Healing in Dental Tissues PDF (2024-25)

Year 2 BDS and DTH Life Sciences 2024/25 Healing in Dental Tissues Dr Amr Elraggal Clinical Lecturer in Dental Education BDS, MSc, PhD [email protected] Wound Healing  Introduction Every tissue or organ in our body is composed of parenchyma...

Year 2 BDS and DTH Life Sciences 2024/25 Healing in Dental Tissues Dr Amr Elraggal Clinical Lecturer in Dental Education BDS, MSc, PhD [email protected] Wound Healing  Introduction Every tissue or organ in our body is composed of parenchymal cells (functional cells) and mesenchymal cells (support cells) contained within an extracellular matrix to form a microenvironment, and these microenvironments collectively form our tissues and organs. A wound is a break in the integrity of skin or mucosae which may be associated with disruption of the structure or function. Loss of continuity of epithelium, with or without loss of underlying connective tissue Following injury to skin or underlying tissues/ organs Caused by surgery, blow, cut, chemicals, heat/ cold, friction/ shear force, pressure or as result of disease, such as leg ulcers or carcinomas. Cell Proliferation Cell proliferation is crucial for tissue restoration. Cells are categorized into groups based on their mitotic activity: Labile cells: unstable, proliferative, divide, like skin, oral mucosa, GIT, etc. NB. Chemotherapy is killing these cells. Stable cells: divide under conditions (as a response to injury), like liver and pancreas and renal tubules cells. Permanent cells: do not divide, like brain and heart cells. NB. They die after injury. Proliferation, migration and differentiation of parenchymal and mesenchymal cells in healing are regulated by a number of growth or differentiation factors and extracellular matrix components. Healing Healing is divided into regeneration and repair. Regeneration is proliferation of parenchymal cell that result in complete restoration of the original tissue. Not all the body tissues divide at the same pace. (what is the main difference between slowly and rapidly dividing cells??) Repair, incomplete regeneration, achieves healing by replacing lost or damaged tissue with granulation tissue that matures into fibrous tissue and finally a scar. Phases of wound healing Oral Mucosal Wound Healing Oral mucosal wounds heal with minimal scar formation compared to skin wounds. Scarring would be detrimental to food intake. Gingival wounds heal without scars. Tongue wounds heal quickly with little inflammation and altered TGF-β (Transforming Growth Factor) response. Oral Mucosal Wound Healing Possible reasons: Distinct fibroblast phenotype. Presence of bacteria that stimulate wound healing. Moist environment and growth factors present in saliva. Saliva has ↑ concentration of Epidermal Growth Factor (EGF). Rapid but transient inflammatory response. Remodelling of wound matrix more rapid – almost normal tissue architecture by 60 days. Patient factors: Influence of tissue site. Patient age. Periodontol ogy Healthy gum No or minimal (less than 15%) bleeding in probing. No attachment loss. No bone loss. No calculus. No plaque retentive factors. Gingivitis Bleeding on probing. Signs of inflammation and swelling. Redness. Calculus may present. Plaque retentive factors may present. No loss of attachment. No bone loss. Normal Gingiva Chronic Gingivitis B = junctional Bacterial plaque in epithelium gingival sulcus Hyperplasia of junctional Thin, flat, no rete epithelium with ridges elongated rete ridges No inflammation in the Mild inflammatory, underlying fibrous lymphocytic infiltrate replacing some collagen connective tissue in underlying fibrous F = alveolar bone tissue Superficial dilated capillaries Periodontitis Bleeding on probing. Signs of inflammation and swelling. Redness. Supra and subgingival calculus may present. Plaque retentive factors may present. Loss of attachment. (apical migration of junctional epithelium. Bone loss. Furcation involvement may present. Pocket formation. Histopathology of Periodontal Disease Lesion Significant Cells Events Initial (2-4 days) Polymorphs Epithelial (neutrophils) disruption, vascular and perivascular activity, beginning of inflammatory cell infiltrate Early (4-10 days) Lymphocytes Further disruption, Other local collagen mononuclear cells breakdown, significant inflammatory cell infiltrate Established (2-3 Plasma cells Pocket epithelium weeks) lines sulcus, marked collagen breakdown with efforts at repair, dense infiltrate Advanced Plasma cells As above plus Pathogenesis of Periodontal Pocket Bacterial plaque accumulates in gingival crevice. Products of bacterial metabolism diffuse through crevicular and junctional epithelium to reach gingival connective tissue. Products of bacterial metabolism eg