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Gingival bleeding

MedGen UID:
42218
Concept ID:
C0017565
Pathologic Function
Synonyms: Gingival Hemorrhage; Gingival Hemorrhages; Hemorrhage, Gingival
SNOMED CT: Bleeding gums (86276007); Gingival bleeding (86276007); Gingival hemorrhage (86276007)
 
HPO: HP:0000225

Definition

Hemorrhage affecting the gingiva. [from HPO]

Term Hierarchy

CClinical test,  RResearch test,  OOMIM,  GGeneReviews,  VClinVar  
  • CROGVGingival bleeding

Conditions with this feature

Bernard Soulier syndrome
MedGen UID:
2212
Concept ID:
C0005129
Disease or Syndrome
Bernard-Soulier syndrome is an autosomal recessive bleeding disorder caused by a defect in or deficiency of the platelet membrane von Willebrand factor (VWF; 613160) receptor complex, glycoprotein Ib (GP Ib). GP Ib is composed of 4 subunits encoded by 4 separate genes: GP1BA, GP1BB, GP9, and GP5 (173511). Genetic Heterogeneity of Platelet-Type Bleeding Disorders Inherited platelet disorders are a heterogeneous group of bleeding disorders affecting platelet number, function, or both. Functional defects can involve platelet receptors, signaling pathways, cytoskeletal proteins, granule contents, activation, or aggregation (review by Cox et al., 2011 and Nurden and Nurden, 2011). Platelet-type bleeding disorders include Bernard-Soulier syndrome (BDPLT1); Glanzmann thrombasthenia (BDPLT2; 273800), caused by mutation in the ITGA2B (607759) or ITGB3 (173470) gene; pseudo-von Willebrand disease (BDPLT3; 177820), caused by mutation in the GP1BA gene (606672); gray platelet syndrome (BDPLT4; 139090), caused by mutation in the NBEAL2 gene (614169); Quebec platelet disorder (BDPLT5; 601709), caused by tandem duplication of the PLAU gene (191840); May-Hegglin anomaly (BDPLT6; 155100), caused by mutation in the MYH9 gene (160775); Scott syndrome (BDPLT7; 262890), caused by mutation in the TMEM16F gene (608663); BDPLT8 (609821), caused by mutation in the P2RY12 gene (600515); BDPLT9 (614200), associated with deficiency of the glycoprotein Ia/IIa receptor (see ITGA2; 192974); glycoprotein IV deficiency (BDPLT10; 608404), caused by mutation in the CD36 gene (173510); BDPLT11 (614201), caused by mutation in the GP6 gene (605546); BDPLT12 (605735), associated with a deficiency of platelet COX1 (176805); susceptibility to BDPLT13 (614009), caused by mutation in the TBXA2R gene (188070); BDPLT14 (614158), associated with deficiency of thromboxane synthetase (TBXAS1; 274180); BDPLT15 (615193), caused by mutation in the ACTN1 gene (102575); BDPLT16 (187800), caused by mutation in the ITGA2B (607759) or ITGB3 (173470) gene; BDPLT17 (187900), caused by mutation in the GFI1B gene (604383); BDPLT18 (615888), caused by mutation in the RASGRP2 gene (605577); BDPLT19 (616176), caused by mutation in the PRKACG gene (176893); BDPLT20 (616913), caused by mutation in the SLFN14 gene (614958); BDPLT21 (617443), caused by mutation in the FLI1 gene (193067); BDPLT22 (618462), caused by mutation in the EPHB2 gene (600997); BDPLT23 (619267), caused by mutation in the ITGB3 gene (173470); BDPLT24 (619271), caused by mutation in the ITGB3 gene (173470); and BDPLT25 (620486), caused by mutation in the TPM4 gene (600317). See reviews by Rao (2003), Cox et al. (2011), and Nurden and Nurden (2011). For a discussion of the genetic heterogeneity of hereditary thrombocytopenia, see THC1 (313900).
Glanzmann thrombasthenia
MedGen UID:
52736
Concept ID:
C0040015
Disease or Syndrome
Glanzmann thrombasthenia is a bleeding disorder that is characterized by prolonged or spontaneous bleeding starting from birth. People with Glanzmann thrombasthenia tend to bruise easily, have frequent nosebleeds (epistaxis), and may bleed from the gums. They may also develop red or purple spots on the skin caused by bleeding underneath the skin (petechiae) or swelling caused by bleeding within tissues (hematoma). Glanzmann thrombasthenia can also cause prolonged bleeding following injury, trauma, or surgery (including dental work). Women with this condition can have prolonged and sometimes abnormally heavy menstrual bleeding. Affected women also have an increased risk of excessive blood loss during pregnancy and childbirth.\n\nAbout a quarter of individuals with Glanzmann thrombasthenia have bleeding in the gastrointestinal tract, which often occurs later in life. Rarely, affected individuals have bleeding inside the skull (intracranial hemorrhage) or joints (hemarthrosis).\n\nThe severity and frequency of the bleeding episodes in Glanzmann thrombasthenia can vary greatly among affected individuals, even in the same family. Spontaneous bleeding tends to become less frequent with age.
