2023 ECD IV Exam III Study Guide Part 3 PDF

Necrotizing Perio Diseases ● Perio-endo infections Necrotizing Perio Diseases Necrotizing Perio Diseases ● Perio status review ○ Determine probing depths, attachment loss, bone loss, tooth mobility ■ Mobility Grade II or III consider ext if no value in tooth to patient, tx unlikely to improve...

Necrotizing Perio Diseases ● Perio-endo infections Necrotizing Perio Diseases Necrotizing Perio Diseases ● Perio status review ○ Determine probing depths, attachment loss, bone loss, tooth mobility ■ Mobility Grade II or III consider ext if no value in tooth to patient, tx unlikely to improve tooth, or tooth poses risk to adjacent teeth ■ For severe attachment/bone loss consider is there tx that can improve this and if this tx would make the tooth useful to the patient ■ Low probing depth and no bleeding indicated stable perio status (with good predictable outcomes with endo) ● If endo breaks through perio tissue: will have narrow pocket (not wider than perio probe)- compare to perio disease with wide pockets often line angle to line angle or at furcation ● Perio disease-> softer sulcus (not rubber-band like in healthy) (in endo more stretch with soft mushy feel) ● Perio doesn’t always have pain associated unless severe and acute (but endo has pain) Necrotizing Perio Diseases Necrotizing Perio Diseases ● Combo perio exam, pulp testing, periapical testing usually diagnostic ○ Other options, gutta percha to trace sinus track, tooth sleuth for cracked tooth identification, CBCT for fractures or hidden endo infections (good for vague symptoms with inconclusive other testing) ■ Max teeth: test if anesthetic infiltration relieves pain (helps to focus on endo involved teeth) ■ Test cavity: drill into tooth not anesthetized (non-vital will be fine, pt will feel nothing) ■ Exploratory flap surgery: can check if fractured, has root surface abnormalities, perforated or damaged root ■ Exploratory root canal access with microscope and dye (internal root fractures, missed or hidden canals, perforations) Necrotizing Perio Diseases ● Combined perio-endo disease (perio-endo lesions) ○ ○ ○ ○ ○ Prevalence: rae (less than 3%of TDC patients) Signs and symptoms: obvious on radiograph, deep localized PD (10mm+), pulp test either questionable or no response (pulp necrosis), large caries, tooth fracture, occlusal trauma, obvious mobility, fremitus Histo: epithelialization to root apex and large leukocyte infiltrate Diagnosis: usually obvious except when just starting to develop (then can be more subtle), also may be difficult to understand how this lesion developed (can be classified by Glick-Simon-Frank method) ■ Primary endo: root canal infection first to apex/furcation, drains at PDL -> perio lesion ■ Primary perio: severe perio-> destroys blood supply,-> pulp necrosis ■ Secondary perio: endo infection-> PA lesions while also depp pocket eventually-> apex (fusion of both) ■ Secondary endo: perio disease-> accessory canal-> perio bact in pulp-> pulp necrosis-> PA lesion ■ (Ture) combined lesion: severe perio and endo infection independent of each other and separated by PDL Perio-endo lesion recently developed originating as endo lesion and endo lesion still separate from perio lesion may be treatable and reversible Necrotizing Perio Diseases Necrotizing Perio Diseases ● Perio-endo lesion ○ How to identify origin: educated guess using pt hx, past conditions of tooth, size and feel of perio pocket, intuition Necrotizing Perio Diseases Necrotizing Perio Diseases ● Differentials ○ ○ ○ ○ ○ Perio abscess: deep pocket, severe bone loss, vital pulp, bone loss NOT to apex of tooth (more centered at furcation), intact PDL Endo infection: can produce large area bone loss but do not affect perio sulcus and PD not to apex of tooth Localized severe.chronic aggressive periodontitis: vital pulp, 1st molar or incisor most, contributing factors (calculus, occlusal trauma, restorative