Protocol

The structure of the review protocol was developed before the start of the study, and the reporting of findings followed the PRISMA guidelines ( www.prisma-statement.org ). Because the experimental studies on which this systematic review was based were on animals, our protocol could not be registered in the PROSPERO database.

Information resources

A search was made of the MedLine (Entrez PubMed, www.ncbi.nim.nih.gov ), SCOPUS ( www.scopus.com ), and Web of Science ( www.isiknowledge.com ) databases to find possible studies matching our established selection criteria, including all articles published up to January 21, 2016. We searched for gray literature by exploring the OpenGrey database, European Association for Grey Literature Exploitation, also up to January 21, 2016, without applying language restrictions.

Search strategy

Our search strategy used the medical subject heading term “tooth movement” crossed with “inhibition,” “inhibit,” or “decrease” and excluded the terms “relapse” or “increase” or “enhance” or “promotion.” Supplementary Table I summarizes the full search strategy, including animal search filters, in all databases used. Some main orthodontic journals not indexed in the Journal Citation Report index were also hand searched to identify potential studies not found in the electronic search ( Supplementary Table I ).

Eligibility

Articles selected for this study fulfilled the following criteria for inclusion, according to the PICOS format.

• 1.

  Population: animals; any experimental study or clinical investigation that included at least 1 experimental group with a minimum of 5 animals or samples per group.

• 2.

  Intervention: biologic methods of decreasing or inhibiting tooth movement using orthodontic or orthopedic devices to apply forces.

• 3.

  Comparison: control group without a biologic method.

• 4.

  Outcome: rate of OTM deceleration or inhibition.

• 5.

  Study design: experimental controlled trials.

Excluded from the selection were case reports, case series, descriptive studies, review articles, opinion articles, letters, and articles that did not correspond to the objectives of this review or did not have an adequate description of the technique or the administration dose.

Study selection

Eligibility was assessed by 2 observers (M.C-P. and R.M.Y-V.) acting independently. Articles were initially selected on the basis of the title and abstract, with the complete article reviewed whenever there was doubt about whether it should be included. Disagreements were resolved by consensus or by a third experienced reviewer who was requested to arbitrate (A.I-L.). After the 2 reviewers had separately applied the inclusion and exclusion criteria to each article, concordance between them was measured using the kappa index.

Data collection and analysis

Data were extracted by 1 observer (M.C-P.). A data extraction sheet was developed and piloted. Conflicts during data collection were resolved by discussion with a second (R.M.Y-V.) or a third experienced observer (A.I-L.). Data were extracted for the following items: author and year, study design, sample (size, species, age, and sex), a brief description of the methods, applied force, total treatment or experimentation time, decrease in the rate of OTM, and clinical applicability.

Methodologic quality and risk of bias of individual studies

The methodologic quality of the selected articles was assessed using the Methodological Index for Non-Randomized Studies (MINORS). The 12 variables analyzed were clearly stated: aim, inclusion of consecutive patients, prospective collection of data, end points appropriate to the aim of the study, unbiased assessment of the study end point, follow-up period appropriate to the aim of the study, loss to follow-up less than 5%, prospective calculation of the study size, adequate control group, contemporary groups, baseline equivalence of the groups, and adequate statistical analysis. After this analysis, every item scored 0 when not reported, 1 when it was reported but inadequate, and 2 when it was reported and adequate. Articles obtaining between 0 and 7 points were assessed as low quality and therefore had a high risk of bias; studies with 8 to 15 points were considered as medium quality and with a medium risk of bias; and articles obtaining 16 to 24 points were classed as high quality and with a low risk of bias.

Study selection

Two independent observers selected the studies, and good concordance was shown (kappa index, 0.8). A complete flow diagram of the search is given in the Figure .

PRISMA flow diagram.

Study characteristics and quality assessment

Rats were the most frequently used models in the sample (38 of 57 articles: 25 Wistar, 13 Sprague Dawley), followed by mice (9 of 57) and rabbits (4 of 57); guinea pigs and dogs were used in 2 articles each, and cats and monkeys in 1 each. The sample sizes seldom exceeded 25 subjects per group (6 of 57 articles). Randomization of the samples was mentioned in 24 articles, and blinding measures were found in only 14 studies ( Table I ).

