Pulpal Diseases and Diagnosis PDF

Pulpal Diseases and Diagnosis Pulpal and Apical Diagnosis 2 general diagnoses: Pulpal and Apical Pulpal o Normal Pulp o Reversible Pulpitis o Symptomatic Irreversible Pulpits o Asymptomatic Irreversible Pulpitis o Pulp Necrosis o Previously Treated Pulp o Previously Initiated Therapy o Other § Hyper...

Pulpal Diseases and Diagnosis Pulpal and Apical Diagnosis 2 general diagnoses: Pulpal and Apical Pulpal o Normal Pulp o Reversible Pulpitis o Symptomatic Irreversible Pulpits o Asymptomatic Irreversible Pulpitis o Pulp Necrosis o Previously Treated Pulp o Previously Initiated Therapy o Other § Hyperplastic Pulpitis § Internal Resorption Apical (all tissues surrounding tooth) o Symptomatic Apical Periodontitis o Asymptomatic Apical Periodontitis o Acute Apical Abscess o Chronic Apical Abscess o Normal Apical tissue The Pulp – Review Pulp contains: o Nerves o Blood Vessels o Connective Tissue Has an altered ability to respond to irritation o Surrounded by hard tissue, restricting its ability to expand and tolerate edema o Lacks collateral circulation, restricting its ability to cope with bacteria, necrotic tissue and inflammation o Odontoblasts (hard tissue secreting cells) and mesenchymal cells (differentiate into osteoblasts) form more dentin in an attempt to protect the pulp from injury. § Pulp shrinks when inflamed b/c odontoblasts lay down more dentin to protect tender pulp Pulpal Pain A Delta fibers: Quick, sharp, momentary pain (ex. cold, biting on hard) o Superficial pain (near dentin) o Myelinated nerves o Courses coronally through pulp o Easily provoked o A-delta associate with odontoblasts and dentin = pulpodentinal complex C afferent fibers: Deep, throbbing ache à pain dominates signifying irreversible tissue damage o Small fibers o Unmyelinated nerves o Must determine if this is reversible pain or not o Not involved with pulpodentinal complex o Not easily provoked o Occurs with tissue injury o Increases tissue pressure (hot liquid/foods increase intrapulpal pressure that excites C fibers) o Mediated by inflammatory mediators o Vascular changes in blood volume and blood flow Pulpitis o Inflammation of the pulp causes an exaggerated and disproportionate pain called hyperalgesia o Pain can be diffuse, don’t take the pts full word for it, the pain can be ‘referred’ to another tooth o Pain is induced by inflammatory mediators released from inflamed pulp o Progression of pulpal inflammation changes the quality of pain (A-delta pain subsides, pain continues as dull, throbbing ache of C nerve fibers) o Sustained inflammation causes pulpal death (tissue necrosis) Normal Pulp Asymptomatic Mild to mod transient response to thermal and electrical stimuli that Subsides immediately when stimulus removed (return to normal in 3-5 seconds when tooth warms back up) No painful response when percussed or palpated Reversible Pulpitis (RS occurs w/o endo tx) Thermal stimuli causes quick, sharp, hypersensitive response that subsides when stimulus is removed Any irritant that can affect the pulp can cause reversible pulpitis o Early caries o Recurrent Decay o Recession o Periodontal Scaling o Root planning RS is NOT a disease, it is a symptom o Irritant is removed à pulp goes back to normal o Irritant remains/lingers à irreversible pulpitis Reversible vs Symptomatic Irreversible 2 distinguishing factors: o Reversible does NOT involve spontaneous, unprovoked pain (instead it is momentary, sharp, quick pain) o Symptomatic Irreversible has painful response to thermal change that LINGERS even when stimulus removed Frequent bacterial penetration into pulp à Irreversible pulpitis Symptomatic Irreversible Pulpitis (SIP) Pulp damaged beyond repair, even w irritant removal it will not heal Pulp death occurs: quickly or over years, painful or asymptomatic à end result is pulp necrosis o Spontaneous o Unprovoked o Intermittent or continuous pain o Temp changes can elicit prolonged episodes of pain that LINGER after stimulus is removed o Pts report that posture changes induces pain (ex. lying down, bending) X Rays look normal for IP (radiographs are not enough to diagnose IP) o Only helpful to identify if we suspect death o Thick apical PDL becomes evident in advanced stage o Electrical pulp test has little value to diagnose SIP (ex. Tingling or buzzing = tooth is SIP still somewhat vital) Above decay is deep