The textbook Contemporary Orthodontics [2] has an excellent description of the EARR process. For the benefit of the reader, the following is a brief summary.

Frontal resorption of the alveolar lamina dura is a desirable process in orthodontic tooth movement because it is not associated with root resorption, while undermining resorption is an undesirable and pathological process since it is associated with root resorption. Undermining resorption occurs when compression of the periodontal ligament (PDL), produced by a sustained orthodontic force against a tooth, is great enough to totally occlude blood vessels and cut off the blood supply to an area within the PDL. Blood flow impediment results in hyalinization, also known as sterile necrosis. During the initial repair phase of the necrosed areas, clast cells resorb not only the underside of the lamina dura but also the cementum and dentin. Removal of hyalinized tissue leads to removal of cementoid and mature collagen, leaving a raw cemental surface that is readily attacked by dentinoclasts. Once orthodontic movement stops, these root craters usually fill back in with cementum, restoring the original contours of the root. However, if the attack on the root surface produced large defects at the apex, they eventually become separated from the root surface. Once an island of cementum or dentin has been cut totally free from the root surface, it will be resorbed and will not be replaced. Thus, shortening of the root occurs when cavities coalesce at the apex, so that peninsulas of root structure are cut off as islands. Then the repair process smoothes over the new root surface and a net loss of root length occurs. Forces are concentrated at the root apex because orthodontic tooth movement is never entirely translatory, which places the narrow periapical region in harm’s way. The coronal third of a root is covered with acellular cementum, whereas the apical third is cellular and the middle third is intermediate. Cellular cementum forms more rapidly and is more active than acellular cementum, but this cellular periapical cementum depends on a patent vasculature. Accordingly, periapical cementum is more friable and easily injured in the face of heavy forces and concomitant vascular stasis. Despite the clinician’s best efforts to keep forces light and well distributed to induce only frontal resorption, some areas of undermining resorption are probably produced in every patient [2].

Light forces are precisely what orthodontists have been applying since the late 1970s when brackets welded to bands were replaced by direct bonding. Bonding brackets to enamel obligated orthodontists to diminish the magnitude of applied force by using lighter wires to avoid accidental dislodgement of brackets. Currently, narrower brackets are available in order to increase the interbracket distance, resulting in additional force reduction due to increased wire springiness. Many orthodontists are using .018″ instead of .022″ slot brackets, which also diminishes the magnitude of forces that can be applied. Further, some orthodontists are even using glass ionomer cement to bond brackets to minimize the development of white spot lesions. This type of cement limits even more the magnitude of forces that can be applied, particularly during the first 24 h after bonding, because of the diminished bonding adhesion of this cement when compared to composite resin. If orthodontic force magnitude would be the main cause for severe EARR, the incidence should have diminished dramatically since less force magnitude has been used for the past 40 years (due to the use of direct bonded brackets). Unfortunately, this has not occurred.

EARR is a common iatrogenic consequence of orthodontic treatment. In an extensive literature review of the evidence for EARR and orthodontic treatment, Weltman [3] made several critical observations. First, post-orthodontic treatment incidence of EARR is 73 % (detected radiographically). Cross-sectional as well as longitudinal studies show that EARR is a small problem for the average orthodontic patient with a radiographic mean resorption of less than 2.5 mm. This magnitude of resorption has no adverse clinical consequences, but unfortunately, 1–5 % of orthodontic patients experience a severe form of EARR (defined as exceeding 4 mm or one-third of the original root length). Severe root resorption mainly occurs in maxillary incisors followed by mandibular incisors and mandibular first molars. Finally, this magnitude of EARR compromises crown-root ratios and can unfortunately result in tooth mobility. Incisor mobility sometimes requires splinting (Fig. 3.2).

More recent studies [4–9] investigating EARR incidence and comparing the severity with lighter forces and studies [10–12] investigating heavier forces, used before the introduction of direct bonding, show similar results. The conclusion is that development of EARR may not necessarily be due to the degree of applied orthodontic force per se but also to a patient’s individual genetic predisposition or susceptibility.

Many factors have been proposed as risk factors for the appearance of the severe form of EARR. These can be divided into orthodontic treatment-related risk factors and patient-related risk factors [13]. Examples of treatment-related risk factors are treatment duration [14–25], magnitude of applied force [19, 26–31], direction of tooth movement [11, 24, 25, 27, 32–35], amount of apical displacement [16, 21], method of force application (continuous vs. intermittent) [12, 28, 36–41], type of appliance [42–44], and treatment technique [24, 32, 44–53].

Examples of risk factors related to the patient include previous history of EARR [42, 54–56]; tooth-root morphology, length, and roots with developmental abnormalities [4, 7, 9, 11, 21–23, 57–63]; genetic influences [7, 54, 64–68]; systemic factors [69–72] including drugs (nabumetone) [73]; hormone deficiency, hypothyroidism, and hypopituitarism [74–77]; asthma [41, 58]; root proximity to cortical bone [11, 15, 78]; alveolar bone density [15, 79–81]; chronic alcoholism [82]; previous trauma [9, 12, 41, 47, 54–56, 83–85]; endodontic treatment [4, 10, 35, 41, 55, 56, 86]; severity and type of malocclusion [4, 7–9, 11, 16, 17, 20, 31, 54, 87]; and patient age [12, 14, 17, 21, 22, 36, 88–92], patient gender [7, 17, 21, 31, 56, 57, 65, 78, 93], and patient habits [94].

