{"id":58096,"date":"2024-06-25T11:54:35","date_gmt":"2024-06-25T11:54:35","guid":{"rendered":"https:\/\/biomedpharmajournal.org\/?p=58096"},"modified":"2024-07-04T11:07:36","modified_gmt":"2024-07-04T11:07:36","slug":"acquired-high-flow-arteriovenous-malformation-of-the-lower-lip-induced-by-hormonal-variation-report-of-a-rare-case-and-review","status":"publish","type":"post","link":"https:\/\/biomedpharmajournal.org\/staging\/vol17no2\/acquired-high-flow-arteriovenous-malformation-of-the-lower-lip-induced-by-hormonal-variation-report-of-a-rare-case-and-review\/","title":{"rendered":"Acquired High Flow Arteriovenous Malformation of the Lower Lip Induced by Hormonal Variation- Report of a Rare Case and Review"},"content":{"rendered":"\n

Introduction<\/strong><\/p>\n\n\n\n

Arteriovenous\nmalformations (AVMs) are uncommon vascular lesions consisting of aberrant connections\nbetween arteries and veins without normal intervening capillaries.1<\/sup> AVMs\noccurring in the head and neck region are rare lesions that affect only 0.1% of\nthe general population, while extracranial AVMs make up only 8.1% of those\ncases.2,<\/strong>3,<\/strong>4<\/sup> AVMs may be congenital or acquired.2<\/sup>Most of the oral AVMs are congenital and the acquired type is very\nrarely reported.5<\/sup>Congenital AVMs are vascular malformations\ncaused by the differentiation failure of the embryonic vascular network.1<\/sup>The most common causes identified for acquired AVMs are trauma and\nhormonal changes. Oral-acquired AVM can be a fatal benign disease and is\nchronic and progressive.5<\/sup><\/p>\n\n\n\n

AVMs\nin the oral cavity can obstruct speech, mastication, and deglutition and\nfrequently get traumatized resulting in ulceration and secondary infections.1<\/sup>Due to the possibility of uncontrolled bleeding during invasive oral\noperations or examinations, they are among the most infamous vascular lesions.4<\/sup>Spontaneous haemorrhage is also a possible hazard.1<\/sup>They\nmight be asymptomatic or produce functional and cosmetic issues such as\nasymmetry of the face, discomfort, bone destruction and sudden haemorrhage.6<\/sup> Accurate diagnosis of AVMs is critical and their management\nremains challenging.1<\/sup>The likelihood of progression and\nrecurrence is also very high.7<\/sup>Recurrence of the lesion frequently\nlarger than its original size is a common consequence of inadequate excision.5<\/sup><\/p>\n\n\n\n

The\nlips play an important role in mastication, speech and facial aesthetics. Lip vascular\nanomalies can adversely impact functionality and facial appearance.8<\/sup> In this article, we discuss a very rare case of\nacquired AVM of the lower lip occurring due to hormonal variation in a female\npatient of 58 years age. <\/p>\n\n\n\n

Case report<\/strong><\/p>\n\n\n\n

A\nfemale patient of 58\u2011years age reported to the dental hospital with swelling of\nthe lower lip as the chief complaint. The swelling was painless and started as\na peanut-sized lesion 6 years ago and slowly increased to the current size; it bled\noccasionally on mild manipulation. There was no history of trauma to the lips. The\npatient reported that the appearance of the swelling coincided with the onset\nof her menopause phase. Dental, medical and family history were not relevant. On\ngeneral physical examination, all vital signs were normal. <\/p>\n\n\n\n

Extra\noral examination revealed a diffuse swelling on the left lateral side of the lower\nlip measuring approximately 2 \u00d72\u00d71.5 cm in size. (Figure 1)<\/strong> The\nvermilion border of the lip appeared slightly erythematous in colour. Intraoral\nexamination of swelling revealed erythematous but intact overlying mucosa. The\nswelling existed opposite the left mandibular lateral incisor-canine region.\nHard tissue examination was not contributory. On palpation, the swelling was\nnon-tender, had diffuse borders, soft consistency and was readily compressible with\nblanching and pulsations. <\/p>\n\n\n\n\n\n
\"\"<\/td>\n\n