Wiskott-Aldrich syndrome
MedGen UID:
21921
Concept ID:
C0043194
Disease or Syndrome
The WAS-related disorders, which include Wiskott-Aldrich syndrome, X-linked thrombocytopenia (XLT), and X-linked congenital neutropenia (XLN), are a spectrum of disorders of hematopoietic cells, with predominant defects of platelets and lymphocytes caused by pathogenic variants in WAS. WAS-related disorders usually present in infancy. Affected males have thrombocytopenia with intermittent mucosal bleeding, bloody diarrhea, and intermittent or chronic petechiae and purpura; eczema; and recurrent bacterial and viral infections, particularly of the ear. At least 40% of those who survive the early complications develop one or more autoimmune conditions including hemolytic anemia, immune thrombocytopenic purpura, immune-mediated neutropenia, rheumatoid arthritis, vasculitis, and immune-mediated damage to the kidneys and liver. Individuals with a WAS-related disorder, particularly those who have been exposed to Epstein-Barr virus (EBV), are at increased risk of developing lymphomas, which often occur in unusual, extranodal locations including the brain, lung, or gastrointestinal tract. Males with XLT have thrombocytopenia with small platelets; other complications of Wiskott-Aldrich syndrome, including eczema and immune dysfunction, are usually mild or absent. Males with XLN have congenital neutropenia, myeloid dysplasia, and lymphoid cell abnormalities.
Congenital prothrombin deficiency
MedGen UID:
124425
Concept ID:
C0272317
Disease or Syndrome
Prothrombin deficiency is an extremely rare autosomal recessive bleeding disorder characterized by low levels of circulating prothrombin; it affects about 1 in 2,000,000 individuals. There are 2 main types: type I deficiency, known as true prothrombin deficiency or 'hypoprothrombinemia,' is defined as plasma levels of prothrombin being less than 10% of normal with a concomitant decrease in activity. These patients have severe bleeding from birth, including umbilical cord hemorrhage, hematomas, ecchymoses, hematuria, mucosal bleeding, hemarthroses, intracranial bleeding, gastrointestinal bleeding, and menorrhagia. Type II deficiency, known as 'dysprothrombinemia,' is characterized by normal or low-normal synthesis of a dysfunctional protein. Bleeding symptoms are more variable, depending on the amount of residual functional activity. Variant prothrombin gene alleles can result in 'hypoprothrombinemia' or 'dysprothrombinemia,' and individuals who are compound heterozygous for these 2 types of alleles have variable manifestations. Heterozygous mutation carriers, who have plasma levels between 40 and 60% of normal, are usually asymptomatic, but can show bleeding after tooth extraction or surgical procedures (review by Lancellotti and De Cristofaro, 2009).
Hereditary factor X deficiency disease
MedGen UID:
543976
Concept ID:
C0272327
Disease or Syndrome
A rare inherited bleeding disorder with a decreased antigen and/or activity of factor X (FX) and characterized by mild to severe bleeding symptoms.
Primary intraosseous venous malformation
MedGen UID:
376071
Concept ID:
C1847197
Disease or Syndrome
Primary intraosseous vascular malformation (VMPI), previously called intraosseous hemangioma, is a rare malformation that usually involves the vertebral column and the skull. The most commonly affected bones in the skull are the mandible and the maxilla, and life-threatening bleeding after a simple tooth extraction is frequent (Vargel et al., 2002).
Congenital afibrinogenemia
MedGen UID:
749036
Concept ID:
C2584774
Disease or Syndrome
Inherited disorders of fibrinogen affect either the quantity (afibrinogenemia and hypofibrinogenemia; 202400) or the quality (dysfibrinogenemia; 616004) of the circulating fibrinogen or both (hypodysfibrinogenemia; see 616004). Afibrinogenemia is characterized by the complete absence of immunoreactive fibrinogen. Bleeding due to afibrinogenemia usually manifests in the neonatal period, with 85% of cases presenting umbilical cord bleeding, but a later age of onst is not unusual. Bleeding may occur in the skin, gastrointestinal tract, genitourinary tract, or the central nervous system, with intracranial hemorrhage being reported as the major cause of death. Patients are susceptible to spontaneous rupture of the spleen. Menstruating women may experience menometrorrhagia. First-trimester abortion is common. Both arterial and venous thromboembolic complications have been reported (summary by de Moerloose and Neerman-Arbez, 2009). Hypofibrinogenemia is characterized by reduced amounts of immunoreactive fibrinogen. Patients are often heterozygous carriers of afibrinogenemia mutations and are usually asymptomatic. However, they may bleed when exposed to trauma or if they have a second associated hemostatic abnormality. Women may experience miscarriages. Liver disease occurs in rare cases (summary by de Moerloose and Neerman-Arbez, 2009).
