Chapter 47 Tooth Movement In Periodontally Compromised Patient Flashcards
Stage IV periodontitis
Severity
— Interdental CAL >=5mm
— RBL extending to middle third of root and beyond
— Tooth loss due to periodontitis >=5
Complexity
— Probing depth >=6mm
— Vertical bone loss >=3mm
— Furcation involvement Class II or III
— Severe ridge defect
— Masticatory dysfunction
— Secondary occlusal trauma (tooth mobility degree >=2)
— Bite collapse, drifting, flaring
— <20 remaining teeth (10 opposing pairs)
- Stage 4 periodontitis will usually need not only the appropriate treatment of the periodontal condition but also a multidisciplinary rehabilitation including orthodontic tooth movements to restore the patient’s functional dentition.
Describe the basic biological processes involves in tooth movements (physiological and orthodontic).
In both types of movements, the basic processes are similar: the transmission of a mechanical force from the root to the PDL affecting the homeostasis between the cells and the extracellular matrix, and leading to a series of biological events characterised by modelling and remodelling processes of the alveolar bone, which results in changes in tooth position. The forces applied to the tooth crown elicit a of series of cell-matrix interactions within the PDL that convert physical distortion into changes in the extracellular, cell membrane, and nuclear transduction mechanisms that alter cell behaviour through a chain of biochemical cascades. These highly sophisticated biological pathways transforming mechanical forces into controlled active cellular processes represent a controlled inflammatory response (aseptic inflammation).
Depending on the amount and direction of the mechanical force applied to the tooth, the resulting tooth movement will be different. In general terms, the tension areas will widen the PDL space by stretching the periodontal fibres, which will distend the blood vessels and increase the fibroblasts oriented in the direction of the applied force. This phenotypic alteration of the fibroblast will induce the differentiation of the osteoblast precursors into functional osteoblast that will form osteoid leading to bone apposition and reformation of the Sharpey’s fibres within the new calcified formation. On the contrary, on the pressure zones, there will be compression of the PDL space, with partial obliteration of the blood vessels and collagen tissue remodelling, leading to a pro-inflammatory biological cascade with a differentiation of bone resorbing cells (osteoclasts), resulting in bone resorption and change of tooth position towards the force direction. Once the tooth has been displaced and escaped from the physical force, homeostasis will return with new vessel formation, osteoplast recruitment, and reformation of the periodontal fibre attachment to the newly formed bone.
Explain possible reasons for patient variability in response to similar mechanical forces in orthodontic practice.
Application of light mechanical forces (approximately 50-100g/tooth) on the pressure side is associated with direct bone resorption. In these situations, the vessels are patent, and the physiology of the cells and tissues is preserved. In contrast, stronger mechanical forces will cause a crushing injury to PDL tissues, with cell death, hyalinisation, and the formation of cell-free areas between the PDL and the adjacent alveolar bone, which will interfere with the tooth movement and will slow biologic processes.
Possible reasons — differences in alveolar bone mineral density, vascularity, the number of available bone cells, and in the many inherent cellular and metabolic responses due to differences in the patient’s genome that dictate differences in cell recruitment, differentiation, and function, as well as in the expression of the many proteins and regulatory molecules that intervene in bone metabolism.
Common medications that may affect orthodontic therapy.
— NSAID
The use of non-steroidal anti-inflammatory drugs may alter the behaviour of those cells targeted by the orthodontic forces during to movement . They not only effectively reduce inflammation and pain, but also affect the sequence of two movement by inhibiting, or at least reducing, the controlled inflammatory and bone resorptive processes.
— Muscle relaxants (such as cyclobenzaprine) ;Tricyclic antidepressants (such as amitriptyline) ; SSRI antidepressants ( such as benzodiazepines)
Negatively affect the proper maintenance of oral hygiene, hence proper periodontal health during orthodontic therapy, due to xerostomia.
— Antiresorptives, which may slow the remodelling phase of bone turnover and potentially interfere with orthodontic therapy.
— In patients suffering from rheumatoid arthritis or other chronic inflammatory conditions, therapy aims to block the catabolic cytokine production responsible for the damage to soft tissues and bones. These immune-modulatory agents might also interfere with orthodontic tooth movement.
— Phenytoin used for seizures; Calcium blockers used as antihypertensive drugs; Cyclosporine-A used organ transplant patients
These drugs induce gingival hyperplasia which might prevent the application of certain orthodontic mechanics as well as interfering with the maintenance of proper oral hygiene and periodontal health.
— Chemotherapy with busulfan/cyclophosphamide (<2 years of disease-free life), because these drugs are known to produce damage to the precursor cells involved in the bone remodelling processes.
What is the endpoint of periodontal therapy?
The timing of initiating orthodontic treatment after periodontal therapy?
— No pockets of >=6mm AND No probing depth >4mm with bleeding on probing
— Once proper infection control has been implemented and the endpoint of periodontal therapy achieved, it is advisable to start the orthodontic treatment as soon as possible in order to benefit from the high bone turnover secondary to the healing of the periodontal interventions, which may accelerate orthodontic tooth movements.
Does orthodontic tooth movement cause periodontal attachment loss / gingival recession? p. 1237
Orthodontic tooth movements per se do not cause periodontal attachment loss and/or gingival recession. However, in areas of thin buccal cortical bone, labial or proinclination orthodontic tooth movements can result in bone dehiscence defects, which when accompanied by a thin gingival phenotype in conjunction with presence of plaque-derived gingival inflammation and/or toothbrush trauma may lead to attachment loss and the development of localised gingival recessions. In the presence of thick gingival tissues, gingival marginal tissue recessions will not occur, even when labial or expansive tooth movements are carried out.
In children and adolescents, studies have not found a correlation between orthodontic labial inclination of mandibular central incisors with the development of gingival recessions. In adults, however, study showed a significant correlation between the incidence and the severity of recession lesions with excessive proinclination (>10 degrees) of the mandibular incisors. Other studies in patients with mandibular prognathism subjected to orthognathic surgery reported that in spite of extensive labial tipping of the mandibular incisors, there were no negative outcomes in the periodontal tissues. It is the combination of the final tooth inclination and the thickness of the marginal gingival tissues (<1mm) that has been associated with the occurrence of recessions in mandibular central incisors and, therefore, the main risk factors are the presence of a thin gingival phenotype combined with an insufficient width of keratinised gingival, and/or presence of gingival inflammation.
