Dental News - The role of biology in the orthodontic practice (Page 5)

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The role of biology in the orthodontic practice (Page 5)

Young Guk Park & Ze'ev Davidovitch

Young Guk Park & Ze'ev Davidovitch

Wed. 10. August 2011

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The goal of this article is to enhance the biological awareness of the orthodontic practitioner in order to minimise and avoid tissue damage during orthodontic treatment. In this part, Profs Park and Davidovitch discuss the etiology of orthodontic root resorption and how to identify high-risk subjects.

Ketcham made the first reports on severe root resorption associated with orthodontic treatment in 1927. Subsequent reports attributed orthodontic root resorption to hormonal imbalances, malnutrition, genetic predisposition, dental root morphology, and specific treatment-related details, such as force magnitude, duration and direction. A comparison of the rates of tooth movement and the degree of root resorption between human premolars that had been moved buccally for 12 weeks by either a stainless steel wire that exerted dissipating forces, or by a superelastic wire that applied constant forces, revealed that the latter wires had moved the teeth faster, but at a cost of significantly greater amounts of root resorption (Weiland, 2003).

The most susceptible teeth for orthodontic root resorption are the maxillary incisors, probably because these teeth are usually moved the longest distances during the course of treatment. In a number of current orthodontic techniques, much of this incisor root movement is redundant. As discussed below in the section titled Optimal Orthodontics, maxillary incisor root resorption is frequently associated with uncontrolled tipping of the incisors, where the crown move palatally, while the root apex moves labially, into contact with and even through the labial plate of compact alveolar bone. This movement is then followed by a torque of the incisor roots, in order to return them to a proper angulation and position. In many such cases, about 90% of the root movement is unwarranted.

Although root resorption can occur on any surface of the root, it is most frequently observed radiographically in the apical region, where both cementum and dentine are removed irreversibly. Severe root resorption, which accounts for the loss of at least 25% of the root length, occurs in 1 to 3% of the orthodontic patient population. Despite this excessive loss, the affected teeth’s longevity is usually not jeopardized, provided the resorptive process is halted when orthodontic treatment ceases, and when periodontal health is good, with maintenance of the height of the alveolar crest.

Cells participating in the remodelling of dental and paradental tissues during tooth movement are derived from the native cell population of these tissues, from the circulation (platelets and leukocytes), and from alveolar bone marrow cavities. These cavities are connected with the periodontal ligament (PDL) by intra-bony channels that provide passageways for marrow cells with osteogenic potential (McCulloch et al., 1987). In human patients, periapical radiographs have revealed that the largest marrow cavities are situated around the apical region of the root, thus potentially providing a plethora of marrow-derived cells to the PDL in this area, increasing the probability of root resorption, in comparison to the coronal section of the root.

Apparently, the PDL cells themselves contribute to the formation of odontoclasts, a conclusion reached by Shiraishi et al (2001). They transplanted rat molar roots into the dorsal skin, with or without the PDL, for 1-28 days. After a period of 7 to 10 days, TRAP-positive odontoclasts were found around roots with intact PDL, but not around roots transplanted without PDL. Cyclo-oxygenase-2 was found in the PDL in the early days following transplantation. Root-resorbing cells are derived from a macrophge-lineage, like osteoclasts, in an effort to determine whether these progenitors are derived from resident macrophages or from cells exiting PDL capillaries, Nakamura et al. (2001) applied antibodies against specific markers to each cell type in rat jaw sections after 1 to 7 days of tooth movement. This experiment revealed that most of the cells that contribute to the formation of odontoclasts are derived from exudative macrophages.

The finding that inflammation is an integral part of the tissue response to orthodontic forces may explain, at least in part, the reasons for orthodontic root resorption. In inflammation, paradental capillaries become hyperpermeable, facilitating the migration of circulating leukocytes into the extravascular space. These migratory cells are derived from the immune system, and some are osteoclast and odontoclast progenitors. Therefore, the authors hypothesized that individuals who have medical conditions that affect the immune system, common as they might be, may be at a high level of risk to develop excessive root resorption during the course of orthodontic treatment.

The records of 102 orthodontic patients who had presented excessive root resorption of one or more teeth at the completion of orthodontic treatment were reviewed, and of 102 pair-matched controls who had received orthodontic treatment, but showed no signs of root resorption. The review revealed that the incidence of asthma, allergies, and signs indicative of psychological stress, was significantly higher in the root resorption cohort (Davidovitch, 2000). In all these conditions, the immune system is either altered or adversely affected. Therefore, we concluded that excessive root resorption may occur in patients who are psychologically stressed, or who have asthma and allergy, or any other local or systemic condition that may adversely affect and modify the immune system.