Ehlers-Danlos syndrome, dermatosparaxis type
MedGen UID:
397792
Concept ID:
C2700425
Disease or Syndrome
Dermatosparaxis (meaning 'tearing of skin') is an autosomal recessive disorder of connective tissue resulting from deficiency of procollagen peptidase, an enzyme that aids in the processing of type I procollagen. The disorder and the responsible biochemical defect was first observed in cattle (Lapiere et al., 1971). Lapiere and Nusgens (1993) reviewed the discovery of dermatosparaxis in cattle, the elucidation of the disorder, its occurrence in other animals, and the delayed recognition of the disorder in the human.
Factor XIII, A subunit, deficiency of
MedGen UID:
442497
Concept ID:
C2750514
Disease or Syndrome
Factor XIII deficiency is an autosomal recessive hematologic disorder characterized by increased bleeding and poor wound healing. Most cases of congenital factor XIII deficiency result from mutation in the A subunit (Kangsadalampai et al., 1999). Ichinose et al. (1996, 2000) proposed a classification of factor XIII deficiency: XIIIA deficiency (formerly 'type II' F13 deficiency) and XIIIB deficiency (formerly 'type I' F13 deficiency), as well as a possible combined deficiency of the 2.
Hermansky-Pudlak syndrome 1
MedGen UID:
419514
Concept ID:
C2931875
Disease or Syndrome
Hermansky-Pudlak syndrome (HPS) is characterized by oculocutaneous albinism, a bleeding diathesis, and, in some individuals, pulmonary fibrosis, granulomatous colitis, or immunodeficiency. Ocular findings include reduced iris pigment with iris transillumination, reduced retinal pigment, foveal hypoplasia with significant reduction in visual acuity (usually in the range of 20/50 to 20/400), nystagmus, and increased crossing of the optic nerve fibers. Hair color ranges from white to brown; skin color ranges from white to olive and is usually a shade lighter than that of other family members. The bleeding diathesis can result in variable bruising, epistaxis, gingival bleeding, postpartum hemorrhage, colonic bleeding, and prolonged bleeding with menses or after tooth extraction, circumcision, and other surgeries. Pulmonary fibrosis, a restrictive lung disease, typically causes symptoms in the early thirties and can progress to death within a decade. Granulomatous colitis is severe in about 15% of affected individuals. Neutropenia and/or immune defects occur primarily in individuals with pathogenic variants in AP3B1 and AP3D1.
Bernard-Soulier syndrome, type A2, autosomal dominant
MedGen UID:
478706
Concept ID:
C3277076
Disease or Syndrome
Autosomal dominant Bernard-Soulier syndrome type A2 (BSSA2) is characterized by chronic macrothrombocytopenia with mild or no clinical symptoms, normal platelet function, and normal megakaryocyte count. When present, clinical findings include excessive ecchymoses, frequent epistaxis, gingival bleeding, prolonged menstrual periods, or prolonged bleeding after tooth extraction (Savoia et al., 2001). Genetic Heterogeneity of Bernard-Soulier Syndrome Homozygous or compound heterozygous mutations in the GP1BA gene cause classic autosomal recessive Bernard-Soulier syndrome (BSSA1; 231200).
Hermansky-Pudlak syndrome 3
MedGen UID:
854708
Concept ID:
C3888001
Disease or Syndrome
Hermansky-Pudlak syndrome (HPS) is characterized by oculocutaneous albinism, a bleeding diathesis, and, in some individuals, pulmonary fibrosis, granulomatous colitis, or immunodeficiency. Ocular findings include reduced iris pigment with iris transillumination, reduced retinal pigment, foveal hypoplasia with significant reduction in visual acuity (usually in the range of 20/50 to 20/400), nystagmus, and increased crossing of the optic nerve fibers. Hair color ranges from white to brown; skin color ranges from white to olive and is usually a shade lighter than that of other family members. The bleeding diathesis can result in variable bruising, epistaxis, gingival bleeding, postpartum hemorrhage, colonic bleeding, and prolonged bleeding with menses or after tooth extraction, circumcision, and other surgeries. Pulmonary fibrosis, a restrictive lung disease, typically causes symptoms in the early thirties and can progress to death within a decade. Granulomatous colitis is severe in about 15% of affected individuals. Neutropenia and/or immune defects occur primarily in individuals with pathogenic variants in AP3B1 and AP3D1.