protease, hyaluronidase, collagenase, damage crevicular and junctional epithelium and gingival connective tissue. This damage provokes an inflammatory reaction Because there is persistence of tissue damaging factors chronic inflammation ensues. Pathogenesis of Periodontal Pocket Damage to junctional epithelium increases permeability to plaque microbial products. Products of bacterial metabolism are chemotactic for neutrophils which accumulate in gingival crevice where they may phagocytose plaque bacteria. Neutrophils in gingival crevice die and release lysosomal enzymes which damage both junctional epithelium and connective tissue. Pathogenesis of Periodontal Pocket Turnover of gingival connective tissue is high; interference in balance between catabolism and synthesis may lead to net loss of gingival connective tissue; damaged fibroblasts are seen in inflamed areas. Inflammatory and immune reactions in gingival and periodontal tissues are usually protective and restrict bacterial penetration of gingiva. Tissue damage remains localised and minor. When balance is altered, either by alterations in amount or character of plaque flora, or alteration in host response to plaque products, tissue damage may occur producing a burst of tissue destruction. Objectives of Periodontal Therapy Complete restoration of structure and function of tissues damaged by periodontal disease. Process of removing aetiological agents which cause inflammation and calculus, thus helping to establish periodontium that is free of disease. This ultimate goal may be achieved by the following: 1. Elimination of factors responsible for periodontal disease may facilitate spontaneous regeneration. This includes living bacteria in biofilm and calcified biofilm microorganisms from tooth surface and adjacent soft tissues. 2. Produce smooth root surface less likely to harbour residual bacteria and that is conducive to healing. 3. Periodontal ligament cells may selectively proliferate via guided tissue regeneration. 4. Advanced techniques in cellular biology may induce tissue regeneration. Healing in Gingivitis Gingivitis can be induced within 7-14 days simply by stopping cleaning and rapidly becomes healthy when cleaning is resumed. Gingivitis is essentially caused by plaque accumulation at gingival margins. Gingivitis is infinitely reversible if plaque levels are kept minimal. Gingivitis proceeds to periodontitis only in about 15% of individuals. Once oral hygiene instruction takes effect, the patient keeps themselves healthy. Healing in Periodontitis Elimination of risk factors (plaque retentive factors, smoking, alcohol, systemic diseases, etc.) Maintaining good oral hygiene (teeth brushing, flossing, mouthwash). Professional Mechanical Plaque Removal (PMPR) with supra and subgingival scaling. Antimicrobials are only adjuncts to plaque control and mechanical biofilm disruption. Periodontal surgeries and bone graft could be necessary to regain bone resorption and attachment loss. Earlier identification of “at risk” genotype will radically alter prevalence and treatment in future. Healing in Periodontium Cells that are first to proliferate on the exposed root surface are ones to establish nature of attachment that develops. Potential for repair may depend on which cell type wins race to populate root surface first. Healing in Periodontium If epithelial cells populate root surface first, specifically growing on surface of gingival granulation tissue, long junctional epithelium will be the ultimate result. If gingival connective tissue cells populate root surface first, attachment will be one of connective tissue adhesion. If bone cells are first to proliferate and make contact with tooth surface, root resorption and ankylosis are result. If periodontal ligament cells are first to migrate and cover denuded root surface, then new connective tissue attachment forms and this is ideal attachment. Clinical Healing Following periodontal treatment bacterial remnants continue to be washed out of pocket by blood and crevicular fluid. After 14 days new gingival sulcus will be formed near to crest of gingiva. Some shrinkage of gingiva will occur due to resolution of oedema. Collage repair ultimately takes about 12 weeks to mature fully. There is little/ no connective tissue re-attachment between treated pocket lining and root surface, instead close adaptation between gingivae and instrumented root surface relies on long junctional epithelium and tissue tone in gingivae. Histological Healing Within few hours an acute inflammatory reaction occurs in soft tissue pocket wall. Remnants of pocket epithelium will proliferate, and pocket wall will be fully epithelialized after 2 days. After 5 days, epithelial reattachment will commence at apical extremity of pocket and progress coronally. Involution