis  Down Syndrome  Neutropenais, Leukemia  Leukocyte Adhesion Deficiency (defiency in the cell adhesion molecule CD 18- an integrin)  Papillon-Lefevre Syndrome  Hypophosphatasia  Langerhans Cell Histiocytosis  Chediak Higashi Syndrome  Acrodynia  Ehlers Danlos Syndrome, Glycogen storage diseases  Cohen Syndrome  Infantile Genetic Agranulocytosis  Autoimmune disorders (Rheumatoid arthritis, lupus, CREST)  Allergy to dental materials  HIV-RELATED PERIODONTAL PROBLEMS i. The only condition that appears to be specific to HIV infection is “Linear Gingival Erythema” ii. HIV positive patients do NOT usually need prophylactic antibiotic coverage for routine dental procedures—including tooth extraction iii. Other diseases of the gingival tissues that are associated with HIV infection include: 1. Acute Herpetic Gingivitis 2. Papilloma Virus Gingival Hyperplasia 3. Varicella Zoster Gingivitis 4. Kaposi’s Sarcoma of the Gingiva 5. Gingival Candidiasis 6. NUG 7. Necrotizing Ulcerative Periodontitis 8. Periodontal Abscesses (may be multple) 9. Pericoronitis (can be very serious and may spread to become a necrotizing stomatitis) b. Periodontitis associated with endodontic lesions a. For a true combined lesion, treat endo FIRST then perio (“E before P”) c. Necrotizing Periodontal Diseases A. NECROTIZING GINGIVITIS & NECROTIZING PERIODONTITIS i. Often an underlying medical condition or factor (Immunosuppression/HIV, smoking, stress, etc) 1. NG in pts with HIV is strongly associated with neutropenia ii. Local debridement is the MOST important first step of treatment Version- by S Ashrafi- 11-11-20 updated 5  1. Antibiotics may be needed if the disease is widespread of anesthesia is difficult to obtain (debridement should follow in 24 to 48 hours) 2. Comprehensive periodontal treatment is often necessary to treat residual problems of ANG (e.g. tissue architecture) iii. PMN= Dominant WBC in ANUG iv. P. intermedia, T. denticola, Fusobacterium, Selenomas d. Periodontal Abscesses MOST common periodontal emergency a. Abscesses & Cysts: i. Acute Gingival Abscess 1. Located CORONAL to the alveolar bone in gingiva 2. Usually caused by impacted foreign object (ex: popcorn kernel) 3. Treatment is removal of object when present and drainage ii. Acute Periodontal Abscess 1. Etiology of most periodontal abscesses is blockage of a pre-existing periodontal pocket 2. Rapid loss of bone may occur Establishing 3. Treatment is drainage (usually by curettage through the pocket) DRAINAGE is the 4. Most numerous cell= PMN MOST important 5. Most common symptoms= acute pain that is constant and severe & a dull throbbing objective. Antibiotics that does not change to thermal changes should ONLY be 6. Radiographic findings are NOT specific used as an adjunct 7. The surrounding teeth will be VITAL! if the patient has 8. May become chronic-- drainage frequently occurs through the pocket but may occur systemic symptoms by a sinus tract through the alveolar bone & gingiva (fever, malaise) or if 9. Always check for the possibility of an underlying systemic condition (ex: DM, HIV) in there is a serious patients with periodontal abscesses—particularly multiple abscesses underlying disease. iii. Periodontal Cyst 1. Localized tender swelling 2. Often located in mandibular canine/premolar area 3. Treatment is surgical removal without extraction of teeth e. Developmental or Acquired Deformities 6. Peri-implant Diseases and Conditions a) Peri-Implant Health b) Peri-Implant Mucositis c) Peri-Implantitis d) Peri-Implant Soft and Hard Tissue Deficiencies CLINICAL FEATURES OF GINGIVITIS & PERIODONTISIS  GINGIVITIS REVERSIBLE o Color changes: red/blue/purple o Texture changes: loss of stippling/increased smoothness o Consistency changes o Swelling: edema/fibrotic o Tendency to bleed  Bleeding on probing is the BEST clinical indicator of gingival inflammation o *NO RADIOGRAPHIC FEATURES  PERIODONTITIS IRREVERSIBLE (Evidence of inflammation AND tissue destruction) O Periodontal pockets &/or gingival recession O Bleeding on probing O Attachment loss O Alveolar bone loss (horizontal and vertical defects) Version- by S Ashrafi- 11-11-20 updated 6  O Tooth mobility (usually advanced disease) O Furcation involvement O *MUST have radiographic evidence of bone loss DIAGNOSIS