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Periodontitis-definition the inflammation of the supporting tissues of the teeth, specifically the periodontal ligament, cementum, and alveolar bone
Periodontitis-condition o tissue inflammation, loss of connective tissue and destruction of collagen fibers, migration of the junctional epithelium, recession and/or bone loss
Periodonitis-• Related to the plaque accumulation, microflora presence and retention o Multibacterial, Primary pathogen associated with periodontitis is P. gingivalis, Other anaerobic gram- bacteria: B. forsythus, P. intermedia, C. rectus, actinomycetemcomitans, Eikenella corrodens, F. nucleatum, Treponema, Eubacterium
Periodontitis-Classification (based on) *AAP revised the classification in 1999* Etiology Clinical presentation Pathogenesis Progression Response to therapy
Periodontitis-Treatment Requires the treatment or removal of all local etiologic factors: Plaque and calculus removal by RDH and patient, Patient education to maintain plaque control, Control of overhangs, etc, Smoking cessation, Possible periodontal surgery
Chronic Periodontitis • The most common form of periodontal disease, May begin in adolescence and progress slowly (up to 1mm per year)
Chronic Periodontitis • Severity of the disease is directly related to the accumulation of plaque and calculus on the teeth, Rate of destruction varies depending on the disease activity and patient’s resistance, Progression of periodontitis occurs in episodic burst of activity
Chronic Periodontitis • The most reliable method to monitor the progression of the disease is to document the loss of periodontal attachment (clinical attachment loss) over time, The degree of severity is related to the amount of periodontal ligament and bone lost, Probing poc
Chronic Periodontitis • Patients with slight to possibly moderate periodontitis “may” be treated in a general dental practice
Aggressive Periodontitis periodontal disease that progress rapidly with massive
Early onset Periodontitis • Periodontal disease that affect people younger than 30, Includes: Prepubertal, Juvenile (General and Localized) and Rapidly Progressive Periodontitis
Early onset perio differs from chronic periodontitis in o Microflora, Age of onset, Rate of tissue destruction, Possible defects in the immune system
Prepubertal Periodontitis • Very rare condition that may be localized or generalized and affect primary and secondary teeth, Severe gingival inflammation, rapid bone loss, and early tooth loss, WBC defects also leave them susceptible to other infections, Bacteria involved: P. gin
Prepubertal Periodontitis • Treatment – poor response to conventional treatment, antibiotic therapy may help, and treatment slows rather than stops the disease
Localized Juvenile Periodontitis • Extreme bone loss around 1st molars and incisors in patients younger than 20, Not a lot of plaque or inflammation, but radiographs may show advanced bone loss, More common in girls than boys and blacks than whites; can run in families, Predominant bacte
Localized Juvenile Periodontitis-Treatment scaling and root planning, systemic antibiotics, and periodontal surgery
Generalized Juvenile Periodontitis • More rare than Localized Juvenile Periodontitis, Affects most or all of the teeth of young adolescents, Also associated with a neutrophil chemotactic disorder, Usually have significant inflammation, heavy plaque and calculus formation, Bacteria involved
Generalized Juvenile Periodontitis-Treatment improved plaque control, scaling and root planning, antibiotic therapy and periodontal surgery
Post-Juvenile Periodontitis • Localized or generalized juvenile periodontitis that has stopped or slowed, Seen in adults rather than adolescents, Diagnosis primarily based on severe bone loss around incisors or first molars, Probably late diagnosis of Juvenile Periodontitis, Lesions
Post-Juvenile Periodontitis-Treatment scaling and root planning, home care instruction, antibiotic therapy and periodontal surgery
Rapidly Progressive Periodontitis • Occurs in young adults between 20 and 30, Usually involves most of the teeth, but localized forms have been reported, There is severe inflammation, varying amounts of plaque and calculus and rapid (over weeks or months) bone loss, May have a genetic com
Rapidly Progressive Periodontitis-Treatment plaque control, scaling and root planning, antibiotic therapy and surgery
Refractory Periodontitis • Periodontal disease that is unresponsive to standard or appropriate treatment, May occur at single or multiple sites, No single bacterial agent. Organisms found: B. forsythus, P. intermedia, C. rectus, A. actinomycetemcomitans, F. nucleatum, Peptostre