Figure 1: <\/strong>Diffuse swelling on the lateral part of the lower lip.<\/strong><\/p>\n

<\/p>\n

Click here to view Figure<\/a><\/p>\n<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n\n\n

The\nlesion was diagnosed provisionally as Haemangioma based on clinical findings\nand history. Vascular malformations (VM), vascular tumours, pyogenic granuloma,\nmucocele, and cheilitis granulomatosum were considered differential diagnoses. On routine blood investigations,\nall values were within the normal range. To confirm diagnosis Colour Doppler Ultrasonography\nof the lower lip was suggested.<\/p>\n\n\n\n

Ultrasonography investigation revealed submucosal soft tissue thickening with tufts of vascular channels showing both arterial and venous flow. The arterial feeder appeared to be a branch of the buccal and superior alveolar arteries. The findings suggested High-flow Arteriovenous malformation of the lower lip. (Figure 2)<\/p>\n\n\n\n\n\n
\"\"<\/td>\n\n

Figure 2: <\/strong>Colour Doppler Ultrasonography of lower lip showing tuft of vascular channels with both arterial and venous flow.<\/strong><\/p>\n

<\/p>\n

Click here to view Figure<\/a><\/p>\n<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n\n\n

Following\nthe diagnosis of High flow AVM, sclerotherapy was opted as the treatment choice.\n1% sodium tetradecyl sulphate was used as the sclerosing agent to induce\nvascular sclerosis. 1 ml of the sclerosant was directly injected into the centre\nof the lesion with slow infiltration using an insulin needle. The patient was\ngiven post-operative instructions and was prescribed antibiotics and\nanalgesics. She was recalled after a week for a second dose of the sclerosant. The\npatient decided against further interventions and reported that the lesion had\nreduced in size and the result was aesthetically satisfactory to her.  On examination of the lesion at 1-month\nfollow-up, it had undergone fibrosis and a significant reduction in size. At 6\nmonths follow-up, the lesion remained stable and the patient was comfortable\nwith the result. Since then, the patient has been on regular follow-up with no\nsubsequent consequences. <\/p>\n\n\n\n

Discussion<\/strong><\/p>\n\n\n\n

AVMs\nare vascular malformations of fast-flow type, composed of an abnormal capillary\nnetwork between the arterial and venous systems, resulting in the shunting of\nblood. AVMs are dangerous types of VMs, causing substantial deformity and\nfunctional disability.9<\/sup>They present in congenital (defective\nTGF\u2011\u03b2), acquired and familial forms (RASA1 gene mutation).4<\/sup>Terms\nsuch as arteriovenous shunt, arteriovenous aneurysm and arteriovenous fistula are\nalso used synonymously to refer to AVMs.1<\/sup><\/p>\n\n\n\n

Clinical features: AVMs can be asymptomatic or can create functional impairments. They can present clinically as compressible pulsatile swellings1<\/sup>with some lesions exhibiting a palpable thrill and can occasionally be auscultated for a bruit.5<\/sup>An audible bruit is not produced by Intraosseous lesions.1<\/sup>The overlying skin may appear erythematous;10<\/sup>or have a true port-wine stain.11<\/sup>Neurosensory alterations can sometimes cause numbness in the affected area.1<\/sup>Local hyperthermia, bleeding, ulceration, impaired function due to arterial steal and ischaemia may also be noted.<\/p>\n\n\n\n

In\nthe oral cavity, the anterior portion of the tongue is the most frequent location\nof occurrence of AVMs followed by the palate, gingiva and buccal mucosa.11<\/sup>Intraoral lesions may be symptomless in many cases.1<\/sup> Intraosseous VM involving alveolar bone can result in\nmobile teeth, widening of periodontal ligament spaces, pericoronal bleeding, facial\nasymmetry and occlusal anomalies.1,5<\/sup> Acquired\nAVMs typically occur as asymptomatic, soft or firm pulsatile swellings.5  <\/strong><\/sup>Our case presented with the typical\nfeatures of acquired AVMs and was painless, slow growing, pulsatile, diffuse swelling\non the lower lip with occasional history of bleeding. <\/p>\n\n\n\n