Hermansky-Pudlak syndrome 8
MedGen UID:
854728
Concept ID:
C3888026
Disease or Syndrome
Hermansky-Pudlak syndrome (HPS) is characterized by oculocutaneous albinism, a bleeding diathesis, and, in some individuals, pulmonary fibrosis, granulomatous colitis, or immunodeficiency. Ocular findings include reduced iris pigment with iris transillumination, reduced retinal pigment, foveal hypoplasia with significant reduction in visual acuity (usually in the range of 20/50 to 20/400), nystagmus, and increased crossing of the optic nerve fibers. Hair color ranges from white to brown; skin color ranges from white to olive and is usually a shade lighter than that of other family members. The bleeding diathesis can result in variable bruising, epistaxis, gingival bleeding, postpartum hemorrhage, colonic bleeding, and prolonged bleeding with menses or after tooth extraction, circumcision, and other surgeries. Pulmonary fibrosis, a restrictive lung disease, typically causes symptoms in the early thirties and can progress to death within a decade. Granulomatous colitis is severe in about 15% of affected individuals. Neutropenia and/or immune defects occur primarily in individuals with pathogenic variants in AP3B1 and AP3D1.
Ehlers-Danlos syndrome, periodontal type 2
MedGen UID:
934648
Concept ID:
C4310681
Disease or Syndrome
Periodontal Ehlers-Danlos syndrome (pEDS) is characterized by distinct oral manifestations. Periodontal tissue breakdown beginning in the teens results in premature loss of teeth. Lack of attached gingiva and thin and fragile gums lead to gingival recession. Connective tissue abnormalities of pEDS typically include easy bruising, pretibial plaques, distal joint hypermobility, hoarse voice, and less commonly manifestations such as organ or vessel rupture. Since the first descriptions of pEDS in the 1970s, 148 individuals have been reported in the literature; however, future in-depth descriptions of non-oral manifestations in newly diagnosed individuals with a molecularly confirmed diagnosis of pEDS will be important to further define the clinical features.
Ehlers-Danlos syndrome, periodontal type 1
MedGen UID:
1642148
Concept ID:
C4551499
Disease or Syndrome
Periodontal Ehlers-Danlos syndrome (pEDS) is characterized by distinct oral manifestations. Periodontal tissue breakdown beginning in the teens results in premature loss of teeth. Lack of attached gingiva and thin and fragile gums lead to gingival recession. Connective tissue abnormalities of pEDS typically include easy bruising, pretibial plaques, distal joint hypermobility, hoarse voice, and less commonly manifestations such as organ or vessel rupture. Since the first descriptions of pEDS in the 1970s, 148 individuals have been reported in the literature; however, future in-depth descriptions of non-oral manifestations in newly diagnosed individuals with a molecularly confirmed diagnosis of pEDS will be important to further define the clinical features.
Hepatitis, fulminant viral, susceptibility to
MedGen UID:
1684882
Concept ID:
C5231406
Finding
Hermansky-Pudlak syndrome 11
MedGen UID:
1727728
Concept ID:
C5436936
Disease or Syndrome
Hermansky-Pudlak syndrome (HPS) is characterized by oculocutaneous albinism, a bleeding diathesis, and, in some individuals, pulmonary fibrosis, granulomatous colitis, or immunodeficiency. Ocular findings include reduced iris pigment with iris transillumination, reduced retinal pigment, foveal hypoplasia with significant reduction in visual acuity (usually in the range of 20/50 to 20/400), nystagmus, and increased crossing of the optic nerve fibers. Hair color ranges from white to brown; skin color ranges from white to olive and is usually a shade lighter than that of other family members. The bleeding diathesis can result in variable bruising, epistaxis, gingival bleeding, postpartum hemorrhage, colonic bleeding, and prolonged bleeding with menses or after tooth extraction, circumcision, and other surgeries. Pulmonary fibrosis, a restrictive lung disease, typically causes symptoms in the early thirties and can progress to death within a decade. Granulomatous colitis is severe in about 15% of affected individuals. Neutropenia and/or immune defects occur primarily in individuals with pathogenic variants in AP3B1 and AP3D1.