prob, anatomic defect, tipped tooth) Histiocytosis and malignancies: v. rare-> free floating tooth, vital pulp, destruction usually wider and more diffuse (endo-perio lesion more 203 mm within tooth surface), systemic symptoms as well, site will not heal with tooth ext (so always biopsy non-healing ext sites) External root resorption (pink tooth): area of bone loss and radiographic shadow near pulp, prognosis poor, tx is RCT with surgical access, clean with curette and trichloroacetic acid, then GI cement Necrotizing Perio Diseases ● Etiology ○ ○ ○ ○ ○ ○ ○ ○ Bacteria and local contributing factors (poss fungi in some with viruses exacerbating inflammation) Can be started by non-living etiologic agents (foreign material into pulp or PDL space- ie cement, core material, restorative material) Chronic trauma-> loss of vitality All lead to tissue die off and release of toxic materials to periodontal tissue Accessory canals, wide dentinal tubules, apical foramina can provide extra passageway for bact to spread to pulp-> necrosis or for irritants to leech to PDL to perio tissue Root resorption reduced distance bw perio pocket and endo infection Malformation can predispose tooth to perio or endo Iatrogenic factors Necrotizing Perio Diseases ● Prognosis ○ ○ ○ ● Tx ○ ○ ● Most: ext tooth If know origin: perform RCT first (especially if tooth not mobile and lesion is of endo origin) then treat perio disease Perio destruction and treatment have no relationship to pulp status ○ ● Questionable to hopeless with unknown hx (prog improves when know origin of lesion) Primary endo: good (RCT can reverse bone loss) Primary perio: poor No evidence aggressive SRP causes pulp infection, no evidence perio disease can cause bact into furcation Dentists can cause perio-endo lesions ○ Perforations in RCT tx, root fractures from occlusal overload due to faulty prosthetic design Rare Perio Diseases ● Non plaque induced gingival diseases ○ ○ ○ ● Rare, inflam not limited to gingival margin, can produce soft tissue ulcers, OHI and plaque removal has little effect, biopsy needed, see associated with med conditions Does not cause attachment/bone loss Diagnosis: with other signs/symptoms treat as pathology, perform OHI and perio tx, re-eval in 2-3 weeks, in f no improvement then biopsy Neisseria infections ○ ○ Very rare, generalized erythema in mouth with shallow ulcers, no pain to severe pain Will have sore throat that will not resolve on own (refer to PCP), dental tx will not resolve, need microbial culture and typically antibiotics Rare Perio Diseases ● Syphilis ○ ○ ● Tb ○ ○ ● Very rare, red, raised, shallow ulcers and tissue necrosis (primary chancre at infection site, secondary patches, tertiary gumma), similar to SSC Refer to PCP, dental tx wil not resolve, need microbial culture and antibiotics V. rare, systemic signs as well (productive cough, weight loss, fever, malaise) Biopsy (confused with oral cancer), med tx for Tb Streptococcal gingivitis ○ ○ Rare, swollen, bright red, large soft tissue swelling on mucosa with shallow ulcer, fever, malaise, submandibular lymphadenitis Chlorhexidine rinse and antibiotics Rare Perio Diseases ● Coxsackie virus ○ ○ ● Herpes ○ ○ ○ ● Rare, viral, see in children <5, intraoral lesion plus patchy vesicular rash on extremities, mild fever, sore throat, pain Self limiting but can be fatal, severe needs tx for dehydration risk, antiviral tx Severe mouth pain, fever, can’t eat or drink due to pain, shallow, painful, small, irreg ulcers with yellow-gray pseudomem with erythematous halo, HSV-1 Resolves on own in 1-2 weeks, young children may need IV infusion to prevent dehydration , supportive tx (rest, fluids, tylenol), poss antiviral to shorten and dec symptoms Chicken pox/shingles/varicella ○ ○ Fever, sharp pain (neuralgia), unable to eat.drink, shallow, painful irreg ulcers with yellow-gray pseudomem with erythematous halo, follows dermatome and stops t midline for shingles IV infusion for