Year : 2012 | Volume
: 3 | Issue : 2 | Page : 72--75
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
14#, 3rd Section, Renmin Nan Road, Chengdu 610 041
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.
|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;3:72-75
|How to cite this URL:|
Yi J, Zhang L, Yan B, Yang L, Li Y, Zhao Z. Drinking coffee may help accelerate orthodontic tooth movement. Dent Hypotheses [serial online] 2012 [cited 2020 Jan 29 ];3:72-75
Available from: http://www.dentalhypotheses.com/text.asp?2012/3/2/72/100391
Orthodontic tooth movement (OTM), as a consequence of force-induced periodontal tissue remodeling, , 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.  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,  RANKL,  osteocalcin  and prostaglandins,  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. , 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. ,, 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.  As bone remodeling is the essential biological process in OTM, , and lower bone mineral density (BMD) can lead to faster bone remodeling,  decreased BMD may well elicit accelerated OTM. 
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.  Many studies have shown that caffeine consumption is related to low bone density. ,,, The mechanisms, however, are complicated.
Evidence has suggested that caffeine consumption increases the urinary calcium excretion.  The loss of calcium induced by caffeine has been verified to be the consequence of reduction in renal reabsorption  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. , 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),  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,  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,  results in the lack of activated osteoblast and consequently bring about decreased BMD.  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;  firstly caffeine inhibits the phosphodiesterase which breaks cAMP down, , and secondly caffeine induces an enhancement in prostaglandin E 2 (PGE 2 ) output in vitro and in vivo.  High concentration of PGE 2 can increase intracellular cAMP in osteoblasts and has also been reported to up-regulates osteoclasts activity  and inhibits collagen synthesis, , leading to faster bone resorption and slower bone deposition. , 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.  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. 
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.  (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.  (3) Low BMD accelerates the bone remodeling and thus shortens the duration of orthodontic treatment. ,,,
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  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.
|1||Mabuchi R, Matsuzaka K, Shimono M. Cell proliferation and cell death in periodontal ligaments during orthodontic tooth movement. J Periodontal Res 2002;37:118-24.|
|2||Krishnan V, Davidovitch Z. Cellular, molecular, and tissue-level reactions to orthodontic force. Am J Orthod Dentofacial Orthop 2006;129:469 e1-32.|
|3||Chen Y, Cao Z, Zhang L, Xu X. Low level laser can be a novel adjuvant method for orthodontic tooth movement on postmenopausal women. Med Hypotheses 2011;76:479-81.|
|4||Soma S, Iwamoto M, Higuchi Y, Kurisu K. Effects of continuous infusion of PTH on experimental tooth movement in rats. J Bone Miner Res 1999;14:546-54.|
|5||Kanzaki H, Chiba M, Arai K, Takahashi I, Haruyama N, Nishimura M, et al. Local RANKL gene transfer to the periodontal tissue accelerates orthodontic tooth movement. Gene Ther 2006;13:678-85.|
|6||Hashimoto F, Kobayashi Y, Mataki S, Kobayashi K, Kato Y, Sakai H. Administration of osteocalcin accelerates orthodontic tooth movement induced by a closed coil spring in rats. Eur J Orthod 2001;23:535-45.|
|7||Lee WC. Experimental study of the effect of prostaglandin administration on tooth movement-with particular emphasis on the relationship to the method of PGE1 administration. Am J Orthod Dentofacial Orthop 1990;98:231-41.|
|8||Shen G, Liu K. A biomechanical analysis for the effect of EB iontophoresis on accelerating tooth movement of human canines [In Chinese]. J Appl Biomech 1994;9:95-8.|
|9||Liu CG, Huang SG, Lin TY, Feng DY, Huang P, Zhang JX. Effect of Erigeron Breviscapus on the expression of vascular endothelial growth factor in the periodontal tissues of rabbits during orthodontic tooth movement [In Chinese]. Hua Xi Kou Qiang Yi Xue Za Zhi 2006;24:458-61.|
|10||Leung FY, Rabie AB, Wong RW. Osteoporosis, osteonecrosis, and orthodontics. World J Orthod 2009;10:261-71.|
