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Tooth resorption Resorption is a condition associated with either a physiologic or a pathologic process resulting in a loss of dentin, Cementum or bone. Etiology Traumatic luxation injuries orthodontic tooth movement chronic infections of the pulp or periodontal structures. Process Similar to that of bone resorption. Involves an elaborate interaction among inflammatory cells, resorbing cells, and hard tissue structures. The clastic cell is the key cell type responsible for all hard tissue resorptive processes. It is joined by cells like Macrophages and Monocytes in resorptive activities. Collectively, these cells orchestrate a complex interplay of molecular biologic events, involving cytokines, enzymes, and hormones, that influence the resorptive activity. key cells and factors involved in the mechanisms of resorption Monocytes macrophages, osteoclasts, they are found in tissue sections adjacent to bone-resorbing surfaces of rheumatoid arthritis, periodontal disease, peri-radicular granulomas and cysts, and in metastatic bone tumors. Interaction of Monocytes- cytokines- macrophages ( whose major role is wound debridement). Although macrophages have a structure similar to that of osteoclasts and, like osteoclasts, can also become multinucleated giant cells, macrophage lake a ruffled border that is attached to hard tissue substrate during resorption and do not create lacunae on the dentinal surface. Osteoclasts Bone-resorbing cells derived from hemopoietic cells of the Monocytes-macrophage lineage life span of approximately 2 weeks active cell and has ability to move between resorbing sites highly vacuolated and have numerous mitochondria (20 to 30 nuclei) characterized by specialized membrane structures, clear zones, and ruffled borders. found in tiny depressions, pits or irregular grooves, termed Howship lacunae. Resorptive mechanism Establish a microenvironment between the ruffled border and the bone in which resorption takes process is bimodal-involving the degradation of the inorganic crystal structure of hydroxyapatite and the organic structure of collagen, principally type I. The activated osteoclasts produce an acidic pH (3.0 to 4.5) at Ph 5.0 or lower, the solubility of hydroxyapatite increases dramatically, and re-sorption of hard tissue can occur. Acidic environment is primarily achieved through the action of a highly active polarized proton pump contained within the ruffled border. Osteoclasts contain enzyme carbonic anhydrase II (CA II) -specific to osteoclasts, CA II catalyzes the intracellular conversion of CO2, to H2 CO3---provides a readily available Source of H+ ions to be pumped into the subosteoclastic region. organic matrix degradation accomplished by three groups of proteinase enzymes: collagenases matrix metalloproteinase's (MMP) both act at neutral or just below neutral pH (7.4) cysteine proteinase family act at an acidic pH.close to the ruffled border Systemic regulatory factors Parathyroid hormone (PTH) active at the resorbing surface 1.25-dihydroxyvitamin D3 -calcitonin PTH- promote bone resorption by increasing both the number of cells present and the rate of activity among individual clastic cells- multifactor. 1. Stimulation of osteoblasts using a receptor-mediated, cAMP-dependent pathway to increase the production of neutral proteases and to decrease the amount of protease inhibitor and matrix deposition. 2. Direct action on the osteoclasts to increase CA II activity by cAMP-mediated phosphorylation of the enzyme. 3. Promotion of the fusion of marrow cells, leading to the formation of the multinucleated giant cell of osteoclastic phenotype. Systemic regulatory factors D3 -increase the resorbing activity of osteoclasts Calcitonin- inhibits resorption by inhibiting cytoplasmic motility and producing cell retraction. Local regulatory factors macrophage colony-stimulating factors: (M-CSF),(IL-1),(IL-6),(IL-11) and (TNF-α) Macrophage colony-stimulation factor is probably the most important soluble factor. Interleukin-6 acts on osteoblastic stromal cells to induce osteoclast differentiation factor. Interleukin-1 was one of the first bone-resorbing cytokines to be identified . The major effect of TNF-α on hard tissues is to stimulate osteoclastic activity Bacteria-induced resorption Produce acids and proteases production of osteolytic factor. Odontoclasts dissimilarities with osteoclasts smaller in size have a ruffled border contain fewer nuclei have smaller or no clear zone Similarities with osteoclasts enzymatic properties intense tartrate-resistant acid phosphatase activity. types Mononuclear odontoclasts 4% -participate in tooth resorption. Multinucleated odontoclasts 94% -form lacunae on the dentin. Having 10 or fewer nuclei. Oligonuclear odontoclasts (cells with fewer than five nuclei) resorb more dentin per nucleus than do cells with a higher number of nuclei Types of tooth resorption Internal resorption external resorption combined internal and external resorption. Internal resorption Rare in permanent teeth asymptomatic discovered during a routine radiographic examination. types : root canal replacement resorption internal inflammatory resorption Root canal replacement resorption (metaplastic resorption) Etiology: Low-grade irritation to pulp localized to small area of the root canal resorption of the dentin deposition tissue that resembles bone or Cementum but not dentin. Clinical evaluation: Asymptomatic can become painful if perforate. Radiographic evaluation: Enlargement of canal. Histological evaluation: Pulpal tissue is replaced by a cancellous tissue. Variations: Internal tunneling resorption. Treatment: RCT / Critical that the pulp and granulation tissue with odontoclasts