dehydration, supportive (rest, fluids, tylenol, poss neurologist if neuralgia Rare Perio Diseases ● Molluscum contagiosum (pox virus) ○ ○ ● V. rare on gingiva, rare intraorally, extraoral more common, painless nodules on gingiva (can be tender and pruritic/itchy), immunocomprosmied state, oral sex Resolve in 6-9 mo for immunocompetent, excise HPV: various forms (squamous papilloma, condyloma acuminatum, verruca vulgaris, focal epithelial hyperplasia) ○ ○ Very rare on gingiva (more tongue and mucosa), wart-like or slowly enlarging whte wrinkled lesion, verrucous leukoplakia can progress to SCC) Biopsy, leukoplakic lesions recur, OMFS Rare Perio Diseases ● Candidiasis ○ ○ ● Generalized redness outline denture, pseudomem type rare on gingiva (severe immunosuppression) Antifungal tx Histoplasmosis ○ ○ Solitary, slowly enlarging tissue mass with central ulcer like SSC, hx immunocompromised Biopsy (histoplasma spores), refer to infectious disease specialist, antifungal tx Rare Perio Diseases ● Genetic conditions cause non-plaque induced gingival disease: grouped as Hereditary gingival fibromatosis (slow growing gingival enlargement independent of plaque with a disturbance of collagen metabolism -> collagen matrix build-up in soft tissue) ○ ● Tx usually involves: genetic counseling, OHI with frequent maintenance, gingivectomy Autoimmune: sometimes see first in gingiva due to frequent mechanical force here ○ ○ Desquamative gingivitis describes condition Characteristics: uncommon, patchy, diffuse gingiva, erythema to ulceration, soreness to severe pain, OHI and plaque removal won’t help, tx with med professional Rare Perio Diseases- Autoimmune ● Pemphigus vulgaris ○ ○ ○ ● V. rare, skin blisters with mechanical friction, intraoral blisters to shallow ulcers (if tissue isrubbed- Nikolski sign), need biopsy HIsto: blister from within epi, tombstone cells (basal cell layer forms single layer at base of blister), Tzank cells (free floating round epi cells in blister), IgG (antibodies against Desmoglein within epi cells) Tx: smooth restorative surfaces, mild, bland toothpaste/mouthwash, topical corticosteroids (fluocinonide), short term prednisone before prophy or perio tx, dermatologist referral Pemphigoid ○ ○ ○ Same as above Refer to PCP If controlled, root coverage procedures by periodontist may resolve recession defects Rare Perio Diseases- Autoimmune ● Lichen Planus ○ ○ ○ ○ Common, can be triggered by meds, varied appearance, reticular (painless, white striations), erosive (sore, red tissue with pinpoint ulcer), vesicular (like pemphigoid lesion), atrophic (thin, friable gingiva) Diagnose with biopsy Histo; cell layer thickened or inc keratin, dense T-cell infiltrate in lamina dura, degen basal layer, saw tooth rete pegs, mimics early SSC, fibrin deposits in basement mem Tx: none for reticular, oral cancer screenings, topical corticosteroid cream, refer to PCP if systemic Rare Perio Diseases- Autoimmune ● Lupus erythematosus (systemic and discoid) ○ ○ ○ ○ Systemic: with internal organ involvement; discoid: only affects skin and mucosal surface but can become systemic Oral signs uncommon (like lichen planus or pemphigoid with +Nikolsky sign), skin lesions more common (red purple macules, hyperkeratotic plaque with erythema and hyperpig at border, central scar and hypopig area, patchy loss of hair, scaly around hair follicles, itching/burning) Histo: perivascular accumulation of leukocytes, dense lymphocytic infiltration at epi CT junction, loss basement mem Tx: OHI and plaque removal won’t resolve, biopsy, refer to PCP (diagnose with autoantibodies), systemic steroids or cytotoxic meds (cyclophosphamide,, azathioprine), topical corticosteroids Rare Perio Diseases- Autoimmune ● Crohn's Disease ○ ○ ○ ● Sarcoidosis ○ ○ ● Usually see in children and diagnosed with internal signs/symptoms (food sensitivity, pain/ab cramping, irreg bowel mvmt, diarrhea) Oral signs: crusty, cracked lips, diffuse inflamed