Professional guidelines

PubMed

Di Stefano M, Polizzi A, Santonocito S, Romano A, Lombardi T, Isola G
Int J Mol Sci 2022 May 5;23(9) doi: 10.3390/ijms23095142. PMID: 35563531Free PMC Article
Innes NP, Ricketts D, Chong LY, Keightley AJ, Lamont T, Santamaria RM
Cochrane Database Syst Rev 2015 Dec 31;2015(12):CD005512. doi: 10.1002/14651858.CD005512.pub3. PMID: 26718872Free PMC Article
Teughels W, Dhondt R, Dekeyser C, Quirynen M
Periodontol 2000 2014 Jun;65(1):107-33. doi: 10.1111/prd.12020. PMID: 24738589

Recent clinical studies

Etiology

Geetha Priya PR, Asokan S, Janani RG, Kandaswamy D
Indian J Dent Res 2019 May-Jun;30(3):437-449. doi: 10.4103/ijdr.IJDR_805_18. PMID: 31397422
Ccahuana-Vasquez RA, Adam R, Conde E, Grender JM, Cunningham P, Goyal CR, Qaqish J
Int J Dent Hyg 2019 May;17(2):153-160. Epub 2018 Dec 19 doi: 10.1111/idh.12372. PMID: 30375187Free PMC Article
Pawlaczyk-Kamieńska T, Torlińska-Walkowiak N, Borysewicz-Lewicka M
Adv Clin Exp Med 2018 Oct;27(10):1397-1401. doi: 10.17219/acem/70417. PMID: 30058781
Newbrun E
J Periodontol 1996 Jun;67(6):555-61. doi: 10.1902/jop.1996.67.6.555. PMID: 8794964
Tiainen L, Asikainen S, Saxén L
Community Dent Oral Epidemiol 1992 Apr;20(2):87-9. doi: 10.1111/j.1600-0528.1992.tb00683.x. PMID: 1555394

Diagnosis

Pawlaczyk-Kamieńska T, Torlińska-Walkowiak N, Borysewicz-Lewicka M
Adv Clin Exp Med 2018 Oct;27(10):1397-1401. doi: 10.17219/acem/70417. PMID: 30058781
Hujoel PP, Lingström P
J Clin Periodontol 2017 Mar;44 Suppl 18:S79-S84. doi: 10.1111/jcpe.12672. PMID: 28266117
Herrera D, Alonso B, de Arriba L, Santa Cruz I, Serrano C, Sanz M
Periodontol 2000 2014 Jun;65(1):149-77. doi: 10.1111/prd.12022. PMID: 24738591
Teughels W, Dhondt R, Dekeyser C, Quirynen M
Periodontol 2000 2014 Jun;65(1):107-33. doi: 10.1111/prd.12020. PMID: 24738589
Newbrun E
J Periodontol 1996 Jun;67(6):555-61. doi: 10.1902/jop.1996.67.6.555. PMID: 8794964

Therapy

Zini A, Mazor S, Timm H, Barker ML, Grender JM, Gerlach RW, Biesbrock AR
Can J Dent Hyg 2021 Jun 1;55(2):85-94. PMID: 34221032Free PMC Article
Geetha Priya PR, Asokan S, Janani RG, Kandaswamy D
Indian J Dent Res 2019 May-Jun;30(3):437-449. doi: 10.4103/ijdr.IJDR_805_18. PMID: 31397422
Hujoel PP, Lingström P
J Clin Periodontol 2017 Mar;44 Suppl 18:S79-S84. doi: 10.1111/jcpe.12672. PMID: 28266117
Littlewood SJ, Millett DT, Doubleday B, Bearn DR, Worthington HV
Cochrane Database Syst Rev 2016 Jan 29;2016(1):CD002283. doi: 10.1002/14651858.CD002283.pub4. PMID: 26824885Free PMC Article
Innes NP, Ricketts D, Chong LY, Keightley AJ, Lamont T, Santamaria RM
Cochrane Database Syst Rev 2015 Dec 31;2015(12):CD005512. doi: 10.1002/14651858.CD005512.pub3. PMID: 26718872Free PMC Article