OF PERIODONTAL DISEASE Clinical Diagnosis  ATTACHMENT LOSS MOST significant clinical criteria indicating periodontal disease o Definitions:  Histological Attachment Loss= distance between the CEJ & the base of the pocket  Clinical Attachment Loss= distance from the CEJ to the tip of the probe o Histology Review:  Junctional Epithelium  Approx 1mm long, 10-20 cells thick at the sulcus & 2-3 cells thick towards the apical end  Attaches the gingiva to the tooth via hemidesmosomes & allows transmigration of neutrophils & other host defense molecules into the periodontal pocket  Biologic Width  Approx 2mm in length (1mm JE + 1mm supra-alveolar CT)  Need to allow for at least 3mm (and more if in the esthetic zone) between the restorative margin and the alveolar bone o Calculation Review:  CAL= Recession + Probing Depth  CAL= Probing Depth – overgrowth  EX: #8 has 2mm recession and a probing depth of 3mm, what is the clinical attachment loss? ANS: 5mm  PROBING MOST accurate assessment of pocket depth o Facts:  Clinical probing is ALWAYS greater than the histological depth  Early attachment loss can be detected with probing BEFORE bone loss can be detected on radiographs o Health vs Disease:  In health: the tip of the probe may end in the junctional epithelium (located on enamel)  In disease: the tip may end in connective tissue o Technique:  Angle 10-degrees under contact  Gentle force= ~25gm of force or to depress thumb pad 1-2mm  Tapered shaft= ~0.5mm diameter at tip  Excessive angling is the MOST common error (keep parallel to tooth) o Periodontal Probe Measures & Detects:  Probing depth  Gingival recession  Clinical attachment loss  Bleeding on probing  MOBILITY o Classifications:  Cl I= 0.2-1mm horizontal movement  Cl II= 1-2mm horizontal movement  Cl III= >2mm horizontal & vertical movement o Splints  External- prepared easily, economic, conserves tooth structure  Intracoronal- tooth structure is removed  FURCATIONS o Classifications:  Cl I= Incipient furcations  Cl II= Bone loss into furcation but not through and through (cul-de-sac with definitive horizontal component)  Cl III= bone loss through and through Version- by S Ashrafi- 11-11-20 updated 7   Cl IV= bone loss through and through with gingival recession (can see clinically) o Predisposing Factors:  Short root trunk  Short roots  Narrow inter-radicular dimension  Presence of cervical enamel projections o Facts:  Furcations in maxillary molars may appear as “furcation arrows” on radiographs  Over 50% of furcations may be too narrow for hand instruments to gain access  Buccal furcations of first maxillary molars are usually the narrowest Radiographic Diagnosis  Facts: o Presence of periodontal pockets CANNOT be determined from the X-ray o Radiographs are NOT a sensitive means of detecting early bone loss or the presence of calculus o Need >30% bone loss to visualize it on an x-ray o A reduction of only 0.5-1mm thickness of the cortical plate is enough to see destruction of cancellous trabecular on an x-ray  Helpful in Detecting: o Interdental/interradicular bone loss (NOT buccal/lingual bone loss) o Pattern of bone loss (horizontal or vertical) o Tooth trunk and root anatomy o Crown:root ratio o Furcation involvement  BITEWINGS o BEST way to view bone loss o Crest of the alveolar bone parallels a line drawn between adjacent CEJs  In health the alveolar bone is 1-2mm apical to the CEJ ETIOLOGY OF PERIODONTAL DISEASE Bacteria Associated with Periodontal Health and Diseases Bacterium Disease Association Streptococcus sanguinis Periodontal health (gram + facultative cocci & rods) Actinomyces species Gingivitis (gram +) Aggregatibacter actinomycetemcomitans Localized Aggressive Periodontitis Porphyromonas gingivalis Periodontitis Tannerella forsythia Periodontitis Prevotella intermedia Gingivitis of pregnancy, NG, Downs Syndrome Treponema denticola (spirochetes) Periodontitis, ANG F. nucleatum Bridges primary & secondary colonizers P. aeruginosa Peri-implantitis Major Pathogens Involved in Periodontitis  Porphyromonas gingivalis Bacteria produce low o Gram – rod, anaerobic, nonmotile “Red Complex”= molecular weight  Tannerella forsythia P. gingivalis + compounds (hydrogen o Gram – rod, anaerobe, nonmotile T. forsythia + sulfide & butyrate) that  