oral cavity, burning pain in mouth Tx: med eval (biopsy, systemic steroids, poss surgerybowel obstructions-, mngmt side effects of corticosteroid therapy), avoid triggering foods, counseling Rare, YA, affects lungs, symptoms depend on what organ involved, non-caseating inflammatory granuloma, no tissue necrosis inside granuloma Tx: PCP, diagnostic tests to rule out Tb, systemic corticosteroids, tx for specific organ damage Others: chronic ulcerative stomatitis, linear IgA disease, dermatitis herpetiformis, GVHD, epidermolysis bullosa acquisita, Wegener's granulomatosis, mucositis caused by chemo/rad Rare Perio Diseases ● Allergic Rxns ○ ○ ○ ○ ○ Slight local redness to massive swelling and ulceration (from varying levels of inflam (from type 1- immediate, to type 4-cytotoxic Signs of perio disease (gingival redness and bleeding, maybe burning, maybe ulcerated) Perio therapy, OHI, avoid spicy foods, avoid alcohol, use baking soda, warm salt water rinse Re-eval in 2 weeks- if gone slowly start reintroducing food and OH productsone at a timeto find cause, if not gone then biopsy Refer to allergist Rare Perio Diseases- Allergic Rxns ● Plasma cell gingivitis ○ ○ ● Sudden onset burning sensation, diffuse erythema, patchy, generalize beefy, red look, low plaque levels, inflam not limited to margin or related to plaque, see with cinnamaldehyde Tx: bland diet, OH, resolves in 2 weeks, allergy testing as needed Erythema multiforme ○ ○ ○ ○ ○ ○ Immune complement fixation rxn -> capillary vessel damage and poss necrosis, can be ife threatening (Steve Johnson syndrome)- due to electrolyte loss and shock Skin: mild (patchy areas erythema with ligh center- target lesion), severe (ulceration, blood encrusted vermillion border of lips, erythema encomppases entire skin surface) Oral: mild (erythema similar to plasma cell gingivitis), severe (erythematous area that ulcerate and bleed profusely Histo: degen basement mem, degen superficial epi, intra-epi microvesicles, no blisters Triggers: herpes, mycoplasma, allergy to sulfonamides, phenylbutazone, phenytoin, dilantin, penicillin Tx: mild (none, resolve in 4weeks once stop med), severe (emergency med tx with IV antihistamines, steroids, fluids, life support, IV antibiotics) Rare Perio Diseases ● Traumatic Injury ○ ○ ○ ○ ○ ○ ○ Thermal: food burn, electric burn (children most at risk), heat burns from dental tx Chemical: overly acidic substance (aspirin) caustic substance (bleach), dehydrating agents (alcohol), irritants (tobacco) Physical: cut from dental tool (floss, tooth brush, explorer), food (tortilla chips), haits (nail digging), intruded dental material (polishing paste, com- see with cement retained implants and with prophy cups used to aggressive) Tissue necrosis, tissue sloughing (chem and thermal), leukoplakia, scarring (chem), linear cut/tear (physical), sharp pain, ulceration, peristnat inflammation See, find out cause, have pt stop cause, re-check in 2 weeks Tx: have patient protect area, let heal (most heal in 2 weeks, biopsy non-healing areas, soft tissue graft as needed) Floss cut: small, linear cut causing sharp gum pain- tx is do not floss here for 1 weeks and use extrasoft brush with alcohol free mouth wash, if doesnt heal can form gingival cleft Rare Perio Diseases ● ● Localized gingival enlargement affecting multiple interdental papilla with normal or unaffected facial gingiva: see with phenytoin/dilantin (siezure med), cyclosporine (immunosuppressive drug), calciium channel blockers (HTN), neuroligc meds (amphetamines and valproic acid Clinical signs ○ ● Rounded papilla point, tissue reaches coronally to IP point and is thicker than 3mm, pebbly lumpy texture, gingiva covers >3mm of enamel Cause ○ See with edema from inflam, inc tissue matrix (matrix deposition by fibroblasts from hereditary gingival fibromatosis or phenytoin), or lower collagen breakdown (Ca channel blockers), malignant cell infiltrate, or inc bulk from underlying