into the pulp. Decay Microscopic Findings: o Microabscesses of the pulp begin as tiny zones of necrosis within dense acute is 20% larger than what radiographs shows inflammatory cells o Histologically intact myelinated and unmyelinated nerves observed in areas with dense inflammation and cellular degeneration Asymptomatic Irreversible Pulpitis No pain, is the only difference from symptomatic Dead nerve- no thermal response Microscopic Findings: o Microabscesses of the pulp begin as tiny zones of necrosis within dense acute inflammatory cells o Histologically intact myelinated and unmyelinated nerves observed in areas with dense inflammation and cellular degeneration No clinical symptoms, but inflammation is produced by caries, caries excavation, or trauma o Carious lesion went into pulp o Patient has no pain o RCT required Pulp Necrosis Death of Pulp results from: o Untreated irreversible pulpits (IP) o Traumatic injury o Any event that causes long-term interruption of the blood supply to the pulp Can be partial or total o Total: asymptomatic before it affects the PDL o Partial: symptoms of irreversible pulpitis (ex. multirooted tooth has one canal with necrotic pulp and one canal with inflamed pulp) Anterior teeth may show some crown discoloration w pulp necrosis o Protein b/d and bacteria toxins can thicken the PDL, manifest tenderness to percussion/chewing Microscopic findings: o Tissue disintegrates in the center to form an increasing region of liquefaction necrosis o Lack of collateral circulation + unyielding walls of d entin = insufficient drainage of inflammatory fluids § Results in localized increases in tissue pressure § Destruction progresses unchecked until the entire pulp is necrotic o Bacteria can penetrate and invade dentinal tubules (must remove superficial layers of dentin when cleaning/shaping) Previously Treated Pulp An RCT already existing Indicates tooth has been endodontically treated and canals are obturated w filling other than intracanal medicaments (CaOH) o CaOH will be reabsorbed by macrophages o “Milholm’s Rule of Thumb”: A Lower tooth with a big lesion should be made into a 2-visit appt esp if they come in with no pain. Bacteria gets stirred up and will cause pain the day after tx, so a Partial endo therapy preemptive talk is advised. (pulpotomy or pulpectomy We DO NOT see CaOH intracanal medicament Previously Initiated Therapy Indicates tooth has been previously treated by partial endo therapy o Pulpotomy: cut part of pulp off o Pulpectomy: cut full nerve out Hyperplastic Pulp Reddish, cauliflower-like growth of pulp tissue through and around caries Low-grade, chronic irritation of the pulp Generous vascular supply Characteristically found in young people Internal Resorption Chronic pulpitis Most commonly identified during routine radiographic exam Will perforate root if undetected Prompt therapy restores tooth Partial vitality (active internal resorption) Necrotic pulp coronal to defect Histo: o Chronic inflammatory cells o Multinucleated giant cells adj to granulation tissue Cvek Pulpotomy: removal of coronal pulp (medicate then fill) Used in young teeth that haven’t fully formed roots yet, allows roots to finish developing. Internal resorption cannot continue b/c no nutrients Apical Diseases Inflammatory response to irritant from root canal system Pt can be asymptomatic, symptomatic o Sensitivity to chewing o Feeling of tooth elongation, hitting upon bite (tx: check bite) o Intense pain o Swelling o Fever o Malaise Proprioceptive nerve fibers detect pressure, not thermal Most indicative sign: radiographic bone resorption o Frequently not visible on x-rays o CBCT helps to identify apical lesions Do not occur as individual entities Acute and Chronic variants only applies to clinical symptoms 4 classifications o Symptomatic Apical Periodontitis (SAP) *most common o Asymptomatic Apical Periodontitis (AAP) o Acute Apical Abscess (AAA) o Chronic Apical Abscess (CAA) Symptomatic Apical Periodontitis (SAP): Most common Painful localized inflammation of PDL Can occur around vital and nonvital teeth (conducting pulp test is only way to confirm) o In assc w dental work that isn’t well adjusted § If pain is deep it’s most likely a pathology and not high occlusion § Cracked teeth hurt upon release of tooth slooth Can be caused by: o Extension of pulpal dz into apical tissue o Canal