Treponema denticola T. denticola can induce early signs of o Gram – spirochete, strict anaerobe inflammation  Aggregatibacter actinomycetemcomitans o Gram – rod, nonmotile ENDOTOXIN= LPS  Associated with GRAM NEGATIVE bacteria (major virulence factor) Gingival changes  Consists of 3 components: Lipid A, R polysaccharide, O-polysaccharide during pregnancy Version- by S Ashrafi- 11-11-20 updated are due to PROGESTERONE 8 & INCREASED MAST CELLS which   Promotes bone resorption & inhibits osteogenesis & chemotaxis  Free endotoxin is found in plaque & inflamed gingiva PLAQUE  Basics: o Plaque= complex microbial community with >1010 bacteria/mg o PRIMARY etiological factor in initiating PD o MAJOR factor in the growth of plaque is surface roughness  Composition: o 80% water o 20% solids  Major organic constituents= polysaccharides, proteins, glycoproteins, lipids  Major inorganic constituents= calcium, phosphorus  Source= saliva (supragingival) & crevicular fluid (subgingival)  DEXTRAN MATRIX  Types: o SUPRAGINGIVAL  Gram + cocci & rods (tooth associated)  Gram – filaments & spirochetes (outer surface) o SUBGINGIVAL  Gram – rods  Provides the MOST likely source of bacteria in disease tissues  Formation: o Pellicle forms= glycoproteins, proline rich proteins, phosphoproteins, histidine-rich proteins o Adhesion occurs (reversible; electrostatic forces & van der waals) o Attachment occurs (receptor mediated) o Colonization & maturation= Gram +  Gram - anaerobes  Primary colonizers= gram + facultative (s sanguis, s. mutans, actinomyces)  Secondary colonizers= gram – (f. nucleatum, p. intermedia, capnocytphaga sp)  Tertiary colonizers= gram – anaerobic rods (p. gingivals, campylobacter rectus, erkenella, corrodens, AA, oral spirochetes (treponema sp))  Microbiology Review: BIOFILMS o Plaque= biofilm= microbial community in an extracellular matrix where bacteria interact with each other o Bacteria in biofilms may resist antibiotics & antimicrobials several hundreds of times more than bacteria in suspension because…  Extracellular matrix is relatively impermeable  Antibiotic resistance genes may be transferred between bacteria  Bacteria in biofilms may be metabolically inactive  Bacteria producing enzymes that breakdown antibiotics may protect neighboring susceptible bacteria (friendly neighbors) CALCULUS  Basics: o Calculus= precipitation of mineral salts into soft plaque o Starts 1-14 days after plaque formation  12 days= average time for entire calculus formation process to occur o MOST important plaque retentive factor (calculus is bad because it is always covered in plaque & promotes plaque retention on teeth) o MOST commonly located on the lingual of the lower anteriors & buccal surfaces of the maxillary molars o MOST significant contributing local factor for periodontal disease  Composition: o 70-90% inorganic (at least 2/3 in crystalline state) o 10-15% organic  Types: o SUPRAGINGIVAL (yellow/white)  Brushite= recent calculus Version- by S Ashrafi- 11-11-20 updated 9   Oactacalciumphosphate= outer layers  Hydroxyapatite= inner layers o SUBGINGIVAL (darker due to blood breakdown pigments, harder, more dense)  Whitlockite= main component  Attachment: o Via pellicle on enamel  Salivary pellicle= MOST important mechanism that allow supragingival calculus to attach to enamel o Mechanical locking into surface irregularities o Adaptation to depressions on cementum o Penetration into cementum  Plaque Free Zone o Zone of ~0.5mm in width at the base of the periodontal pocket that appears to be free of plaque and calculus HOST RESPONSE TO MICROBIAL PLAQUE CREVICULAR FLUID  Contains Neutrophils (95%) which phagocytose & kill bacteria o Neutrophils (PMNs) migrate from gingival blood vessels into the crevicular fluid via the junctional epithelium & pocket epithelium  PMNs= 1st line of defect & 1st cells to migrate to sulcus  PMNs= MOST abundant cell in acute inflammation  Immunoglobulins (antibodies) & complement which facilitate phagocytosis (act as opsonins) o IgG= MOST abundant immunoglobulin in gingival exudates in gingivitis GINGIVAL TISSUES  Macrophages o Ingest antigen & present it o Release cytokines o Represent transition between acute & chronic inflammation  B cells o Plasma cells (predominate in established