AVMs can progress through four stages and can be graded by severity using the ISSVA (International Society for the Study of Vascular Anomalies) recognized clinical staging system introduced by Schobinger in 1990.5<\/sup>The clinical stages of AVM are presented in Table 1. <\/p>\n\n\n\n

Table 1: Clinical stages of Arteriovenous malformations<\/strong>9<\/sup> <\/p>\n\n\n\n\n\n\n\n\n\n
\n

Stage<\/strong><\/p>\n<\/td>\n

\n

Clinical features<\/strong><\/p>\n<\/td>\n<\/tr>\n

\n

Stage 1- Quiescence<\/p>\n<\/td>\n

\n

Pink-bluish stain, local hyperthermia and arteriovenous shunting demonstrated by Doppler.9<\/sup> (Progression to the next stage is usually induced by trauma, puberty, pregnancy or any interventions like ligation of feeder arteries, incomplete excision and laser treatment)5<\/sup><\/p>\n<\/td>\n<\/tr>\n

\n

Stage 2- Expansion<\/p>\n<\/td>\n

\n

Stage 1 lesion showing enlargement, pulsations, thrill, bruit and tense\/tortuous veins.<\/p>\n<\/td>\n<\/tr>\n

\n

Stage 3- Destruction<\/p>\n<\/td>\n

\n

Stage 2 lesion showing dystrophic skin changes, ulceration, tissue necrosis, bleeding or persisting pain.<\/p>\n<\/td>\n<\/tr>\n

\n

Stage 4- Decompensation<\/p>\n<\/td>\n

\n

Extensive AVM causing increased cardiac output and heart failure.<\/p>\n<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

 <\/p>\n\n\n

Classification<\/strong><\/p>\n\n\n\n

Vascular malformations are a diverse group of vessel disorders that can involve any part of the vascular system.2<\/sup>VMs can be classified depending on the vessel type involved as capillary, venous, lymphatic, and arteriovenous. Forbes et al. further differentiated VMs into high-flow (arteriovenous) and low-flow lesions (capillary, venous, lymphatic, or combinations thereof) based on the fluid velocity through their system.2,6,10<\/sup> AVMs are the most aggressive of all VMs, that can cause severe morbidity and deformity.2<\/sup> Our case was classified as High-flow arteriovenous malformation.<\/p>\n\n\n\n

Etiopathogenesis<\/strong><\/p>\n\n\n\n

VMs are a type of vascular anomaly induced by the aberrant formation of vascular elements during embryogenesis.9<\/sup>Few prevailing theories of pathogenesis are TGF-beta signalling defects and a genetic two-hit hypothesis.11,12<\/sup>They are usually congenital but may not be evident clinically; later on, they show growth in proportion to the body volume and do not exhibit spontaneous involution.6<\/sup>The lesion enlarges due to variations in the blood flow and pressure, vascular channel dilatation, shunting and collateral proliferation. These do not exhibit endothelial cell turnover elevation as observed in vascular neoplasms.9<\/sup> Occasionally, rapid growth can follow after trauma, hormonal changes such as puberty or pregnancy, infections6<\/sup>and iatrogenic injury (biopsy, proximal ligation, or subtotal excision).10<\/sup>VMs may sometimes be associated with underlying systemic conditions. Some AVMs associated syndromes are Parkes-Weber syndrome, Bonnet-Dechaume-Blanc syndrome or Wyburn-Mason syndrome, Capillary malformation-AVM syndrome and Cobb syndrome.11<\/sup><\/p>\n\n\n\n

In\nthe case of acquired AVM, a history of trauma, hormonal imbalance or surgery\nusually precedes the proliferation of abnormal vasculature. They usually\nexhibit a single feeder vessel, unlike congenital forms which exhibit several\nfeeder vessels.4<\/sup> In our case, the patient\ngave a history of onset of the lip lesion coinciding with the onset of her\nmenopause phase, thus hormonal variation is the most likely trigger for its\nproliferation. Though hormonal variations occurring during pregnancy and\npuberty have been implicated as the triggers for acquired AVM, on review of the\nliterature, we did not find any other case with menopause as the cause for\nacquired AVM. <\/p>\n\n\n\n