The most commonly used biologic method leading to reduced orthodontic tooth movement was pharmacologic administration, and a wide range of substances were used (53 of 57 articles). The main substances evaluated in the selected articles were nonsteroidal anti-inflammatory drugs (NSAIDS) in 14 articles, followed by cytokines and bisphosphonates in 10 articles each. Three articles were based on antihistamines, and 2 articles each on hormones, fluoride, and beta blockers. Finally, 10 articles concentrated on other substances, such as immunosuppressants, morphine, nitric oxide, phenytoin, nicotine, simvastatin, endothelin, and tetracycline, or Nrf2 activators. Twenty-five studies were categorized as high quality with a low risk of bias (over 16 points), although on the 24-point scale used, no article scored more than 20 points. The remaining articles were considered to be medium quality.

Outcomes

The methods included in this review fall into 3 major categories: chemical or pharmacologic methods, gene therapy, and low-level laser therapy ( Table II ). Fifty-three of the 57 studies were classed as chemical methods. These comprised a wide range of substances, ranging from NSAIDs to bisphosphonates and cytokines, and were mainly administered in 1 of 2 forms: local or systemic. NSAIDS and other selective COX-2 inhibitors were the most frequently described substances (14 of 53 studies). Diclofenac seems to have the strongest inhibitory effect on OTM; de Carlos et al, in a study rated as high quality, described complete inhibition when diclofenac was used on rats under 100 and 50 g of force ( P <0.01), and partial inhibition with rofecoxib under 50 g of force ( P <0.01), although some movement was found (a reduction of approximately 70%) with rofecoxib and 100 g of force, compared with the controls ( P <0.05). In another article by the same authors, no statistically significant reduction in OTM was found with parecoxib or celecoxib compared with the controls at 50 g of force. However, short-term use of celecoxib slowed down OTM by 30% and long-term use by 46% ( P <0.01), as determined by a study of high methodologic quality, whereas in another, assessed as medium quality, 50% less tooth movement was found with the same drug ( P <0.01). However, a higher decrease in OTM was found by Hammad et al with paracetamol and ketorolac than with celecoxib ( P <0.01). Indomethacin obtained different results; it was reported to reduce the rate of OTM by half compared with the controls ( P <0.01), as described in a study rated as high quality, and to reduce OTM by 40% ( P <0.05) and 25% ( P <0.01) in 2 studies of medium methodologic quality. In the latter study, the prostaglandin (PG) analogs, prostacyclin (PGI2) and thromboxane A2 (TxA2), were compared with 2 PG inhibitors, indomethacin (a PGI2 inhibitor) and imidazole (a TxA2 inhibitor). The PG analogs—PGI2 much more than TxA2—significantly increased the rate of OTM in rats, whereas indomethacin and imidazole reduced OTM, with no significant differences in their inhibitory effects. Leukotriene inhibitors—and not only PG—were also reported to decrease OTM (application of AA861 resulted in 29.8% less OTM and 36% less tooth movement combined with indomethacin) ( P <0.05), as 1 high-quality study demonstrated ( Table II ).