lesions)  Elevated levels of antibodies to periodontal pathogens are found in serum & crevicular fluid in patients with PD  T cells HOST FACTORS  CT destruction & bone resorption are, at least in part, the result of HOST FACTORS o Tissue metalloproteinases (MMPs)  MOST important proteinase involved in destruction of periodontal tissues  PMNs produces lots of these o Cytokines Polymorphisms in IL-1=  IL-1- causes bone resorption  IL-1 &  risk for tooth loss  IL-6  IL-8- responsible for chemotaxis (moves PMNs from blood vessels to infection so they can phagocytose via oxygen radicals)  TNF-alpha- activates macrophages o Prostaglandins (PGE-2) ROLE OF OCCLUSION IN PERIODONTAL TISSUE DESTRUCTION  Basics: o Damage from occlusal forces occurs in the PDL  Gingival (supra-alveolar) tissues are NOT affected by occlusal forces Early effect of  Occlusal trauma= damage in the PDL (NOT forces on the teeth) OT= o Damage from occlusal forces include the following changes in the PDL: hemorrhage & Version- by S Ashrafi- 11-11-20 updated thrombosis of 10 PDL & blood vessels   Hemorrhage  Edema  Thrombosis  Disorganization of PDL fibers  Resorption of bone (occasionally resorption of cementum)  Resorption is frontal (on the PDL surface of the bone) or rear (in the marrow spaces) if there is extreme forces that cause necrosis of the PDL o There is NO evidence that occlusal trauma causes attachment loss in patients. The co-destructive influences of occlusal trauma and inflammation are still unclear.  OT does NOT cause periodontal pockets!  Classifications: o Primary Occlusal Trauma  Associated with EXCESSIVE forces exceeding the capacity of a relatively INTACT PERIODONTIUM to withstand it  Exs: Restorations in supra-occlusaion, parafunctional habits (bruxism) o Secondary Occlusal Trauma  Caused by INCREASED forces or NORMAL occlusal forces (eating, swallowing) on teeth with an INFLAMMED periodontium (reduced support)  Signs of Occlusal Trauma: o Mobility MOST common sign of occlusal trauma  Fremitus= movement induced by occlusal contact o Widened PDL (normal width= 0.25mm)  Teeth with excessive occlusal loads have WIDER PDLs  Teeth with too little occlusal loads/ unopposed have NARROWER PDLs. o Wear facets o Cemental tears o Tooth fracture o Migration of teeth o Soreness of muscles of mastication o Temporomandibular disease (TMD) NON-SURGICAL PERIODONTAL THERAPY  Rationale: Most forms of periodontal disease are treatable microbial infections. The severity and extent of most periodontal diseases are related to the sum of the local and systemic risk factors present.  Goals: o Control risk factors o Establish an environment which…  Can be maintained with minimal further loss of periodontal tissues  Is esthetically pleasing to the patient  Has stable occlusal relationships Establishing Good Oral Hygiene is the MOST important aspect of initial therapy  Toothbrush bristles enters 1mm into the sulcus, floss enters 2-3mm into the sulcus  Toothbrushing: o Components:  Pyrophosphate= anti-calculus agent  Humectant= retains moisture  Surfactant= sodium lauryl sulfate (foams)  Binder= flowability  Polish= silica, calcium carbonate, or alumina o Toothbrush abrasion= MOST common cause of recession  Typically occurs around the canine & premolars on the opposite side of handedness  Stains: o Exogenous stains originate from outside the tooth but become incorporated in (Ex: amalgam, tobacco, fluoride, green) o Brown strain from brushing Tanin Version- by S Ashrafi- 11-11-20 updated 11  o Black & orange stain Chromogenic Bacteria o Green & yellow stain Fluorescent bacteria  Polishing: Do not polish in pts with… o Communicable disease o “Green stain” o Newly erupted teeth o Pts at risk for caries SCALING & ROOT PLANING  Purpose: To remove plaque biofilm and calculus from supra and subgingival surfaces of the teeth and to make sure that the root surfaces are as smooth as possible without over-instrumenting them o To alter or eliminate microbial etiology & contributing factors o Shifts Gram Neg Gram Pos  Problems/Difficulties with SRP: o The deeper the pocket, the less effective the removal of calculus. Removal of calculus is LESS effective in pockets deeper than 5mm. o Removal of calculus is LESS effective in furcations  Trifurcations of maxillary