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| ORIGINAL HYPOTHESES |
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| Year : 2012 | Volume
: 3
| Issue : 2 | Page : 72-75 |
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Drinking coffee may help accelerate orthodontic tooth movement
Jianru Yi1, Liang Zhang2, Boxi Yan1, Liang Yang1, Yu Li1, Zhihe Zhao1
1 Department of Orthodontics, State Key Laboratory of Oral Diseases, West China Stomatology Hospital, Sichuan University, Chengdu, Sichuan, China
2 Department of Dental Implants, State Key Laboratory of Oral Diseases, West China Stomatology Hospital, Sichuan University, Chengdu, Sichuan, China
| Date of Web Publication | 3-Sep-2012 |
Correspondence Address:
Yu Li
14#, 3rd Section, Renmin Nan Road, Chengdu 610 041
China
 Source of Support: This study is supported by the National Nature Science Foundation of China (Grant No. 11002095), Conflict of Interest: None  | Check |
DOI: 10.4103/2155-8213.100391
Introduction: Developing new methods to enhance orthodontic tooth movement and shorten the duration of treatment has always been desired. However, to date, no therapies have been widely used in clinics. Recent studies and feedback information from patients have shown that drinking coffee may accelerate orthodontic tooth movement. The Hypothesis: Drinking coffee, as a daily habit of many people, can be an effective accelerator of tooth movement with little side effect for caffeine can break the calcium balance in bone tissue and directly inhibit the development of osteoblasts, leading to temporary decreased bone mineral density and consequently inducing faster orthodontic tooth movement. Evaluation of the Hypothesis: Much effort has been made to explore therapies to shorten orthodontic treatment period with limited success. Daily coffee consumption may be a promising approach to enhance orthodontic tooth movement for its reversible effect on bone mineral density and calcium balance. Keywords: Bone density, caffeine, coffee, orthodontic tooth movement
How to cite this article:
Yi J, Zhang L, Yan B, Yang L, Li Y, Zhao Z. Drinking coffee may help accelerate orthodontic tooth movement. Dent Hypotheses 2012;3:72-5 |
| Introduction | |  |
Orthodontic tooth movement (OTM), as a consequence of force-induced periodontal tissue remodeling, [1],[2] involves stretching of the periodontal ligament (PDL), deposition of the alveolar bones at the tension side coupling with compression of the PDL and resorption of the alveolar bones at the pressure side, and finally approaching a new balance within the cementum-periodontal ligament-alveolar bone complex. [3] Since the tooth movement is related to such complicated changes, the orthodontic treatment has a common period of 1-2 years, during which orthodontic devices have to be placed, making oral hygiene maintenance more difficult and time-consuming, patients are thus more vulnerable to periodontal diseases and caries. To shorten the treatment period, orthodontists never stopped exploring methods to accelerate the rate of OTM. A variety of therapies, including local application of PTH, [4] RANKL, [5] osteocalcin [6] and prostaglandins, [7] have been shown to elicit faster OTM. However, great difficulties lie in the clinical application of these agents. Moreover, using such medication will impose additional burden on patients, for example potential adverse effects.
Interestingly, feedback from some orthodontic patients demonstrates that daily intake of coffee may contribute to faster tooth movement. What is more, previous research showed that Erigeron Breviscapus, a traditional Chinese medicine which contains caffeine, the major effective component of coffee, indeed accelerated OTM. [8],[9] In this theoretical article, therefore, we hypothesize that daily coffee consumption may help enhance OTM, and consequently shorten the duration in which patients have to wear braces.
| Orthodontic Tooth Movement-Related Bone Remodeling | | |
When proper orthodontic force is applied to a tooth, compression of PDL leads to an immediate but slight tooth movement due to the distortion of the extracellular matrix of PDL and changes of the cellular shape and cytoskeletal configuration, and then tooth movement pauses for a few days, during which the necrotic tissue emerges at the compression side owing to acute inflammation in response to biomechanical forces. [10],[11],[12] At the compression side, osteoclast progenitors disseminate into bone from blood, proliferate and differentiate by interaction with osteoblasts, inducing the early bone resorption. After the necrotic tissue eliminated, osteoclasts in periodontal space resorb the alveolar bone on the compression side, and the tooth then moves at a consistent rate. [12] As bone remodeling is the essential biological process in OTM, [13],[14] and lower bone mineral density (BMD) can lead to faster bone remodeling, [15] decreased BMD may well elicit accelerated OTM. [16]
| Caffeine-Induced Temporary Decrease of BMD | | |
Caffeine (1, 3, 7-methylxanthine), a member of the methylxanthine family, is the most commonly consumed psychoactive substance with its presence in coffee, tea, and carbonated drinks like cola. [17] Many studies have shown that caffeine consumption is related to low bone density. [18],[19],[20],[21] The mechanisms, however, are complicated.