Prognosis

Pawlaczyk-Kamieńska T, Torlińska-Walkowiak N, Borysewicz-Lewicka M
Adv Clin Exp Med 2018 Oct;27(10):1397-1401. doi: 10.17219/acem/70417. PMID: 30058781
Hujoel PP, Lingström P
J Clin Periodontol 2017 Mar;44 Suppl 18:S79-S84. doi: 10.1111/jcpe.12672. PMID: 28266117
Chapple IL, Bouchard P, Cagetti MG, Campus G, Carra MC, Cocco F, Nibali L, Hujoel P, Laine ML, Lingstrom P, Manton DJ, Montero E, Pitts N, Rangé H, Schlueter N, Teughels W, Twetman S, Van Loveren C, Van der Weijden F, Vieira AR, Schulte AG
J Clin Periodontol 2017 Mar;44 Suppl 18:S39-S51. doi: 10.1111/jcpe.12685. PMID: 28266114
Herrera D, Alonso B, de Arriba L, Santa Cruz I, Serrano C, Sanz M
Periodontol 2000 2014 Jun;65(1):149-77. doi: 10.1111/prd.12022. PMID: 24738591
Newbrun E
J Periodontol 1996 Jun;67(6):555-61. doi: 10.1902/jop.1996.67.6.555. PMID: 8794964

Clinical prediction guides

Geetha Priya PR, Asokan S, Janani RG, Kandaswamy D
Indian J Dent Res 2019 May-Jun;30(3):437-449. doi: 10.4103/ijdr.IJDR_805_18. PMID: 31397422
Pawlaczyk-Kamieńska T, Torlińska-Walkowiak N, Borysewicz-Lewicka M
Adv Clin Exp Med 2018 Oct;27(10):1397-1401. doi: 10.17219/acem/70417. PMID: 30058781
Delwel S, Binnekade TT, Perez RSGM, Hertogh CMPM, Scherder EJA, Lobbezoo F
Clin Oral Investig 2018 Jan;22(1):93-108. Epub 2017 Nov 15 doi: 10.1007/s00784-017-2264-2. PMID: 29143189Free PMC Article
Hujoel PP, Lingström P
J Clin Periodontol 2017 Mar;44 Suppl 18:S79-S84. doi: 10.1111/jcpe.12672. PMID: 28266117
Newbrun E
J Periodontol 1996 Jun;67(6):555-61. doi: 10.1902/jop.1996.67.6.555. PMID: 8794964

Recent systematic reviews

Geetha Priya PR, Asokan S, Janani RG, Kandaswamy D
Indian J Dent Res 2019 May-Jun;30(3):437-449. doi: 10.4103/ijdr.IJDR_805_18. PMID: 31397422
Kotsakis GA, Lian Q, Ioannou AL, Michalowicz BS, John MT, Chu H
J Periodontol 2018 May;89(5):558-570. doi: 10.1002/JPER.17-0368. PMID: 29520910Free PMC Article
Delwel S, Binnekade TT, Perez RSGM, Hertogh CMPM, Scherder EJA, Lobbezoo F
Clin Oral Investig 2018 Jan;22(1):93-108. Epub 2017 Nov 15 doi: 10.1007/s00784-017-2264-2. PMID: 29143189Free PMC Article
Littlewood SJ, Millett DT, Doubleday B, Bearn DR, Worthington HV
Cochrane Database Syst Rev 2016 Jan 29;2016(1):CD002283. doi: 10.1002/14651858.CD002283.pub4. PMID: 26824885Free PMC Article
Innes NP, Ricketts D, Chong LY, Keightley AJ, Lamont T, Santamaria RM
Cochrane Database Syst Rev 2015 Dec 31;2015(12):CD005512. doi: 10.1002/14651858.CD005512.pub3. PMID: 26718872Free PMC Article

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