Histology<\/strong><\/p>\n\n\n\n

AVM is an unencapsulated aggregation of blood vessels within the submucosa.5<\/sup> They consist of numerous abnormal arteriovenous shunts without normal intervening capillary plexus. These convoluted vessels consist of multiple compartments of arteries and veins devoid of muscle support, endothelial cell proliferation and giant cells.6<\/sup>The lining of the vessels consists of flattened endothelial cells. The arterial internal elastic lamina may be, interrupted, distorted or reduplicated. The thickness of the muscularis mucosa varies significantly. In close proximity, feeder arteries and veins may be observed.5<\/sup>Unlike proliferative phase haemangiomas, VMs do not exhibit high mitotic activity, or elevated concentrations of type IV collagenase and are negative for basic fibroblast growth factor (bFGF), vascular endothelial growth factor (VEGF) and urokinase markers.13,14,15<\/sup> Inour case, a biopsy was not undertaken to avoid the risk of haemorrhage. Hence the lesion was not histopathologically evaluated. <\/p>\n\n\n\n

Differential diagnosis<\/strong><\/p>\n\n\n\n

Vascular neoplasms, other VMs, and other forms of neoplasms are included in the differential diagnosis of AVM. Haemangiomas should not be confused with AVMs.5<\/sup> They are the most frequent vascular tumours and must be distinguished from vascular malformations as they are managed differently.2<\/sup>Differential diagnoses can also include pyogenic granuloma and hematoma. These are non-pulsatile and do not reveal a combination of arterioles and venules.5<\/sup>Our case was provisionally diagnosed as Haemangioma. Vascular malformations, vascular tumours, pyogenic granuloma, mucocele and cheilitis granulomatosum were considered as differential diagnoses.<\/p>\n\n\n\n

Diagnosis<\/strong><\/p>\n\n\n\n

Fine needle aspiration is a diagnostic aid for evaluating AVMs, albeit it may not differentiate between high and low-flow types. This method is safe, effective, and lowers the risk of fatal or extensive haemorrhage associated with biopsies. Recent advances in imaging modalities for evaluating AVMs have been made.5<\/sup>Doppler ultrasound is usually recommended for evaluation1<\/sup> as it enables quick differentiation between low and high-flow lesions.5<\/sup> It can be best supplemented with MRI and Computed tomography. Angiography is the gold standard diagnostic imaging modality used for the identification of entire VMs, their contributing vessels, flow characteristics1<\/sup>and dangerous anastomosis.4<\/sup>Colour Doppler Ultrasonography was employed in the diagnosis of our case and it revealed the vessel type, feeder vessel and flow characteristics of the lesion.<\/p>\n\n\n\n

Management<\/strong><\/p>\n\n\n\n

Management of AVMs is quite difficult and requires a multidisciplinary strategy1,16<\/sup>which includes interventional radiologists, surgeons, plastic surgeons, anaesthetists and the blood bank. The appropriate management of vascular anomalies depends upon an accurate diagnosis. It is vital to differentiate between haemangiomas and AVMs, and further between high and low-flow types of AVMs.10<\/sup>It is also important to rule out a vascular anomaly when evaluating pulsatile swellings with a history of spontaneous bleeding, before proceeding with any intervention as it may result in uncontrolled and massive haemorrhage.5<\/sup> <\/p>\n\n\n\n

When\nAVM is small and symptomless, close monitoring will suffice, but if it is accompanied\nby pain, ulceration, haemorrhage, deformity or cardiac issues, active treatment\nis necessary.5,6,11,17<\/sup>Treatment varies depending on the\nlesion’s location, extent and flow characteristics. Intraoral lesions can be managed\nby embolization, sclerotherapy, ligation of vessels, curettage, steroid\ninjection, cryotherapy, laser therapy and surgical resection or a combination\nof the above modalities.1,6<\/sup> Combination\ntherapy is the most effective and is considered the gold standard of treatment.7<\/sup>\nThe most frequently used management technique for AVMs is preoperative\nsclerosing agents or embolization, followed by complete surgical removal.2<\/sup><\/p>\n\n\n\n

Surgical\nexcision of lips vascular anomalies should be considered with care, since the\nlips have a distinctive anatomical structure that can be damaged during\nexcision, causing aesthetic issues. Therefore, vascular anomalies should\nideally be surgically excised only when they are minor, well-localized, or\nsolitary lesions.8<\/sup> Regular follow-up with Doppler sonography is\nsuggested as the lesion has a high rate of recurrence.9,18,19<\/sup><\/p>\n\n\n\n