Table II

Summary of articles included in the review

Authors, year	Study design	Sample (n)	Description of groups	Species	Age, sex	Force (g)	Time (d)	Decrease in rate of OTM	Human clinical applicability tested
Chemical methods
Olteanu et al, 2015	CS	24	G1) CG: OTM only; G2) 1.5 mL aspirin by gastric gavage + OTM; G3) 1.2 mL algocalmin by gastric gavage + OT	WR	NM, 24 M	25	28	Decrease of OTM with aspirin and algocalmin ( P = 0.0001)	Yes
Kanzaki et al, 2015	CS	20	G1) CG: no OTM; G2) OTM + right hemi-maxilla: 2 μL intragingival SFN (Nrf2 activator) in DMF, left hemi-maxilla DMF only; G3) OTM + right hemi-maxilla: 2 μL intragingival EGCG (Nrf2 activator) in DMF, left hemi-maxilla DMF only	Mi	6 wk, 20 M	10	21	60% less OTM compared with controls ( P <0.05)	No
Hakami et al, 2015	CS	32	G1) CG: no OTM; G2) 1.5 μg/d intragingival IL-4 + OTM; G3) intragingival PBS + OTM; G4) 0.015 μg/d intragingival IL-4 + OTM; G5) 0.15 μg/d intragingival IL-4 + OTM	Mi	10-12 wk, 32 M	10	12	Less OTM with 1.5 μg/d IL-4 but not with the rest of the doses ( P <0.01)	No
Fernandez-González et al, 2015	CS	42	G1) CG: OTM only; G2: OTM + twice/w subgingival injections of 5 mg/kg OPG-Fc mesial and distal to maxillary first molar	SDR	6 mo, 42 M	50	21	52%, 31%, and 22% less OTM at days 7, 14 ( P <0.01), and 21 ( P <0.05), respectively	Yes
Venkataramana et al, 2014b	CS	20	G1) CG: 1 mL IP saline solution + OTM; G2) 1.5 mg/kg IP pamidronate + OTM	R	16 wk, 20 M	100	21	Less OTM with pamidronate ( P <0.05)	Yes
Venkataramana et al, 2014a	CS	20	G1) CG: 1 mL IP saline solution + OTM; G2) 0.3 mg/kg intragingival ibandronate + OTM	R	16 wk, NM	100	21	Less OTM with ibandronate ( P <0.05)	Yes
Oliveira et al, 2014	CS	20	G1) vehicle only; G2) OTM + vehicle; G3) OTM + 0.1 mg/kg/d oral propranolol; G4) OTM + 20 mg/kg/d oral propranolol	WR	3 mo, 20 M	50	10	Low dose propranolol (0.1 mg/kg) reduced OTM by 41%; a higher dose did not ( P <0.05)	No
Nagaie et al, 2014	CS	20	G1) CG, OTM + oral administration of basal pure water; G2) OTM + 13 μg/mL TSC water containing 1 μg/mL nicotine	WR	13 wk, 20 M	NM	10	28% less OTM with nicotine ( P <0.01)	No
Toro et al, 2013	CS	30	G1) 2-wk SC injection vehicle then OTM; G2) 2-wk SC injections 25 mg/kg BE, then OTM; G3) 2-wk SC injections 1 mg/kg alendronate, then OTM	SDR	NM, 30 M	13	28	BE and alendronate reduced OTM by 64% and 84%, respectively ( P <0.05)	No
Kaipatur et al, 2013	CS	20	G1) OTM + SC injection 0.015 mg/kg alendronate; G2) OTM + vehicle; G3) 3-mo alendronate, then OTM; G4) 3-mo vehicle, then OTM	SDR	12 wk, 20 F	50	56	65% less OTM on G1/G2 ( P = 0.05), 86% less OTM on G3/G4 (prior intake bisphosphonates) ( P <0.01)	No
Yabumoto et al, 2013	CS	80	G1) wild-type mice, OTM + saline solution; G2) wild-type mice, OTM + injection of 15 mg/kg IP reveromycin A; G3) OPG deficient KO mice, OTM + saline solution; G4) OPG deficient KO mice, OTM + 15 mg/kg IP reveromycin A	Mi	8 wk, 80 M	NM	3	NSRD after 3 days between groups	No
Olyaee et al, 2013	CS	48	G1) OTM + 100 mg/kg/d ethinyl estradiol by gavage + 1 mg/kg/d norgestrel by gavage; G2) CG OTM + saline solution	WR	12 wk, 48 F	30	14	39% less OTM with estradiol and norgestrel ( P <0.05)	No