molars are MOST difficult o Instrumenting the mesial surface of the maxillary premolar and the proximal surfaces of the mandibular incisors are also difficult o SRP in quadrants- do NOT do gross debridement o Can get an abscess if only superficial scaling is performed in a deep periodontal pocket  Results: o ScRP has a long lasting (2-3 mo) effect on the levels of many periodontal pathogens in the periodontal pockets o PMNs predominate immediately after curettage o BEST criteria to evaluate the success of SRP= no bleeding on probing o MOST important factor to determine the amount of shrinkage= degree of edema in the tissues o Pocket depth reduction after ScRP varies considerably:  More inflammation—usually GREATER reduction in pocket depths  Deep pockets – usually GREATER reduction in pocket depth  On average:  5mm pockets are reduced by approx 1mm  8mm pockets are reduced by approx 2mm  Healing: o As a result of SRP  Decreases blood vessels & inflammatory cells  Causes gingival shrinkage & adaptation of pocket epithelium to the root at the base of the pocket  Increases fibroblasts & collagen synthesis forming a long junctional epithelium (re- epithelialization occurs within 7-10 days) o Healing is almost complete after 3-4 weeks but may continue slowly for up to 1 year o Re-evaluation should occur 4-6 weeks after completion of initial therapy  Indications for Referral to a Periodontist: o Nonresponsive sites (continued loss of attachment, bleeding) BEST clinical aid  Check roughness- may need to clean more to determine if o Pocket depth not eliminated & bleeding on probing SubG calculus o Alveolar bone defects was removed= o Insufficient crown forms BWs & explorer o Pseudopockets/overgrowth o Mucogingival defects  HAND INSTRUMENTS: Hand instruments and ultrasonic scalers are comparable in terms of long term results measured by probing depths, clinical attachment levels, and bleeding on probing when used to treat periodontitis o Scalers/Sickles  Basics: Used for SUPRAgingival p/c removal (do not use on root surfaces!) Triangular in cross section, pointed tip, and have two cutting edges per working-end. There is an anterior sickle and posterior sickle. Version- by S Ashrafi- 11-11-20 updated 12   Instrumentation: Hold instrument with modified pen grasp and establish a finger rest. Adapt the leading third of the working end to the tooth. Slightly tilt the lower shank toward the tooth surface to be instrumented to establish the proper 70-80o angulation. Press against the tooth with the ring finger and apply firm lateral pressure against the handle with the finger and thumb to active a pull stroke. Use brief, tiny, biting strokes.  Special Notes: Make sure the lower shank is PARALLEL to the tooth surface and the functional shank goes up and over the tooth! Do not wrap the posterior scaler around the tooth! o Universal Curettes  Basics: Used for supra & sub-G p/c removal for BOTH anterior and posterior teeth. Rounded back and toe, two cutting edges, and semi-circular in cross-section. Face is PERPENDICULAR to the lower shank (both cutting edges are level).  Instrumentation: Same as above. Make sure the instrument face tilts towards the tooth surface when placing the working end against the midline of the facial or lingual surface (as you look down on the working end, the face is partially hidden). Use short strokes for scaling and longer pull strokes for root planing.  Special Notes: Columbia 13/14 has a shorter cutting edge and shorter lower shank to instrument for normal sulci or shallower pockets. Barnhart 1/2 has a longer cutting edge and longer lower shank to instrument root surfaces in deep pockets. o Gracey Curettes  Basics: Used for supra & sub-G p/c removal. SITE SPECIFIC. Do not cause trauma to the pocket epithelium and suitable for root surface debridement within the periodontal pocket. Rounded back, rounded toe, and semi-circular in cross-section. Face is TILTED to the lower shank (cutting edges are curved.) Only the lower cutting edge is used for calculus removal (one cutting edge on each blade.)  Instrumentation: Same as above, except the lower cutting edge is automatically at a 70 o angle to the tooth surface when the lower shank is parallel (hold the lower shank parallel and do not tilt the instrument to establish the proper working angle.)  