Gingivitis vs. Periodontitis Overview Gingivitis affects Epithelium, Gingival connective tissue Periodontitis affects: Connective tissue, Junctional epithelium, Alveolar bone
Necrotizing Ulcerative Gingivitis • Associated with stress, systemic disease, blood dyscrasias, HIV infection, and nutritional deficiencies, Recurrent NUG can result in attachment loss and develop into NUP, Most reliable criteria for recognizing the disease is necrosis and ulceration of t
Necrotizing Ulcerative Periodontitis • Massive tissue destroying process that is an extension of NUG, Bone loss and connective tissue attachment loss are present, Same clinical gingival features as NUG, May occur in AIDS patients, individual with nutritional deficiencies or patients under ex
Treatment of NUG and NUP • May need to progress with multiple visits over a few days during the acute phase
Periodontitis as a Manifestation of Systemic Disease • Systemic diseases can increase the severity of periodontal disease due to decreased resistance, Minimal plaque and calculus with significant disease warrants a thorough medical evaluation, Excellent plaque control and frequent recall visits are essentia
Periodontitis as a Risk Factor for Systemic Diseases cardiovascular disease, pre-term and low birth weight infants, bacterial pneumonia and diabetes
Periodontitis and Cardiovascular disease • Periodontal disease has been associated with an increased risk of heart attack and death, Adverse health effects are related to chronic infections and inflammatory agents
Periodontitis and Pre-Term Birth • Inflammatory mediators produce cytokines that affect the fetus, Lipopolysaccharides from plaque bacteria act directly on the placental membrane
Periodontitis and Bacterial Pneumonia • A number of periodontal pathogenic bacteria found in plaque have been associated with pneumonia and a number of respiratory pathogens reside in dental plaque
Periodontitis and Non-insulin Dependent diabetes • Diabetes increases patient susceptibility to many types of infection, Diabetic patients may have increased clinical attachment loss
calculus formed by deposition of calcium and phosphate salts in plaque
Plaque etiologic agent in perio disease
Supragingival Calculus yellow-white accumulation above the gingival margin, most abundent near Wharten's and Stenson's ducts
Mineralization of supragingival calculus can begin w/in 24-72 hours
supragingival calculus minerals: calcium phosphate & carbonate
supragingival calculus crystals: hydroxyapatite, octacalcium phosphate, whitlockite, and brushite
subgingival calculus mineral content derived from crevicular fluid versus saliva in supragingival calculus
distribution of supragingival calculus maxillary molars and mandibular incisors
distribution of subgingival calculus more evenly distributed throughout the mouth
Supragingival calculus; pathogenesis rough and porous and provides an area for plaque to grow
Subgingival calculus; pathogenesis provides a resevoir for bacteria and endotoxins
pyrophosphates inhibit the growth of the hydroxyapatite crystals-only reduce the formation of new supragingival calculus
marginal discrepancies can cause detrimental periodontal changes
overcontoured crowns can lead to gingival inflammation and periodontal disease
amalgam overhangs cause gingival inflammation
prior to restorative treatment a healthy sulcus is required
a thin line of cement may contribute to plaque adherence
temporary crowns need a good fit and need to be polished to decrease roughness
all restorations should preserve the embrasure space
crowns must be contoured to facilitate oral hygiene procedures
partial dentures can collect calculus, clean properly and remove nightly
natural teeth in function with dentures may have more and deeper pockets
abutment teeth are more susceptible to caries
conditions that affect periodontal health orthodontic appliances, malocclusion, unreplaced teeth, mouth breathing, and tobacco use
Malocclusion NOT a cause of periodontal disease, misaligned teeth can leave spaces & complicate daily plaque control, demostrate appropriate aids
Missing teeth allow for more occlusal pressure on remaining teeth contributing to migration, creates food impaction & makes cleaning harder, educate patient and encourage replacement
First Molar Loss Syndrome if lost in childhood can affect progress/severity of periodontal disease; 2nd and 3rd molars mesially drift and tilt creating space and loss of vertical dimension etc.