Since incisors, particularly maxillary, are the teeth most susceptible to root resorption, it was recommended to obtain periapical radiographs of these teeth every six months, or at least once a year. This routine may assist the clinician in identifying individuals who display early signs of resorption, and in modifying their treatment plan to minimize the risk of severe resorption. On rare occasions, treatment must be stopped altogether, at least for a few months, to give the tissues time for resting.

A comparison between patients with a Class II division 1 malocclusion, with an overjet sameller than 7 milimetres, who had been subjected to either a one-phase or a two-phase orthodontic treatment with fixed appliances revealed that the proportion of maxillary incisors with moderate to severe resorption was slightly higher in the one-phase treatment group (Brin et al., 2003). There was only a slight increase in frequency of root resorption in teeth with irregular root morphology. However, significant associations were found to exist between root resorption, the magnitude of overjet reduction, and the duration of treatment.

The question arises whether all orthodontic techniques are responsible for causing equal frequencies and extents of root resorption. The comparison of periapical radiographs by a number of research teams has revealed differences in this regard between certain methods of tooth movement. In one study, patients treated with a standard edgewise were compared with patients treated with a straight wire edgewise technique (Mavragani et al., 2000). There was significantly more apical root resorption of maxillary central incisors in the standard than in the straight wire edgewise group. No difference was found for the lateral incisors. In another study (Janson et al., 2000), the effects of treatment with these two techniques on 30 patients were compared with those achieved with the Bioefficient Therapy, a method based on the utilization of heat-activated and superelastic wires. It was found that the latter group was showing less root resorption than the other. This effect was attributed to the superelastic wires, and the use of a smaller diameter rectangular wire, 0.018 x 0.025 inches, in a larger bracket slot, 0.022 x 0.028 inches, during incisor retraction and the finishing stages. There was no root resorption in only 2.25% of all the examined teeth, slight resorption in 42.56%, moderate in 53.37%, severe in 1.4%, and extreme in 0.42%. As discussed below in the section titled Optimal Orthodontics , one of the prerequisites for avoiding orthodontic root resorption is the use of rectangular wires with a diameter smaller than that of the bracket, thereby applying light torque forces to the teeth.

With regards to the incidence of orthodontic root resorption, it might be interesting to know which teeth are more susceptible, those with fully-formed roots or those with immature, short roots. Measurements of maxillary incisors’ root length before and after treatment for correction of a Class II/1 malocclusion (Mavragani et al., 2002) revealed that the immature teeth have continued to grow and elongate during treatment, while the mature teeth were shortened by resorption.

A similar question to the one whether there is a specific gene or combination of genes whose activation will precipitate orthodontic root resorption had been asked regarding the identity of genes responsible for the development of orofacial clefts (Peruchini, 2002). Here, there is a complex mode of inheritence with the possible involvement of 2 to 20 genes. Transgenic mice lacking transforming growth factor μ3 are born with a cleft palate phenotype. An association between TGFμ3 and cleft lip was detected in an Iowa population, leading to a search for mutations in this gene in this population, as well as in families with cleft lip from Colombia. No mutations were identified in the coding region of TGFμ3. However, a polymorphic variant was found in the upstream regulatory that may alter the gene’s function.

A similar search was performed in families whose members have had orthodontic root resorption (Al-Qawasmi et al., 2003). Here, linkage and association were examined between polymorphisms of the interleukin 1 (IL-1μ and IL-1μ) genes and orthodontic root resorption. In this study, evidence emerged of linkage disequilibrium of IL-1μ polymorphism and root resorption, with 15% of maxillary incisor root resorption apparently dependent on this association. Furthermore, individuals homozygous for the IL-1μ allele 1 were found to have a 5.6 fold increased risk of resorption less than 2 milimetres as compared with those who are not homozygous for this gene.

It is concluded that orthodontic root resorption may be caused by a number of contributing elements that are acting individually or in combination. Most prominent factors are faulty mechanics, systemic diseases, and modifications in specific genes. The main tool at the disposal of the orthodontist to avoid causing root resorption is the exclusion of unwarranted tooth movements during the entire course of orthodontic treatment. Patients treated in this way require relatively short time periods for treatment completion. The application of appliances that generate forces that do not injure the PDL also reduces the risk of root resorption. Hence, these conclusions imply that avoidance of root resorption is primarily in the hands of the orthodontist.

Page 1     Introduction

Page 2     Tissue remodelling and orthodontic tooth movement

Page 3     The age factor

Page 4     The effects of pre-existing medical conditions and the development of complications

Page 5     The etiology of tooth resorption

Page 6     The biological nature of an optimal orthodontic force

Page 7     How to move teeth without resorbing their roots

Page 8     Summary
 

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