Special Notes:  1/2: All surfaces of anterior teeth (face is partially hidden when placed against the midline of the facial/lingual surface)  7/8: Buccal and lingual surfaces of posterior teeth  11/12: Mesial surfaces of posterior teeth  13/14: Distal surfaces of posterior teeth (make sure the functional shank goes UP AND OVER the tooth) o Hoes & Files  Basics: For heavy supra & sub-G calculus removal (or gross subgingival if the tissue is flexible and easily displaced)  Instrumentation: Only use vertical strokes  Special Notes: Must always be followed by curettes  Scaling vs Root Planing Strokes: o Sequence & control of stroke is important: deliberate transition from short, powerful scaling strokes to longer, lighter root planing strokes must be made as soon as calculus and roughness are removed o Scaling stroke= generated in forearm  Sharpening Hand Instruments: o Sharper instruments require fewer strokes, provide greater control, & increase tactile feel o Dull instruments fatigue due to heavy handedness, decrease tactile feel, burnish calculus, and are an inefficient use of time o A properly sharpened instrument with no rounded surface area will NOT reflect light o Manual sharpening is preferred:  Avoid “wire edge” by always finishing with a downstroke  Hold 100-110o between flat stone and instrument  Lubricate stone to prevent scratching  Oil for natural stones  Water for synthetic stones o Proper sharpening= BEST way to prevent curette breakage  If a curette tip breaks: seat the pt up, check the floor of the mouth & folds, take a PA, use a curette in a spoon-like stroke (NEVER push) Version- by S Ashrafi- 11-11-20 updated 13  *MOST effective instrument for removing subgingival calculus= sharp curette *MOST effective way to use a curette is short, even working strokes followed by longer strokes *Ideal angle between curette & tooth= 70-80 degrees  ULTRASONIC SCALING: o Cavitation= the production & collapse microscopic vacuum cavities cause high-powered micro-jets of liquid to be propelled around the tip (Acoustic Microsteaming) which assists in plaque removal o Instrumentation:  The tip of the ultrasonic scaler should be held PARALLEL to the tooth or at not more than 15o to the tooth to avoid grooving the tooth surface  Lower power settings should be used with thinner tips  The power knob on the ultrasonic scaler controls the length of the stroke o Ultrasonic Scalers vs Sonic Scalers:  ULTRASONIC SCALERS  Vibrate at 18,000 to 50,000 cycles/second  2 Types: o Magnetostrictive (Cavitron) Motion of tip is ELLIPTICAL (all sides of tip are active) o Piezo-electric Motion of tip is LINEAR (2 sides of tip are active)  Requires more precise orientation to the tooth surface than magnetostrictive scalers  SONIC SCALERS  Vibrate at 2,000 to 6,000 cycles/second using air from high speed handpiece lines Gingival Curettage  Objective: To remove chronically inflamed, diseased epithelial lining and bacteria from the pocket to reduce edema and pocket depth removes diseased soft tissue lining periodontal pockets o Often performed with root planing to promote soft tissue attachment o Pts with edematous and granulomatous inflammation respond better than pts with fibrous hyperplasia  Instrumentation: Cutting edge directed against soft tissue wall of pocket  Coincidental curettage= when soft tissue wall of a pocket is removed by the offset cutting edge during root planing SURGICAL PERIODONTAL THERAPY Periodontal surgery Distal Wedge Flap  Phase II Treatment  Design:  ALWAYS SRP before surgery o Base= periosteum  Surgery is contraindicated in patients with bad oral hygiene overlying bone o Apex= coronal gingival FLAPS surface  Basics:  Uses: Maxillary tuberosity region, o IMPROVE ACCESS mandibular retromolar triangle, o MOST common of all periodontal surgical techniques distal to last tooth in arch, mesial to a tooth next to a space  Types: o Partial Thickness (Mucosal= epithelium + CT)  Used when attached gingiva is THICK (>2mm wide)  Used to prepare recipient site for FGG or if dihescence or fenestration is present in prominent root  Tissue is separated from the periosteum by sharp dissection o Full Thickness (Mucoperiosteal)  Used where attached gingiva is THIN (