over-instrumentation/overfill o Occlusal trauma (ex. bruxism) PDL may appear WNL for a long time and pt can experience pain during percussion Increased pressure from PDL inflammation on nerve causes intense, throbbing pain If tooth is vital: o Occlusal adjustment relieves pain o Only if no other symptoms If pulp is necrotic: o Additional symptoms can occur as dz stage advances (ex. acute apical abscess) Asymptomatic Apical Periodontitis (AAP) No swelling, no sinus tract involvement, no pain? = AAP Long standing asymptomatic or mildly symptomatic lesion (slight tenderness to percussion, palpation) Visible apical bone resorption seen on x-rays Bacteria/endotoxin are in apical region from necrosed pulp causing demineralization of cancellous/cortical bone Diagnose via: o General absence of symptoms o Radiolucency at apex is seen o Pulp necrosis confirmed (cold test, electric test) Total pulp necrosis: o Anaerobic bacteria (no vascularity and no defense cells) o Tissue present as cyst or granuloma (granulomas are thick scar tissue that needs to be removed) No pain No sinus tract Acute Apical Abscess (AAA) Painful and purulent exudate at apex No sinus tract involvement Swelling is seen clearly (infection, rapid tissue destruction) o Localized but can become diffuse and spread (cellulitis) o Extent of swelling is determined by location of apex, muscle attachments, cortical plate thickness Exacerbation of SAP from necrotic pulp PDL and Lamina dura appear thick or WNL bc infection spreads rapidly before demineralization detected Signs/Symptoms: o Rapid onset of swelling o Moderate to severe pain o Pain w percussion and palpation o Mobility of tooth is slightly increased Differentiated from Lateral Periodontal Abscess w pulp vitality testing and probing o Lateral Perio Abscess: normal tooth, abscess tissue around tooth o AAA: Necrosed root Parapharyngeal abscess: Deviated uvula à refer to OS Chronic Apical Abscess No pain, no swelling Cont./intermittent draining sinus tract (Keeps pressure from building up) Mimics periodontal lesion with a ‘pocket’ as it can drain through gingival sulcus Negative pulp vitality test (necrotic pulp) Apical bone loss on radiograph Tx: o Resolve spontaneously w nonsurgical tx o Insert gutta percha into sinus tract, take x-ray to show infection origin Condensing Osteitis Excessive bone mineralization around the apex Asymptomatic vital tooth Radiopacity may be caused by low grade pulp irritation Usually the result of an old restoration Asymptomatic and benign hence, it does not require endo tx Pain? Swelling? Sinus Tract? Symptomatic Apical Periodontitis (SAP) Yes Yes No Apical Diseases Summary Asymptomatic Acute Apical Apical Periodontitis (AAP) Abscess (AAA) No Yes No Yes No No Chronic Apical Abscess (CAA) No No Yes Cracked Tooth Syndrome Large cracks have poor prognosis due to lack of margin required to seat crown. Cracked Tooth Syndrome Clinical Features: o Constant pain during biting o Pain only on release of biting pressure o Occasional, momentary, sharp, pain during mastication that is very difficult to reproduce o Sensitivity to thermal changes o Sensitivity to mild stimuli (ex. sweet, acidic foods) High incidence on Mandibular molars (1st) esp. filled molars Radiographic Evidence: o MD crack is impossible to see on radiographs as the line of fracture is not in the plane of image Crown margin must be below crack A crown is the most conservative approach A crown before pain starts, will prevent an RCT Diagnosis: o Transillumination § Small intense light applied to suspect tooth § Light transmits thru tooth, reflects back from crack o Use of “tooth sloth” or cotton-tipped applicator (main dx tool) § Cusps that occlude when pain occurs aids in fracture location § Start with normal teeth than moved toward suspected tooth § Tip of slooth pyramid touches cusp being tested, while the wide base supports multiple contacts o Stain with methylene blue: the blue gets into the cracks Tx of Cracked Tooth Syndrome Healthy Pulp or Reversible Pulpitis o Splint w ortho band and observe o Or, Prep to crown (sound temp and observe before placing permanent) Irreversible Pulpitis (sympt or asympt) OR Necrosis w Acute apical periodontitis Crowning a tooth that has pain does not resolve the pain Endo treatment! - Minimize removal of tooth structure - Minimize condensation force Restoration: o Sufficient tooth structure remaining: § Place Glass-I or acid-etched, dentin-bonded core WITHOUT post and restore with permanent crown. § Core material can be placed 2 to 3 mm into the canal orifices o Insufficient tooth structure remains: § Place acid-etched, dentin-bonded core WITH passively placed post and restore with permanent crown § Sound tooth structure must have margins ≥ 2 mm (Crown lengthening, extrusion or both may be needed) Prognosis: o Guarded: Presence and extent of isolated probing (probe sinks) -hopeless prognosis o Guarded: Crack extends to the floor of the pulp chamber -hopeless prognosis o Poor: Fracture traceable all the way from M to D Vertical Root Fracture 3 types; o A: Coronally located extending apically as far as one third of the root. o B: Midroot extending along the middle third of the root o C: Apical located extending coronally (can go up to 2/3 of root) Etiologies: o Predisposing factors weaken the root structure by the following: § Extensive enlargement of the canal § Mechanical stress from obturation (ex. pressure w pluggers) § Unfavorable placement of posts (remember posts do not strengthen a root) A. Perio pockets are wide coronally, whereas VRF pockets are narrow and deep B. Perio pockets are loose, allowing probing at various sites and especially located on proximal sides of root VRF pockets can easily be missed and are located on B or L sides A. B. C. D. PA radiograph revealing periradicular boneloss. CBCT confirms boneloss from crestal bone to apex CBCT reveals mesial osseous defect CBCT axial view reveals B and L boneloss “J-Shaped Halo” Radiolucent halo around longstanding VRFs Clinical Findings: o Vertical root fracture starts apically and progresses coronally o Usually in the B L plane of the root o Isolated probing defect at the site of the fracture in most cases o Important dx signs include a radiolucency from apex to middle of root (“J” shape or “teardrop” shape) o J shape/teardrop mimics other entities such as periodontal disease or failed RCT Diagnosis: Confirmed by visualizing fracture w exploratory surgical flap Treatment: Goal – eliminate fracture space o Single-rooted teeth: Extraction o Multirooted teeth § Hemisection or root resection with removal of only the affected root § Extraction Prognosis: Hopeless/Guarded Endodontic-Periodontal Relationships Communication of Pulp and Periodontium Occurs through: o Dentinal tubules o Lateral or accessory canals o Furcation canals o Apical foramen Endo pathosis can cause periodontal dz, but perio usually does NOT cause endo problems (Unless perio involves apex) Perio tx can affect pulp through disturbance by bacteria, causing bacterial penetration into dentinal tubules, this causes thermal sensitivity and pulpitis Types of Endodontic or Periodontal Lesions Primary Endodontic Lesions o Inflammation may/may not be localized at apex § Along roots § In furcation § Sinus tract along PDL appears w “narrow deep pocket” o Tooth tests non-vital o Treatment: Endo therapy ONLY bc primary lesion is of endo origin manifested through PDL Primary Periodontal Lesions o Progressive: starts in sulcus, migrates to apex (plaque and calculus produce inflammation that causes loss of alveolar bone and soft tissues) o Can manifest abscess during acute inflammatory phase o Broad pocket formation o Teeth are vital o Treatment: Periodontal therapy Primary Perio lesions w Secondary Endo Involvement o Deep pockets with hx of extensive periodontal disease o Possible past tx of periodontal therapy o Treatment: Endo therapy followed by Perio tx True Combined Lesions o Endodontic and periodontal lesions coalesce o May be clinically indistinguishable o Treatment: Endo and perio tx -Prognosis depends on amount of periodontal destruction Quiz Take more history if patient says: - Pain is intermittent but can be very intense - Lasts a certain amount of time - Wakes him up at night and he takes OTC med Sickle Cell causes spontaneous pulpal pathosis in non-carious teeth Pt has sharp pain to cold, no swelling, no spontaneous pain, no pain on chewing. Its been hurting for the past 6 weeks, xrays are WNL. The next question to ask is: how long does the pain linger after drinking cold water? Multirooted tooth has a PA lesion on distal root, pain is present when pt chews and eats/drinks cold. Pt points to the same multirooted tooth as the lesion. The pain is coming from multirooted tooth’s mesial root.