of pocket epithelium will occur, giving rise to new long junctional epithelium. Histological Healing The new JE continues initially is becoming weak, so the patient should be careful with the supragingival oral hygiene routine in order to avoid any relapse of the pocket. Formation of functional orientated collagen, to replace granulation tissue, tends to lag behind healing of dento- epithelial junction, immature collagen not appearing until after 3 weeks. This collagen ultimately takes about 12 weeks to mature. Endodonti cs Periapical Disease Inflammatory changes in periapical part of periodontal ligament Periapical Periodontitis Usually as consequence of pulp necrosis Adjacent bone may resorb Removal of source of periapical tissue damage usually allows healing Periapical Disease Causes of pulp necrosis Trauma. Bacteria – caries. Restorative procedures. May also follow endodontic treatment Instrumentation beyond apex. Medicaments through apex. Diffusion of :- i. Products of autolysis of cells of pulp and inflammatory cells. ii. Bacteria, products of bacterial metabolism and bacterial death. From pulp into periapical tissues. Damages cells in adjacent cementum, periodontal ligament and bone. Provokes an inflammatory reaction. Periapical Disease Initial acute inflammatory reaction. Usually mild, with vascular dilation, oedema and neutrophil exudation. Clinically tooth may be extruded from the socket with mild pain on biting. Tooth may be tender to percussion (TTP) Continued diffusion of damaging material from apical foramen leads to progression of lesion. Rate and form of progressive lesion depends on :- Nature and severity of damaging agents. Resistance of host. Periapical Disease Tissue reaction is dynamic. May be acute and chronic. Produces a range of conditions: Acute periapical periodontitis. Periapical granuloma. Periapical cyst. Acute periapical abscess. Pulp Therapy & Wound Healing Methods of pulp therapy: 1. Stepwise Excavation/ Indirect Pulp Capping 2. Direct Pulp Capping 3. Superficial/ Cervical Pulpotomy 4. Pulpectomy NB. Somatic cells, such as fibroblasts, macrophages, cementoblasts and osteoblasts, in pulp and periapical tissues have limited potential for regeneration following injury. After pulp therapy, the healing process involves recruitment of progenitor/ stem cells to the damaged area and transforming them into the specific types of cells needed to restore healthy pulp tissue. Stepwise Excavation/ Indirect Pulp Capping Carious Lesion: Pulps under deep caries are inflamed because of micro-organisms and their by- products. When inflammation is reversible it may be controlled by removal of cause and restoration of tooth to prevent micro- leakage. Leaving small amount of partly demineralised dentine may be necessary to prevent exposure and maintain pulp vitality. Direct Pulp Capping It is indicated in pinpoint pulp exposure, with minimal bleeding and surrounded by sound dentine. Pulps under deep carious lesions are inflamed because of micro- organisms and their biproducts. When inflammation is reversible it may be controlled by removal of micro-organisms and restoration of tooth to prevent further contamination. Exposed pulps can be protected by various materials Pulp capping agent must be biocompatible, bactericidal, initiate secondary dentine formation and ideally provide seal against further microbial ingress. Materials used: calcium hydroxide, MTA, Biodentine. Calcium Hydroxide Paste CaOH2(50%), ZnO (10%), Zn Stearate (0.5%), carrier Paste Glycol salicylate (40%), TiO2, CaSO4, Calcium tungstate Properties Bacteriostatic and antimicrobial pH 9-11 (strongly alkaline) Induces mineralisation (Ca2PO4) Radiopaque Poor compressive strength Soluble in water / acid / saliva Non-adhesive to wet surfaces Initiates dentine bridge formation in 50-90% of cases – bridges often have tunnel defects – therefore incomplete Does not seal well nor prevent microleakage Apexogene sis Apexogenesis is a procedure where vital tissue within the tooth is maintained to facilitate continued development of the immature root. Teeth are vital immature permanent with open apex. Materials used: CaOH and MTA. Apexification Teeth are necrotic immature permanent with open apex. Our aim is to maintain tooth development until apex closure. Materials used: CaOH and MTA. Technique: the used pulp materials activate the Epithelial Rest of Mallassez (ERM) to produce dentine and cementum like material until complete apex closure. It has been shown that the ERM cells are distributed in the PDL in a network-shaped manner along the root surface and in the furcation region, primarily in teeth with incomplete root formation  Thank you Dr Amr Elraggal [email protected] This presentation is a modification of another one introduced by dr Yen Lin.