bone (false gingival enlargement) Rare Perio Diseases ● Diagnosis ○ ○ ○ ● Single, localized gingival enlargements usually: ○ ● Peripheral giant cell granuloma, POF, pyogenic granuloma, other non-odonto malig Localized gingival enlargements ○ ○ ● Treat with perio therapy, OHI, cleaning Re-eval in 2-3 weeks If not resolved then biopsy (incisional for generalized and excisional for localized) Med side effect (Ca channel blocker, phenytoin, cyclosporine, amphetamine, valproic acid Biopsy will show inc tissue matrix or suggest fibroma/granuloma Generalized gingival enlargement ○ Genetic cond, see early in life usually (hereditary gingival fibromatosis, juvenile hyaline fibromatosis), rare systemic disease Rare Perio Diseases ● Single, localized tx ○ ○ ● Localized gingival enlargement of multiple papillae ○ ○ ● Benign reactive lesion: excisional biopsy, regular perio preventative therapy, watch for recurrence Malignancy: OMFS and oncologist referral Drug induced gingival enlargement- refer to periodontist (gingivectomy, regular perio tx) Other systemic disease: refer to PCP, regular perio tx once med condition controlled Generalized gingival enlargement ○ ○ Hereditary gingival fibromatosis and juvenile fibromatosis: refer to perio (gingivectomy, regular perio tx) Other systemic disease: refer to PCP, regular perio tx when med condition controlled Bohem Study Guide (Said these will def be on Exam) *** 1. 2. 3. 4. 5. 6. 7. 8. 9. Systemic Periodontal Relationships & CR session: How does periodontitis favor development of atherosclerosis (vascular disease) Systemic Periodontal Relationships & CR session: What effect does periodontal treatment have on type 2 diabetes? Systemic Periodontal Relationships (Clinical Question): Why do you want to know serum glucose levels and HbA1c levels for diagnosing periodontal disease? Abscesses of the Periodontium : What distinguishes periodontal abscesses from endodontic abscesses? (i.e. how do they differ in pulp status, percussion, pockets, mobility, radiographic appearance, location of fistula/gingival swelling, microbiology, causes?) Abscesses of the Periodontium (Clinical Question): Given a case, how would you distinguish between an endodontic abscess (any kind), periodontal abscess, or any other oral pathology (i.e. some soft tissue tumor in gingiva, drug-induced gingival enlargement)? Periodontics and Orthodontic Treatment & CR Session: Why is oral hygiene important? Necrotizing Periodontal Diseases: What medical conditions predispose to necrotizing periodontitis? What can trigger necrotizing gingivitis in a healthy young adult? Periodontal Disease Caused by Systemic Diseases: What are key distinguishing feature of periodontitis as symptom of a genetic condition (i.e. Chediak-Higashi, Zimmerman-Laband, Leukocyte adhesion syndrome, …) compared to typical periodontitis? Periodontics and Restorative treatment & CR session: Periodontal treatment must be completed before starting any complex prosthetic treatment Boehm Study Guide #1: How does periodontitis favor development of atherosclerosis ● Chronic Perio and Atherosclerosis ○ ○ ○ Most common causes of atherosclerosis: HTN, hyperlipidemia, tobacco, DM, sedentary life, obesity, endocrine dysfunction, thrombosis, hemostasis abnormalities Atheroslcerotic injury: injury to endo lining of blood vessel-> more sticky (monocytes adhere to altered cells)->monocytes enter blood vessel at site and activate -> macrophages (digest abnormal cells and absorb lipids-> endo lifts off from underlying blood vessel->space that gets filled with immune cells, lipid droplets, and tissue/debris and m. cells-> smooth m. cells and macrophages engorge on lipids (fibrofatty streaks)->smooth m. prolif., lipids, immune cells EM keeps depositing-> tissue mass that constricts lumen (atheroma or fibrofatty atheroma)->eventual rupture of atheroma-> fat and tissue debris in circulation-> blood clots-> swept to distant blood vessels and trapped