Sodagar et al, 2013	CS	28	G1) OTM only; G2) OTM + injection of 0.3 mg celecoxib	SDR	5 wk, 28 M	60	18	50% less OTM ( P <0.01)	No
Kondo et al, 2013	CS	NM	G1) 7-d IP injections 20 μg/g propranolol (β-antagonist) then OTM; G2) 7-d IP injections 5 μg/g isoproterenol (β-agonist) then OTM; G3) 7-d IP injections 0.9% saline solution, then OTM	Mi	8 wk, M	NM	5	β-antagonist decreased OTM by 35.7%; β-agonist increased it by 14.3% ( P <0.05)	No
Esfahani et al, 2013	CS	32	G1) CG: OTM + saline solution; G2) OTM + 2.5 mg/kg IP simvastatin	WR	8-10 wk, 32 M	60	17	Significantly less OTM ( P <0.024)	No
Yoshimatsu et al, 2012	CS	32	G1) no OTM or injection (CG); G2) OTM + 0.015 mg/d IL-12; G3) OTM + 0.15 mg/d IL-12; G4) OTM + 1.5 mg/d IL-12 G5) OTM + PBS	Mi	8 wk, 32 M	10	12	1.5 mg/d IL-12 significantly decreases OTM ( P <0.001); with lower doses, NSRD were found	No
Kohara et al, 2012	CS	NM	G1) OTM + injections IFN-g (0.015-1.5 μg per 20 mL); G2) (CG) OTM + PBS	Mi	8 wk, NM	10	12	61.4% less OTM in the group treated with interferon ( P <0.05)	No
Hammad et al, 2012	CS	40	G1) CG: reverse osmosis water + OTM; G2) 10 mg/kg celecoxib + OTM; G3) 3 mg/kg ketorolac + OTM; G4) 150 mg/kg paracetamol + OTM.	WR	12 wk, 40 M	50	60	celecoxib did not reduce OTM compared with ketorolac and paracetamol ( P <0.01)	Yes
Meh et al, 2011	CS	48	G1) oral saline solution; G2) OTM + oral saline solution; G3) 3 mg/kg/d oral cetirizine + OTM	SDR	13 wk, 48 M	25	42	cetirizine reduced OTM by 26.1% ( P <0.01)	No
Hao and Hua, 2011	CS	72	G1) OTM + local injections of PBS (CG); G2, G3, G4) OTM and systemic injections of 0.16, 0.12, 0.08, and 0.04 mg/mL rhsTNF-RI.	SDR	6 wk, 72 M	50	14	NSRD in the 0.04 mg/mL group, but 40% decrease in OTM in the rest of the groups ( P <0.01)	No
Gonzales et al, 2011	CS	50	G1) no OTM, no NaF; G2) OTM, no NaF; G3) OTM + 2-wk 45 ppm oral NaF; G4) OTM + 4-wk 45 ppm oral NaF; G5) OTM + 12-wk 45 ppm oral NaF	WR	NM, 50 M	50	84	74% decrease in OTM ( P <0.01)	Yes
Shoji et al, 2010	CS	48	in OPG -/- mice (a model for juvenile Paget disease): G1) CG: IP saline solution + OTM; G2) 1.25 mg/kg/d IP alendronate + OTM in wild-type mice; G3) CG: IP saline solution + OTM; G4) 1.25 mg/kg/d IP alendronate + OTM	Mi	8 wk, 48 M	NM	3	administration of alendronate to OPG -/- mice decreased OTM ( P <0.01)	No
Santos et al, 2010	CS	120	G1) OTM + saline solution; G2) OTM + FK506; G3) FK506 only; G4) saline solution only	WR	9 wk, 120 M	35	14	19% less OTM with tacrolimus immunosuppressant (FK506) treatment ( P <0.05)	No
Han et al, 2010	CS	32	G1) 2.5 mg simvastatin per kg/d; G2) CG	WR	7-8 wk, 32 M	50	49	45% less OTM ( P <0.001)	Yes
Choi et al, 2010	CS	54	G1) 2.5 mM/L clodronate; G2) 10 mM/L clodronate; G3) CG	WR	8 wk, 27 M/27 F	60	17	OTM reduced by 32% and 36.3%, respectively ( P <0.05)	Yes
Baysal et al, 2010	CS	28	G1) no OTM; G2) OTM + thyroxine; G3) OTM + doxycycline; G4) OTM only	WR	7-8 wk, 28 M	50	14	NSRD	Yes
Akhoundi et al, 2010	CS	40	G1) OTM; G2) OTM + injections 5 mg/d morphine; G3) OTM + 5 mg/d morphine + 20 mg/d naltrexone; G4) OTM + 20 mg/d naltrexone/normal saline solution	WR	NM, 40 M	60	14	morphine reduced OTM by 52% ( P <0.05)	No