tobacco use strongly identified as a risk factor for periodontal disease, deeper pockets, greater attachment loss, more calculus, more bone loss
tobacco induced changes increased keratinization, reduced reaction to inflammation, PMN's can't phagocytize, delayed healing, ginigival and bone distruction in areas where smokeless tobacco used
Plaque principle irritating factor
dental plaque-induced gingivitis gingivitis associated with dental plaque only: systemic factors, medications, malnutrition
non-plaque-induced gingivitis gingival diseases of specific bacterial, viral, fungal, genetic origin, or from systemic conditions, traumatic lesions, or foreign body reactions
gingival diseases range from common forms, ie gingivitis to rate and life-threatening forms, ie squamous cell carcinoma & acute leukemia
microflora in gingival health g+ cocci, g+ facultative anaerobic rods, small numbers of g- rods
gingivitis most common human disease, manifests as color change, edema, exudate,& a tendency to bleed
microflora in gingivitis g+ rods and cocci, g- rods, increase in filamentous bacteria (Actinomyces); in later stages anaerobic g- rods increase (Fusobacterium and P. intermedia), Motile rods & spirochetes appear
Stage I gingivitis (initial)-No outwardly observable clinical signs first few days of contact, acute inflammatory response-dilation of blood vessels, PMN's migrate into the connective tissue, plasma leaks into tissue causing edema, PMN's migrate through sulcular epithelium forming exudate
stage II gingivitis (early)-clinically, tissue appears slightly red, shiny, swollen, and there is bop-earliest clinical evidence of gingivitis lesions in 4-7 days, T-lymphocytes increase in number, inflammatory exudate increases and may be white or yellow, connective tissue collagen fibers are destroyeed, stippling begins to disappear, and the junctional epithelium begins to lengthen
stage III gingivitis (established) after 15-21 days plasma cells associated w/ antigen-antibody response are present, T and B-lymphocytes/tissue destruction, junctional epithelium thickens and extends apically, edema, visible pus, capillary proliferation (redness) & oxygen depletion of rbc's (cyanosis)
chronic gingivitis nonspecific infection related to inflammation from a large number of organisms as a result of poor oral hygiene
Periodontitis specific infection as a result of a limited number of organisms
healing after treatment begins in the connective tissue, inflammatory cells replaced by fibroblasts which lay down collagen and produce dense connective tissue
plaque-induced gingival disease most common symptom of gingivitis is bleeding gums, a lot of people think this is normal
gingivitis associated with plaque only increase in capillaries along gingival margin, sulcular epithelium is ulcerated, and increase in gingival crevicular fluid, mature plaque has a large number of g- bacteria
gingivitis associated with plaque only clinically gingival margin is red, edema, hypertrophy, bleeding and pocket formation
plaque traps do not cause gingivitis but can make plaque control more difficult
gingival disease modified by systemic factors systemic factors may modify the way the immune system responds to plaque; some conditions alone don't cause, but may intensify gingivitis ie, pregnancy, puberty,bcps, hrt, and diabetes
pregnancy gingival changes increase when plaque control is inadequate, gingiva may become dark red, hyperplastic, and bleed easily, may increase as pregnancy progresses, most changes improve with good home care and removal of local irritants
pregnancy localized area of pyogenic granulation tissue may occur, not a neoplasm but an inflammatory response, tissues are inflammed, bleed easily and may cause tooth mobility or migration
pregnancy pregnancy tumor aka pyogenic granuloma, may also occur as a result of trauma in nonpregnant people
gingival enlargement or overgrowth phenytoin (antiepileptic)
gingival enlargement or overgrowth nifedipine and verapamil (cardiovascular)
gingival enlargement or overgrowthgingival enlargement or overgrowth cyclosporine (immune suppressant for organ transplant patients & MS)
gingival enlargement or overgrowth treatment includes good home care, regular debridement, scaling and root planing, and often surgical reduction
malnutrition serious nutritional deficiencies modify the body's response to plaque. Deficiencies in vitamins A, B1, B2, B6, & C can produce changes in the tissues-gingiva becomes very hemorrhagic and swollen, progresses rapidly to advanced periodontitis
gingival diseases of specific bacterial origin strep infection of the throat, std's ie gonorrhea or syphillis, NUG
NUG periodontal disease that can occur with no bone loss and a bacterial component, related to excessive stress, organisms include fusiform bacillus and spirochetes
NUG pain, burning, can't eat, cratered papillae, pseudomembrane, inflammed attached gingiva, possible fever, breath odor
NUG treatment debridement, excellent oral hygiene, rinse w/ peroxide and water. untreated leads to boneloss and NUP