Evidence has suggested that caffeine consumption increases the urinary calcium excretion. [22] The loss of calcium induced by caffeine has been verified to be the consequence of reduction in renal reabsorption [23] caused by its antagonism to adenosine, which plays an important role in the tubuloglomerular feedback response as a mediator, and this antagonism has been identified to be brought about by caffeine's structural similarity with adenosine. [24],[25] Caffeine offsets the effect of adenosine via up-regulating the enzyme adenylyl cyclase, then increasing intracellular cAMP concentration and consequently activating the kinase A protein (PKA), [26] finally leads to the calcium loss via urine. Low concentration of serum calcium produced by the mechanism stated above promotes the secretion of parathyroid hormone (PTH) which stimulates bone mineral content to dissolve into blood and thus brings about a reduction in BMD. However, long-term caffeine administration induces an elevation in intestinal calcium absorption through the enhancement in 1,25-(OH) 2 -D production, which brings the calcium balance back to normal, [20] indicating the decreased bone density may be temporary and return to the normal levels through neuro-humoral regulation.
In addition to the systemic regulation on calcium metabolism, caffeine can directly inhibit the developmental processes of osteoblasts, which includes proliferation, followed by matrix maturation and mineralization, [27] results in the lack of activated osteoblast and consequently bring about decreased BMD. [28] A lot of studies have been carried out to elucidate the mechanism underlying caffeine-induced inhibitory effect on osteoblasts. Previous work found that caffeine through two ways increases the concentration of intracellular cAMP, an upstream mediator to down-regulate osteoblast proliferation; [29] firstly caffeine inhibits the phosphodiesterase which breaks cAMP down, [30],[31] and secondly caffeine induces an enhancement in prostaglandin E 2 (PGE 2 ) output in vitro[32] and in vivo. [33] High concentration of PGE 2 can increase intracellular cAMP in osteoblasts and has also been reported to up-regulates osteoclasts activity [34] and inhibits collagen synthesis, [35],[36] leading to faster bone resorption and slower bone deposition. [37],[38] What is more, caffeine has been shown to decrease the expression of vitamin D receptor (VDR) on the surface of osteoblast cells; and VDR plays an essential role in the pathway through which 1,25-(OH) 2 -D 3 modulates osteoblast proliferation, differentiation and alkaline phosphatase (ALP) activity. [39] Tassinari et al. further found that when osteoblasts were treated with caffeine in a relatively low concentration (0.1 and 0.2 mM), the decreased ALP activity and collagen synthesis that lead to an altered extracellular matrix incompetent for mineralization return to normal levels despite the consistent caffeine interference, indicating that caffeine's negative effect on the development of osteoblast is rather a delay than complete inhibition. [40]
| The Hypothesis | | |
Caffeine widely exists in coffee and other psychoactive beverage for its stimulation effect and has never been identified to promote OTM. Hereby, we put forward a hypothesis that merely drinking coffee may potentially be an effective and safe accelerator for OTM through caffeine-induced temporary low bone density.
The hypothesis is based on the following three points: (1) Caffeine interrupts the calcium balance in bone tissue, leading to low bone density, and this can be compensated by increasing the intestinal calcium absorption through neuro-humoral regulation. [20] (2) When exposed to an appropriate dosage of caffeine, the development of osteoblast cells can be delayed, inducing low BMD, and return to normal despite continuous exposure. [40] (3) Low BMD accelerates the bone remodeling and thus shortens the duration of orthodontic treatment. [13],[14],[15],[16]
| Evaluation of the Hypothesis | | |
Since orthodontic treatment has a common duration of 1-2 years, and it imposes heavy burden of maintaining oral hygiene and great risk of periodontal diseases and caries on patients, reducing the time needed for orthodontic treatment is always being pursued by orthodontists. Previously, investigated therapies may be able to promote OTM; however, the negative impacts on patients and difficulties in clinical operation discouraged their extensive application in clinics. Therefore, drinking coffee has the potentiality to be an unprecedentedly simple and convenient approach to raise the velocity of tooth movement because this daily habit adds little extra burden to patients and has the ability to reduce bone density, more importantly, its effect on bone metabolism is temporary and reversible.
To bring the hypothesized treatment from lab to clinics, the appropriate consumption of coffee intake should be further explored through clinical trials because that Tassinari's research [40] on rat has shown that only the comparatively low concentration caffeine elicits a delay rather than an irreversible inhibition on osteoblasts, moreover, the period of tooth movement cycle and the half-life of caffeine are different between human and rats. Further, studies to investigate the likelihood of adverse effect on tissues other than kidney and jaw bone which are the primary desirable targets of caffeine when exposed to the effective concentration of caffeine need to be conducted to ensure its safety. And in clinical contexts, specific plans to carry out the caffeine therapy must be designed by orthodontists, for orthodontic treatment is highly individualized; for example patients with low BMD may have a tendency to relapse, so wearing retainers for a period of time after orthodontic treatment is necessary for them to help stabilize new occlusion and strengthen cementum-periodontal ligament-alveolar bone complex.
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