at branch points-> cut off blood supply-> infarct (heart attack and stroke) Small but sig inc risk for strokes and heart attacks in pt with chronic perio ■ ■ ■ ○ ○ P. gingivalis and other invasive periodontal bacteria can infiltrate tissues, including blood vessel endothelium, and have been found in atheroma biopsies. P. gingivalis is capable of inducing many cellular changes seen in atheromas such as: ● Inducing foam cell formation from macrophages ● Disrupting endothelial cell function ● Inducing atheroma formation in animals injected with P. gingivalis ● Causing auto-immune antibodies against endothelial tissue as P. gingivalis heat shock protein (hsp) is similar to human protein from these cells Periodontitis causes an increase in systemic levels of inflammatory cytokines, C-reactive protein and fibrinogen, which all favor development of atheromas. No evidence of bidirectional effect No trial has shown perio tx lowering atherosclerosis risk Boehm Study Guide #2: What effect does periodontal treatment have on type 2 diabetes? ● DM and Perio Disease ○ ○ ○ Most researched perio-systemic relationship (aside from tobacco) Untreated DM-> worse perio ■ Adults with DM are 2x as likely to have perio, ⅓ have severe, over 45y/o 3x more likely to have severe (5x if smoke too) Mechanism of DM->Perio: DM-> chronically elevated blood glucose levels (randomly converts glucose-> active aldehyde form)-> active aldehyde reacts with amino groups (Schiff base rxn)->glucosyl residues added to proteins that accumulate at blood vessel walls and in tissues (reactive advanced glycosylation end products- RAGE); RAGE seen as abnormal tissue_> activation and triggering of immune cells to remove (in perio tissues RAGE stim adds to immune cell activation already there->excessive tissue damage); also high lipid levels in blood-> high oxidized lipids that activate immune cells Boehm Study Guide #2 ● DM and Perio cont ○ ○ ○ Mechanism of Perio-> DM: active chronic peiro-> inflam of perio tissue with immune cells that release pro-inflam cytokines to tissues-> blood vessels-> IL-6 TNFalpha to organs like liver and muscle-> lower cell response to insulin-> less glucose absorbed by tissues-> liver release of more lipids-> chronically elevated glucose and wordened pre-existing DM with worse lipid profiles-> tissue damage-> even worse Dm-> feeds back into perio disease In obese patients adipose tissue produces higher cytokines-> insulin resistance and why long term obestiy linked to DM Possible causality- some clinical trials have shown perio tx improves glycemic index Boehm Study Guide #3 Systemic Periodontal Relationships (Clinical Question): Why do you want to know serum glucose levels and HbA1c levels for diagnosing periodontal disease? Because it tells you if diabetes is controlled or not…? Is that it? Because worse DM leads to worse perio, a poor HbA1C will suggest more severe perio. Paragraph below answers previous question moreIt is possible that there is a causal relationship as multiple clinical trials have demonstrated that periodontal treatment improves glycemic control in Type 2 diabetes mellitus. The effect seen in most trials is a reduction in HbA1c levels of about 0.3-0.5% in patients with severe periodontal disease. For comparison, single antiglycemic agents given to Type 2 diabetics produce a reduction of HbA1c of about 0.5-1% on average. While the effect is clinically significant, there are still questions on whether this effect is due to periodontal disease or yet to be discovered as other factors that predispose some individuals to having both diabetes and more severe periodontal disease. Boehm Study Guide #4: What distinguishes periodontal abscesses from endodontic abscesses? - will be 2 questions regarding this IDK different microbiology of them Boehm Study Guide #4 P: periodontal abscess, G: gingival abscess, E: Endodontic abscess; C: Pericoronal abscess; PE: Combined periodontal endodontic lesion