In\nour case, administration of a single dose of 1% sodium tetradecyl sulphate into\nthe lesion was effective in reducing the lesion size. It provided a\nnon-surgical method and aesthetic recovery of the patient. However, as the\npatient did not wish for any further interventions, complete involution of the\nlesion was not achieved. Since then, the patient has been on regular follow-up\nwith no subsequent consequences. <\/p>\n\n\n\n

Conclusion<\/strong><\/p>\n\n\n\n

Although\nacquired AVMs are rarely confronted in the head and neck region, dentists must\nbe aware of them. It is crucial to accurately diagnose oral vascular anomalies\nwith detailed patient history, thorough physical examination and diagnostic\nworkup. Their correct diagnosis and appropriate management need utmost emphasis\nas they can pose unforeseen medical emergencies due to unmanageable bleeding\nwhile performing dental procedures. With the findings of the current case, we\nconclude that hormonal variations occurring during menopause can act as a\ntrigger for the development of acquired AVM. We also recommend menstrual\nhistory be included as part of case history recording in female patients\npresenting with oral vascular lesions. Sclerotherapy is a feasible treatment\nmethod that can effectively resolve vascular malformations. We suggest that early\ndetection, intervention and regular follow-up are required to rule out\npotential recurrence of vascular malformations. <\/p>\n\n\n\n

Declaration of patient consent<\/strong><\/p>\n\n\n\n

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given her consent for her images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.<\/p>\n\n\n\n