Karras et al, 2009	CS	50	G1) CG, OTM only; G2) OTM + injections of alendronate sodium of 7 mg/kg body weight per week	SDR	NM, NM	50	35	42% less OTM in the alendronate group after 4 weeks ( P <0.001)	No
Fujimur et al, 2009	CS	NM	G1) OTM + local bisphosphonate; G2) OTM + PBS	Mi	8 wk, M	NM	12	50% less OTM ( P <0.05)	No
Sprogar et al, 2008	CS	34	G1) no OTM + saline solution; G2) OTM + saline solution; G3) OTM + 10 mg/kg IP famotidine	WR	NM, 34 M	25	42	significantly less OTM ( P <0.001)	No
Kriznar et al, 2008	CS	34	G1) no OTM + saline solution; G2) OTM + saline solution; G3) OTM + 10 mg/kg IP cetirizine	WR	NM, 34 M	25	42	significantly less OTM ( P <0.05)	No
Kitaura et al, 2008	CS	NM	G1) OTM + daily injection 10 μg anti-CFms antibody; G2) OTM + PBS	Mi	8 wk, NM	10	12	anti-CFms antibody reduces OTM by in 36.7% ( P <0.05)	No
Hauber Gameiro et al, 2008	CS	32	G1) OTM + IP injections celecoxib 3 d; G2) OTM + IP injections saline 3 d; G3) OTM + IP injections celecoxib 14 d; G4) OTM + IP injections control 14 d	WR	NM, 32 M	50	14	celecoxib decreases OTM by 30% with short-term dosage, and 46% with long-term dosage ( P <0.05)	No
Sprogar et al, 2007	CS	30	G1) OTM + TBC3214; G2) OTM + placebo; G3) placebo	WR	11-12 wk, 30 M	25	40	daily TBC3214, treatment reduces OTM by 33.3% ( P <0.001)	No
Keles et al, 2007	CS	51	G1) OTM; G2) Pamidronate + OTM; G3) OPG + OTM	Mo	8 wk, 51 M	22,4	12	pamidronate inhibited OTM by 34%, OPG by 77% ( P <0.01)	Yes
Dunn et al, 2007	CS	30	G1) OTM + injection PBS; G2) OTM + 0.5 mg/kg local injections recombinant OPG; G3) OTM + 50 mg/kg local injections recombinant OPG	WR	NM, 30 M	54	21	OTM was inhibited by 70.6% after 14 days in higher-dose group ( P <0.001) and by 31.8% in lower-dose group ( P <0.05)	No
de Carlos et al, 2007	CS	28	G1) OTM + rofecoxib; G2) OTM + celecoxib; G3) OTM + Ppecoxib; G4) control	WR	12 wk, 28 M	50	5	rofecoxib inhibits OTM ( P <0.05); NSRD between parecoxib and celecoxib and controls	Yes
Bildt et al, 2007	CS	18	G1) OTM + PBS injection; G2) OTM + injection 6 mg CMT-3/kg body weight; G3) OTM + injection 30 mg CMT-3/kg body weight	WR	NM, 18 M	10	14	CMT reduced OTM by 15.7% in 6-mg group and 34.3% in 30-mg group, respectively ( P <0.05)	No
de Carlos et al, 2006	CS	42	G1) OTM (50 g) + rofecoxib; G2) OTM (50 g) + diclofenac; G3) control G4) G5) G6) OTM (100 g) + same pharmacologic treatment as 1, 2, and 3	WR	NM, 42 M	50-100	10	Diclofenac inhibits OTM under 50 and 100 g forces ( P <0.01); rofecoxib inhibits OTM under 50 g force ( P <0.01) and reduces it by 73.6% under 100 g force ( P <0.05)	Yes
Arias and Marquez-Orozco, 2006	CS	36	G1) OTM + 100 mg/kg/d ASA; G2) OTM + 30 mg/kg/d ibuprofen; G3) OTM + 200 mg/kg/d acetaminophen; G4) CG: OTM + vehicle	WR	NM, 36 M	30	10	aspirin reduced OTM by 38.75% ( P <0.05), ibuprofen by 41.52% ( P <0.01); acetaminophen did not affect OTM	Yes
Jäger et al, 2005	CS	80	G1) OTM + PBS; G2) OTM + sIL-1-R; G3) OTM + sTNF-a-RI; G4) OTM + both	WR	12 wk, 80 M	50	12	60% less OTM ( P <0.05)	No