Most researchers agree that all of the identified risk factors only explain a small percentage of the variation in EARR. In 1998, Vlaskalic [95] stated: “The long list of suspected causative factors for EARR highlights the state of ignorance that exists with respect to EARR and orthodontic treatment.” Fortunately, more light has been shed since then on the etiology of EARR. Årtun et al. [96], in 2005, reported the results of a multicenter clinical study on EARR in which maxillary incisor periapical radiographs were obtained in 302 consecutively treated orthodontic patients who had fixed appliances. The radiographs were taken at three time periods: pretreatment and 6 and 12 months after appliance placement. The result was that orthodontic patients with detectable EARR during the first 6 months of active treatment are more likely to experience resorption in the following 6-month period than those without such exhibited early EARR. These authors concluded that the low explained variance of identified risk factors, combined with the strong association between the amount of EARR during the first and second 6-month treatment period, suggested a genetic predisposition as the major etiologic factor.

EARR is apparently related to a genetic predisposition. Harris et al. [65], in a study using the sib-pair model, reported that the strongest single association with EARR seems to be a person’s genotype since familial studies showed that a person’s genotype accounts for about two-thirds of the variation in the extent of EARR. These authors concluded that an individual’s genetic background is the single strongest predictor of EARR, as shown by familial analysis. The first report, in which a genetic marker was described identifying people who are susceptible to EARR before beginning orthodontic treatment, was published by Al-Qawasmi et al. [64]. This paper, titled “Genetic predisposition to EARR,” investigated whether there is linkage and association between polymorphisms of the interleukin IL-1 genes and EARR. The sample consisted of 35 white American families. Each family included two or more siblings treated with orthodontics. Genomic DNA was obtained for isolation and analysis from buccal swab cells of the siblings and their parents. Highly significant evidence of linkage disequilibrium of IL-1B polymorphism with EARR in the maxillary central incisors was obtained. Persons carrying two alleles # 1 (one from the father, the other from the mother) of the IL-1B have, on average, 1.3 mm more EARR than those with either the alleles 1 and 2 or the alleles 2 and 2. Persons homozygous for the IL-1B allele # 1 have a 5.6-fold increased risk of EARR greater than 2 mm as compared with those who are not homozygous for the IL-1B allele 1. When the EARR value of 2 mm was used to divide subjects into affected and unaffected, 72 % of EARR occurred in those carrying both alleles # 1, followed by 39 % of EARR in those carrying the two different alleles, 1 and 2, and 0 % incidence in individuals carrying the two protective alleles # 2. Thus, data indicate that allele 1 and the IL-1B gene, known to decrease the production of IL-1 cytokine in vivo, significantly increase the risk of EARR. The authors propose a model for the pathway through which IL-1B genotype modulates the extent of EARR experienced during orthodontic tooth movement. Their hypothesis is that low IL-1B production in the case of allele 1 results in less catabolic bone modeling in the cortical bone interface of PDL because of decreased number of osteoclasts associated with lower levels of this cytokine. Inhibition of bone resorption in the direction of tooth movement results in maintaining prolonged dynamic loading of tooth root adjacent to compressed PDL, resulting in more EARR because of fatigue failure of the root. In the case of high IL-1B production associated with allele 2, compressed PDL space is restored by resorption of bone interface of PDL, resulting in only mild EARR that is controlled by the cementum-healing mechanism. In spite of the authors’ encouraging findings that EARR does indeed have a genetic basis, they concluded that the genetic predictors of EARR are not yet reliable because IL-1B polymorphism accounts for only 15 % of the total variation of maxillary incisor EARR. These authors report that many genes besides IL-1B are probably involved, that a search for the remaining genetic factors that influence EARR is ongoing with the ultimate goal of providing orthodontic treatment that circumvents EARR, and that in the future DNA analysis might provide a more accurate risk assessment for EARR.

This subtopic is subdivided into pretreatment, active treatment, and posttreatment prognosis.

Since orthodontists cannot yet identify which pre-orthodontic patients are susceptible to severe EARR, a signed informed consent is important both for adequate patient education and for proper risk management. Dental histories reporting macro-trauma should alert the clinician because there is an increased risk of EARR associated with macro-trauma [83]. The clinician should also be aware that teeth with short roots have an increased risk of loss in patients who also have crestal alveolar bone height loss [98], particularly if the roots have been shortened even more by EARR. In susceptible patients, the probability of EARR development in its severe form is increased by the following: moving teeth considerable distances [16, 21], using heavy continuous orthodontic forces [19, 26–31], moving teeth that have had previous macro-trauma [83], moving teeth against cortical plates [11, 15, 78] (as is frequently done in patients with severe skeletal discrepancies treated with orthodontics exclusively instead of a combination of orthodontics and orthognathic surgery), and an increased treatment time [14–25]. Specifically, patients who need orthognathic surgery to achieve a successful result, but are treated nonsurgically, usually take longer to treat. Long and narrow roots are also at increased risk for EARR since in tipping movements, the longer the root, the more pressure at the root apex due to longer moment arms. EARR can be minimized in orthodontic patients by moving teeth with light forces, through trabecular bone, with periodic radiographic monitoring and, most importantly, by moving them the least distance possible. This may be accomplished by using the following root-sparing orthodontic treatment regimes:

The ultimate goal of these five recommended treatment strategies is to provide orthodontic treatment that circumvents EARR. The following are clinical examples of some of these regimes.