|11||Knop LA, Shintcovsk RL, Retamoso LB, Ribeiro JS, Tanaka OM. Non-steroidal and steroidal anti-inflammatory use in the context of orthodontic movement. Eur J Orthod 2011. [In press]|
|12||Reitan K. Clinical and histologic observations on tooth movement during and after orthodontic treatment. Am J Orthod 1967;53:721-45.|
|13||Hill PA. Bone remodelling. Br J Orthod 1998;25:101-7.|
|14||Hill PA, Tumber A, Meikle MC. Multiple extracellular signals promote osteoblast survival and apoptosis. Endocrinology 1997;138:3849-58.|
|15||Cosman F, Nieves J, Wilkinson C, Schnering D, Shen V, Lindsay R. Bone density change and biochemical indices of skeletal turnover. Calcif Tissue Int 1996;58:236-43.|
|16||Tyrovola JB, Spyropoulos MN. Effects of drugs and systemic factors on orthodontic treatment. Quintessence Int 2001;32:365-71.|
|17||Barone JJ, Roberts HR. Caffeine consumption. Food Chem Toxicol 1996;34:119-29.|
|18||Heaney RP. Effects of caffeine on bone and the calcium economy. Food Chem Toxicol 2002;40:1263-70.|
|19||Valdes M, Shaye R, Joseph F, Jr, Nakamoto T. The effects of caffeine on the maxillary composition in the newborn rat. Calcif Tissue Int 1992;50:165-8.|
|20||Yeh JK, Aloia JF. Differential effect of caffeine administration on calcium and vitamin D metabolism in young and adult rats. J Bone Miner Res 1986;1:251-8.|
|21||Sakamoto W, Nishihira J, Fujie K, Iizuka T, Handa H, Ozaki M, et al. Effect of coffee consumption on bone metabolism. Bone 2001;28:332-6.|
|22||Heaney RP, Recker RR. Effects of nitrogen, phosphorus, and caffeine on calcium balance in women. J Lab Clin Med 1982;99:46-55.|
|23||Bergman EA, Massey LK, Wise KJ, Sherrard DJ. Effects of dietary caffeine on renal handling of minerals in adult women. Life Sci 1990;47:557-64.|
|24||Massey LK, Whiting SJ. Caffeine, urinary calcium, calcium metabolism and bone. J Nutr 1993;123:1611-4.|
|25||Osswald H, Muhlbauer B, Schenk F. Adenosine mediates tubuloglomerular feedback response: An element of metabolic control of kidney function. Kidney Int Suppl 1991;32:S128-31.|
|26||Yeh JK, Aloia JF, Semla HM, Chen SY. Influence of injected caffeine on the metabolism of calcium and the retention and excretion of sodium, potassium, phosphorus, magnesium, zinc and copper in rats. J Nutr 1986;116:273-80.|
|27||Stein GS, Lian JB, Stein JL, Van Wijnen AJ, Montecino M. Transcriptional control of osteoblast growth and differentiation. Physiol Rev 1996;76:593-629.|
|28||Fernandez MJ, Lopez A, Santa-Maria A. Apoptosis induced by different doses of caffeine on Chinese hamster ovary cells. J Appl Toxicol 2003;23:221-4.|
|29||Kamagata-Kiyoura Y, Ohta M, Cheuk G, Yazdani M, Saltzman MJ, Nakamoto T. Combined effects of caffeine and prostaglandin E2 on the proliferation of osteoblast-like cells (UMR106-01). J Periodontol 1999;70:283-8.|
|30||Fredholm BB. On the mechanism of action of theophylline and caffeine. Acta Med Scand 1985;217:149-53.|
|31||Butcher RW, Sutherland EW. Adenosine 3',5'-phosphate in biological materials. I. Purification and properties of cyclic 3',5'-nucleotide phosphodiesterase and use of this enzyme to characterize adenosine 3',5'-phosphate in human urine. J Biol Chem 1962;237:1244-50.|
|32||Naderali EK, Poyser NL. Effects of caffeine and theophylline on prostaglandin production by guinea-pig endometrium. Prostaglandins Leukot Essent Fatty Acids 1997;56:63-7.|
|33||Whiting SJ. Effect of prostaglandin inhibition on caffeine-induced hypercalciuria in healthy women. J Nutr Biochem 1990;1:201-5.|
|34||Hakeda Y, Yoshino T, Natakani Y, Kurihara N, Maeda N, Kumegawa M. Prostaglandin E2 stimulates DNA synthesis by a cyclic AMP-independent pathway in osteoblastic clone MC3T3-E1 cells. J Cell Physiol 1986;128:155-61.|
|35||Raisz LG, Koolemans-Beynen AR. Inhibition of bone collagen synthesis by prostaglandin E2 in organ culture. Prostaglandins 1974;8:377-85.|
|36||Wahl LM, Lampel LL. Regulation of human peripheral blood monocyte collagenase by prostaglandins and anti-inflammatory drugs. Cell Immunol 1987;105:411-22.|
|37||Klein DC, Raisz LG. Prostaglandins: Stimulation of bone resorption in tissue culture. Endocrinology 1970;86:1436-40.|
|38||Hakeda Y, Nakatani Y, Hiramatsu M, Kurihara N, Tsunoi M, Ikeda E, et al. Inductive effects of prostaglandins on alkaline phosphatase in osteoblastic cells, clone MC3T3-E1. J Biochem 1985;97:97-104.|
|39||Rapuri PB, Gallagher JC, Nawaz Z. Caffeine decreases vitamin D receptor protein expression and 1,25(OH)2D3 stimulated alkaline phosphatase activity in human osteoblast cells. J Steroid Biochem Mol Biol 2007;103:368-71.|
|40||Tassinari MS, Gerstenfeld LC, Stein GS, Lian JB. Effect of caffeine on parameters of osteoblast growth and differentiation of a mineralized extracellular matrix in vitro. J Bone Miner Res 1991;6:1029-36.|