Liu et al, 2004	CS	26	G1) OTM; G2) OTM + 2.5 mM clodronate; G3) OTM + 10 mM clodronate; G4) OTM + 40 mM clodronate	WR	7 wk, 26 M	12	21	56%, 65%, and 81% less OTM, respectively ( P <0.001)	No
Gurton et al, 2004	CS	150	G1) OTM + iloprost; G2) OTM + indomethacin; G3) OTM + U 46619; G4) OTM + imidazole; G5) OTM + 0.9% NaCl; G6) no OTM + NaCl; G7) no OTM or solution	SDR	NM 150 M	20	5	Pg analogs increase OTM by 31.28% Pg antagonists reduce OTM by 20.26% ( P <0.01)	Yes
Shirazi et al, 2002	CS	48	G1) CG, no injections; G2) saline solution group; G3) 200 mg/kg injections of L-arg; G4) 10 mg/kg L-NAME group	SDR	NM, M	60	13	50% less OTM with the L-NAME group (reduced nitric oxide production led to a decrease in OTM) ( P <0.001)	No
Zhou et al, 1997	CS	96	G1) OTM + subcutaneous indomethacin; G2) OTM + saline solution	SDR	5-6 wk, 96 M	40	10	40% less OTM with indomethacin ( P <0.05)	No
Karsten and Hellsing, 1997	CS	20	G1) OTM + phenytoin; G2) control	SDR	3-5 mo, 20 F	15	42	not conclusive.	No
Kehoe et al, 1996	CS	40	G1) CG: OTM + placebo; G2) 100 μg/kg/12-h misoprostol + OTM; G3) 200 mg/kg/12-h acetaminophen + OTM; G4) 30 mg/kg/12-h ibuprofen + OTM	GP	6-8 wk, 40 M	25	11	acetaminophen showed NSRD with controls; ibuprofen reduced OTM by approximately 22% ( P <0.001)	No
Igarashi et al, 1994	CS	77	G1) systemic AHBuBP (bisphosphonate) every 24 h + OTM; G2) OTM only; G3) topical AHBuBP + OTM	WR	9-10 wk, 77 M	16.8	21	40% less OTM with systemic application, 70% less OTM with topical administration ( P <0.001)	No
Wong et al, 1992	CS	11	G1) CG: OTM + sodium bicarbonate; G2) OTM + oral administration of 65 mg/kg/d ASA	GP	NM, NM	8	28	NSRD	No
Hellsing and Hammarstrom, 1991	CS	16	G1) OTM in pregnant rats; G2) OTM in nonpregnant rats; G3) nonpregnant rats + NaF	SDR	3-5 mo, 16 F	15	21	52% less OTM with NaF; 39% more OTM in pregnant rats ( P <0.01)	No
Mohammed et al, 1989	CS	132	G1) OTM + leukotriene synthesis inhibitor; G2) OTM + indomethacin; G3) OTM; G4) OTM + both groups	SDR	NM, NM	60	14	29.8% less OTM with AA861 combined with indomethacin; 36.2% less OTM with indomethacin only ( P <0.05)	No
Chumbley and Tuncay, 1986	CS	12	G1) OTM (CG); G2) OTM + oral administration of 5 mg/kg/d indomethacin	C	12-18 mo, NM	250	21	indomethacin group achieved approximately 50% less than the CG ( P <0.01)	No
Sandy and Harris, 1984	CS	14	G1) CG (OTM + vehicle of MC; G2) OTM + flurbiprofen	R	NM 7 F/7 M	100	14	NSRD	No
Gene therapy
Kanzaki et al, 2004	CS	20	G1) CG, no OTM CG; G2) OTM + PBS; G3) OTM + injections of OPG gene transfer	WR	6 wk, 20 M	17	20	92.8% less OTM ( P <0.001)	Yes
Low-level laser therapy
Kim et al, 2015	CS	10	G1) CG: OTM alone; G2) OTM into the grafted defects; G3) OTM into the grafted defects + LLLT.	D	18-24 mo, 10 M	100	42	LLLT decreased OTM into the bone-grafted surgical defects ( P <0.01)	Yes
Kim et al, 2009	CS	12	G1) CG OTM only; G2) OTM + CO; G3) OTM + LLLT; G4) OTM + CO + LLLT	D	84 wk, 12 M	150	56	LLLT after CO decreases OTM 48.4% ( P <0.001)	No
Seifi et al, 2007	CS	18	G1) CG; G2) LLLT (850 nm); G3) LLLT (630 nm)	R	16 wk, 18 M	10-120	16	Pulsed and continuous LLLT reduced OTM by 40.6% and 50.6% ( P <0.001)	No

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