viral origin-primary herpetic gingivostomatitis children and teenagers, fever common, malaise, vesicles, ulcerative lesions, and possible breath odor, symptoms similiar to NUG. secondary forms occur around the mouth "cold sores"
fungal-candida albicans most common fungal organism affecting gingiva, appears red or white. redness at gingival margin called linear gingival erythema, redness with white patches that rub off exposing ulcerated gingival tissues
candida albicans treatment involves use of antifungals, antiseptics or both
genetic-gingival enlargement (hyperplasia or hypertrophy) can be caused by excessive reactions to plaque, medications, infections or as a side effect of systemic diseases-evaluate for this when tissue appears dramatically different from chronic plaque-induced gingivitis
genetic-gingival enlargement (hyperplasia or hypertrophy) treatment-plaque and calculus removal, oral hygiene instruction, and re-eval in 2-4 weeks. if not resolved consider futher eval or referral
Systemic conditions-blood dycrasias in patients with acute leukemia, tissue tender, swollen, hemorrhagic-NOT plaque induced
dermatologic-lichen planus chronic disease of the skin and mucous membranes that is thought to be immune related, related to stress, no known cure, treat w/ steroids
dermatologic-lichen planus asymptomatic reticular form-lacy white lines (wickham's striae) or erosive form-white lesions altenating with raw, reddened areas, concern about potential to transform into squamous cell carcinoma
dermatologic-mucous membrane pemphigoid autoimmune reaction, appears as blistering of epithelium, more common in older women, may be seen on buccal mucosa and inner surface of lips, treatment is palliative steroid therapy, chx rinses
dermatologic-desquamative gingivitis pemphigoid lesions limited to gingival tissues, epithelium sloughs leaving a raw, red area. autoimmune or possibly allergic reaction
traumatic lesions burns (food or chemical), cuts
foreign body reactions food impaction, removal of body usually brings relief
home care plaque-induced gingivitis most common human disease, care will always consist of education & removal of local irritants to promote healing
periodontal abscess acute, localized purulent bacterial infection fo periodontium, occurs in patients with periodontitis, rapid onset, pain, edema, discomfort-caused by bacteria established in tissue by trauma, advancing disease or incomplete scaling and root planing
acute abscesses pocket becomes occluded, infection moves into adjacent areas, and rapid bone loss occurs, appears shiny, red, raised adn rounded masses on the gingiva or mucosa, can drain through the tissue or pocket opening-throbbing pain, swelling red-blue
acute abcesses tooth sensitivity to pressure, Treatment-drainage, scaling and root planing, curettage, irrigation, antimicrobials, antibiotics, surgery-can become chronic if untreated
chronic abcesses usually painless due to drainage, treatment similar to treatment of an accute abcess
gingival abscess caused by foreign body being forced into sulcus, treatment-drainage, irrigation, scaling and root planing, and possible excision
pericoronitis abcess around partially erupted tooth (3rds) or a fully erupted tooth covered by an operculum - bacteria accumulates under gingiva next to tooth and tissue becomes inflammed and painful-swelling of operculum and distal gingiva, redness pain.
pericoronitits treatment; debridement, irrigation, antibiotics, removal of operculum or tooth
periodontitis associated w/ endo lesions facial pain/tenderness similar to acute perio abcess; results from infection through caries, tooth fracture, or trauma. infection can be spread to pulp of an adjacent infected tooth. Treatment-endo therapy or extraction-
periodontitis associated w/ endo lesions if left untreated can lead to brain abscess or fascitis of the neck or chest wall
combo abcesses abscess can spread from pulp to periodontium or from pocket to pulp-can cause extensive damage to surrounding periodontium b/c symptoms can be intermittent. trmt-extensive therapy, both endo trmt and perio therapy
developmental or acquired deformities and conditions-pseudopockets gingival margin is coronal to CEJ, often seen on distal of 2nd 3rd molars
developmental or acquired deformities and conditions-recession can be underlying osseous defect or acquired defect from trauma; leads to sensitivity, caries, gingivitis ro esthetic problems
other factors may WORSEN (not cause) progression of periodontitis nutritional deficiencies, spaces, missing teeth, hormones, furcations, trauma, calculus, food impaction, anatomy, restorations, deep pockets
tobacco use decrease neutrophil function (def. immune response), and upset balance in natural healing
pathogenesis of periodontitis inflammation extends into attachment apparatus and results in pocket formation, pockets deepen b/c of breakdown of collagen fibers, apical migration of JE and loss of crestal bone
acute herpatic gingivostomatitis herpes virus-infectious and painful-vesicles of oral mucous membrane-lips, tongue, gingiva, and buccal mucosa. NO instrumentation
Created by: jfgwinn