Acknowledgements<\/strong><\/p>\n\n\n\n

None<\/p>\n\n\n\n

Conflict of interest<\/strong><\/p>\n\n\n\n

None<\/p>\n\n\n\n

Funding sources<\/strong><\/p>\n\n\n\n

None<\/p>\n\n\n\n

References<\/strong><\/p>\n\n\n\n

  1. Modak R, Mhapuskar A, Hiremutt D, Hebbale M, Gaikwad S. Arteriovenous malformation of the oral cavity: a case report and review of literature. J Pharmaceut Biomed Sci<\/em>. 2016;6(9):514\u2013517<\/li>
  2. Kolarkodi SH, Alnafisah AM. Arteriovenous Malformation of the Lip: A Rare Case Report. Cureus<\/em>. 2020;12(7): e8979. doi:10.7759\/cureus.8979
    CrossRef <\/a><\/li>
  3. Javeed S, Khan FA, Awais M, Khan R, Ain RU, Waheed A. Arteriovenous Malformation of Upper Lip – a short cure for gross deformity. PJMHS<\/em>. 2022;16(3):188-189. doi:10.53350\/pjmhs22163188
     CrossRef <\/a><\/li>
  4. Mohta A, Gupta D, Jain S. A case of acquired arteriovenous malformation of lip: Clinical and mucoscopic evaluation. Indian Dermatol Online J<\/em>. 2021;12(1):198. doi:10.4103\/idoj.IDOJ_542_19
     CrossRef <\/a><\/li>
  5. Pandhare M, Jyoti DB, Mandale M, Suresh RB. Acquired arteriovenous malformation of lip occurring as an occupational hazard: A case report with review of literature. J Oral Maxillofac Pathol<\/em>. 2018;22(2):287. doi:10.4103\/jomfp.JOMFP_4_16
     CrossRef <\/a><\/li>
  6. Jafarian M, Dehghani N, Shams S, Esmaeelinejad M, Aghdashi F. Comprehensive Treatment of Upper Lip Arteriovenous Malformation. J Maxillofac Oral Surg<\/em>. 2016;15(3):394-399. doi:10.1007\/s12663-015-0836-8
    CrossRef <\/a><\/li>
  7. Shobeirian F, Sanei Taheri M, Yeganeh R, Haghighatkhah H. Huge Arteriovenous Malformation of Upper Lip- A Case Report. Iranian Journal of Otorhinolaryngology<\/em>. 2020;32(1):49-52. doi:10.22038\/ijorl.2019.36848.2207<\/li>
  8. Ryu JY, Lee JS, Lee JW, et al. Clinical Approaches to Vascular Anomalies of the Lip. Arch Plast Surg<\/em>. 2015;42(06):709-715. doi:10.5999\/aps.2015.42.6.709
     CrossRef <\/a><\/li>
  9. Bhat VS, Aroor R, Bhandary BSK, Shetty S. Traumatic Arteriovenous Malformation of Cheek: A Case Report and Review of Literature. An International Journal of Otorhinolaryngology Clinics<\/em>. 2013;5(3):173-177. doi:10.5005\/jp-journals-10003-1138
     CrossRef <\/a><\/li>
  10. Pompa V, Valentini V, Pompa G, Di Carlo S, Bresadola L. Treatment of high-flow arteriovenous malformations (AVMs) of the head and neck with embolization and surgical resection. Ann Ital Chir<\/em>. 2011;82(4):253-259.<\/li>
  11. Manjunath SM, Shetty S, Moon NJ, Sharma B, Metta KK, Gupta N, et al. Arteriovenous   Malformation of the Oral Cavity. Case Reports in Dentistry<\/em>. 2014; Article ID 353580, 5 pages   doi:10.1155\/2014\/353580
     CrossRef <\/a><\/li>
  12. Tan S, Marsh P. Arteriovenous Malformation of the Oral Cavity: A Case Report. Oral Hyg Health<\/em>. 2015;03(01). doi:10.4172\/2332-0702.1000174
     CrossRef <\/a><\/li>
  13. Van Doorne L, De Maeseneer M, Stricker C, Vanrensbergen R, Stricker M. Diagnosis and treatment of vascular lesions of the lip. British Journal of Oral and Maxillofacial Surgery<\/em>. 2002;40(6):497-503. doi:10.1016\/S0266-4356(02)00153-5
     CrossRef <\/a><\/li>
  14. Takahashi K, Mulliken JB, Kozakewich HP, Rogers RA, Folkman J, Ezekowitz RA. Cellular markers that distinguish the phases of hemangioma during infancy and childhood. The Journal of clinical investigation<\/em>. 1994;93(6):2357-2364.
     CrossRef <\/a><\/li>
  15. Kr\u00e4ling BM, Razon MJ, Boon LM, et al. E-selectin is present in proliferating endothelial cells in human hemangiomas. The American journal of pathology<\/em>. 1996;148(4):1181.<\/li>
  16. Churojana A, Khumtong R, Songsaeng D, Chongkolwatana C, Suthipongchai S. Life-Threatening Arteriovenous Malformation of the Maxillomandibular Region and Treatment Outcomes. Interv Neuroradiol<\/em>. 2012;18(1):49-59. doi:10.1177\/159101991201800107
     CrossRef <\/a> <\/li>
  17. Siripurapu S, Pasupuleti S, Manyam R, Moturi K, Puvvada D N L. Arteriovenous Malformation of Upper Lip- A Case Report with Literature Review. J Adv Med Biomed Res<\/em>. 2022;30(142):458-462. doi:10.30699\/jambs.30.142.458
     CrossRef <\/a><\/li>
  18. Richter GT, Friedman AB. Hemangiomas and vascular malformations: current theory and management. International journal of pediatrics<\/em>. 2012.
    CrossRef <\/a><\/li>
  19. Fearon JA. Discussion: extracranial arteriovenous malformations: natural progression and recurrence after treatment. Plastic and reconstructive surgery<\/em>. 2010;125(4):1195-1196.
     CrossRef <\/a><\/li><\/ol>\n","protected":false},"excerpt":{"rendered":"

    Introduction Arteriovenous malformations (AVMs) are uncommon vascular lesions consisting of […]<\/p>\n","protected":false},"author":15,"featured_media":0,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[115],"tags":[],"class_list":["post-58096","post","type-post","status-publish","format-standard","hentry","category-vol17no2"],"_links":{"self":[{"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/posts\/58096","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/users\/15"}],"replies":[{"embeddable":true,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/comments?post=58096"}],"version-history":[{"count":5,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/posts\/58096\/revisions"}],"predecessor-version":[{"id":59724,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/posts\/58096\/revisions\/59724"}],"wp:attachment":[{"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/media?parent=58096"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/categories?post=58096"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/tags?post=58096"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}