be removed to arrest. Internal inflammatory resorption Etiology: progressive loss without deposition of hard tissue. Chronic inflammation of the pulp. Most commonly, internal resorption is found in the cervical region. Clinical evaluation: may be symptomatic the process of resorption is active only if part of the pulp remains vital; therefore, pulp testing can be positive. However, usually the coronal pulp is necrotic while the apical pulp is vital, resulting in a non-responsive test. Can be transient or progressive. The transient type of resorption occurs frequently in traumatized teeth or in teeth that have undergone orthodontic or periodontal treatment. While progressive is via tubules. Radiographic evaluation: Circumscribed, oval enlargement (radioleucency) continuous with the root canal wall, Histological evaluation: A necrotic zone containing bacteria is usually found coronal to resorbing tissue. Treatment: Non-surgical root canal therapy. External resorption of teeth type 1. External surface resorption 2. External inflammatory root resorption 3. Ankylosis 4. Replacement resorption. External resorption can be differentiated from internal resorption by its radio-graphic presentation. External surface resorption Transient phenomenon spontaneous destruction and repair in all teeth likely normal physiologic response self limiting process requires no treatment Etiology indirect physical injury-physiological. trauma. Histologic evaluation- small lacunae in Cementum radiographic evaluation- when visible, it appears as small excavations on the root surface with normal lamina dura and periodontal space. Treatment- nil External inflammatory root resorption (EIRR) Most common bowl-shaped resorptive defect that penetrates dentin and associated with a djacent bony radioleucency. Typically in the apical area. Involve any tooth with necrotic pulp. Replanted teeth that have not had RCT often show these resorptive lesion laterally as well as Apically etiologyInjury pressure pressure-bone lesions periodontium infection orthodontic treatment-initiates an inflammatory response cause. Bacteria, bacterial by-products, and tissue breakdown products from within the root canal system stimulate inflammation in the adjacent periodontal tissue and lead to aggressive progressive inflammatory resorption of the root. cervical resorption Can occur following injury to the epithelial cervical attachment apparatus and to the area of the root surface just below the attachment apparatus. Etiology All forms of tooth trauma surgical procedure Orthodontic treatment bruxism periodontal root planning and scaling Chemical injury- 30% hydrogen peroxide used for internal bleaching- gingival or periodontal tissues can become irritated as the hydrogen peroxide leaches through cervical dentinal tubules Apical External inflammatory resorption (EIRR) etiology pulp remains vital. 1.Trauma 2.Periradicular periodontitis. 3.Orthodontic treatment in which the It is hypothesized that the excessive forces initiate inflammation either as a result of stimulation of a phagocyte process by tissue breakdown products or through some form of Neurogenic inflammation. The resorption can begin 2 to 12weeds after injury. It progresses rapidly, especially after tooth re-plantation in patients between the ages of 6 and 10 years. For resorption to continue, resorbing cells require continues stimulation. The progressive type of external inflammatory re-sorption occurs when the source of inflammation is not removed, causing an ongoing resorptive process. Apical Enternal inflammatory root resorption (EIRR) radiographic evaluation With EIRR, the periodontal ligament space becomes widened and there is a loss of adjacent lamina dura and tooth structure. Treatment of external inflammatory root resorption is dependent on the etiology: 1. Calcium hydroxide 2. Post-treatment complications; High rate of recurrence as inflammatory resorption becomes arrested, ankylosis can occur. Ankylosis Ankylosis is union of bone and tooth, with no intervening connective tissue. Etiology- luxation injuries Ankylosis can be progressive or transient. The likelihood of progressive ankylosis increases dramatically, when greater then 20% of the root surface is damaged. Ankylosis is not a disease process. It occurs as a mistake” because cells involved in the remodeling of bone are not able to distinguish among root, Cementum, dentin, and bone. Resorption of root surface-substitution by bone resulting in ankylosis Resorb tooth structure replaced by bone – ankylosis RCT has no effect. Clinically High pitch or metallic tone. Lose of mobility occurs when more than 10% of the root surface is ankylosed. RADIOGRAPHICALLY-A complete disappearance of the periodontal space and an uneven root surface contour is common. COMPLICATIONS- malocclusion or super-eruption as opposing teeth. External replacement resorption: ETIOLOGY It differs from ankylosis because of the presence of intervening inflamed connective tissue. CLINICALLY such resorption typically follows an asymptomatic course. Radio graphically Disappearance of the periodontal ligament space. treatment this type of resorption usually progresses until where is little or no root left, and tooth extraction is necessary. Transient apical breakdown (TAB) a temporary phenomenon invariably follows surface resorption or pulp oblitration.The injured peri-radicular tissue generally returns to normal following repair, which usually takes place 1 year after trauma Etiology moderate injuries to the pulp, infections, orthodontic treatment , and occlusal insult to the periodontium. Radio logically Transient apical break-down can only be found in teeth with fully formed roots and closed or half-closed apices. Treatment nil