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Wound Healing and Ficus hispida Linn. – Overview

30 Sep


Plants have been the major source of drugs in Indian system of medicine and other ancient systems in the world. Earliest description of curative properties of medicinal plants is found in Rig-Veda, Charaka Samhita and Sushrusha Samhita give extensive description on various medicinal herbs. Information on medicinal plants in India has been systematically organized. India has an ancient heritage of traditional medicine.The materia medica of India provides a great deal of information on the folklore practices and traditional aspects of therapeutically important natural products.Indian traditional medicines based on various systems including Ayurveda, Siddha, Unani and Homeopathy[1].

Wound healing:                                                                                                   

Healing is the process by which the cells in the body regenerate and repair to reduce the size of a damaged or necrotic area. Healing incorporates both the removal of necrotic tissue (demolition), and the replacement of this tissue.

Wound healing is a complex phenomenon that results in the restoration of disrupted anatomical continuity and disturbed functional status of the skin [2] accomplished by several processes which involve fibro genesis, neo-vascularization, wound contraction and epithelization [3] .The basic principle of optimal wound healing is to minimize tissue damage and provide adequate tissue perfusion and oxygenation, proper nutrition and moist wound healing environment to restore the [4].

Herbal medicines have been the basis of Ayurveda, Unani and Siddha. One of the surveys conducted by the WHO reports that more than 80% of the world’s population still depends upon the traditional medicines for various diseases. In the developed countries 25 percent of the chronic wounds may even lead to multiple organ failure of death of the patients. Wounds are the physical injuries that result in an opening or breaking of the skin and appropriate method for healing of wounds is essential for the restoration of disrupted anatomical continuity and disturbed functional status of the skin [5-6].




Wounds are classified as open and closed wound on the underlying cause of wound creation and acute and chronic wounds on the basis of physiology of wound healing.

Open wounds:

In this case blood escapes the body and bleeding is clearly visible. It is further classified as: Incised wound, Laceration or tear wound, Abrasions or superficial wounds, Puncture wounds, Penetration wounds and gunshot wounds [7].

Closed wounds:

In closed wounds blood escapes the circulatory system but remains in the body. It includes Contusion or bruises, heamatomas or blood tumor, Crush injury etc.

Acute wounds:

Acute wound is a tissue injury that normally precedes through an orderly and timely reparative process that results in sustained restoration of anatomic and functional integrity. Acute wounds are usually caused by cuts or surgical incisions and complete the wound healing process within the expected time frame [8].

Chronic wounds:

Chronic wounds are wounds that have failed to progress through the normal stages of healing and therefore entera state of pathologic inflammation chronic wounds either require a prolonged time to heal or recur frequently. Local infection, hypoxia, trauma, foreign bodies and systemic problems such as diabetes mellitus, malnutrition, immunodeficiency or medications are the most frequent causes of chronic wounds [8, 9].


The Inflammatory phase:

The inflammatory phase starts immediately after the injury that usually last between 24 and 48 hrs and may persist for up to 2 weeks in some cases the inflammatory phase launches the haemostatic mechanisms to immediately stop blood loss from the wound site. Clinically recognizable cardinal sign of inflammation, rubor, calor, tumor, dolor and function-laesa appear as the consequence. This phase is characterized by vasoconstriction and platelet aggregation to induce blood clotting and subsequently vasodilatation and phagocytosis to produce inflammation at the wound site [10].

Fibroblastic phase:

The second phase of wound healing is the fibroplastic phase that lasts upto 2 days to 3 weeks after the inflammatory phase. This phase comprises of three steps viz., granulation, contraction and epithelialisation. In the granulation step fibroblasts form a bed of collagen and new capillaries are produced. Fibroblast produces a variety of substances essential for wound repair including glycosaminoglycans and collagen. Under the step of contraction wound edges pull together to reduces the defects in the third step epithelial tissues are formed over the wound site [11].

Epithelization phase:

 Epithelial cell migration is one of the vital processes of wound healing. The stem cells of epithelium must detach from the edges of the wound and migrate into wound. Normally dermal basal cells adhere to each other and to the underline basal layer of the dermis. Following mobilization, epithelial cells begin to enlarge and migrate down and across the wound. Transected hair follicles also contribute to the number of migrating epithelial cells. Epithelial cell migrating across wound usually move along the basal lamina or fibrin deposits, this phenomenon is called contact guidance and is an important factor in epithelial migration. Epithelial migration is followed by increased mytosis of epithelium. Recent evidence suggests that a water soluble heatlabile substance called chalone which is secreted at the wound site is responsible for regulation for mytosis. [12]


Prolifrative phase:

Proliferative Phase (2 days to 3 weeks) includes: Granulation stage: Fibroblasts lay bed of collagenFills defect and produces new capillariesContraction stage: Wound edges pull together to reduce defect. Epithelialization stage: Crosses moist surface cell travel about 3 cm from point of origin in all directions [13].


Wound contraction is caused by the action of differentiated fibroblasts (myofibroblasts) in the granulation tissue, which contain filaments of smooth muscle actin. Contraction of these fibroblasts makes the wound margins move toward the center of the wound.[14,15] Wound contraction started sooner in ponies than in horses and it was significantly more pronounced in ponies .Additionally, it was significantly more pronounced in body wounds compared with the limb wounds. As a result, second intention wound healing was significantly faster in ponies

than in horses, and significantly faster in body wounds than in metatarsal wounds.[16] Histology showed that myofi-broblasts were more organized in the wounds of the ponies: the myofibroblasts in the newly formed granulation tissue were transformed into a regularly organized pattern within 2 weeks, in which the cells were orientated perpendicular to the vessels and parallel to the wound surface. This appears to be a more favorable condition for wound contraction to occur. In the horses, myofibroblast organization took much longer. No differences were found in the number of fibroblasts, the amounts of smooth muscle actin and collagen.[17] Further research was performed to investigate whether the differences in wound contraction between horses and ponies were caused by differences in the inherent contraction capacity of fibroblasts or the local environment of the fibroblasts. It was found that no differences existed in the inherent contraction capacity of fibroblasts from ponies and horses in vitro.[18] However, the level of Transforming Growth Factor , the most important instigator of wound contraction, was significantly higher in the granulation tissue of pony wounds compared with horse wounds.


Remodeling phase:

This phase last for 3 weeks to 2 years. New collagen is formed in this phase. Tissue tensile strength is increased due to intermolecular cross-linking of collagen via vitamin-C dependent hydroxylation. The scar flattens and scar tissues become 80% as strong as the original [19, 20].

The wound healing activities of plants have since been explored in folklore. Many Ayurvedic herbal plants have a very important role in the process of wound healing. Plants are more potent healers because they promote the repair mechanisms in the natural way. Extensive research has been carried out in the area of wound healing management through medicinal plants. Herbal medicines in wound management involve disinfection, debridement and providing a moist environment to encourage the establishment of the suitable environment for natural healing process [21].







Plant Name


Family Plant part used Reference


Agave cantala Roxb. Agavaceaae LF 22


Annona squamosa L Annonaceae LF 23
3  Aporusa lindleyana


Euphorbiaceae LF 24
4  Bidens biternata


Asteraceae LF 25
5  Blumea lacera


Asteraceae LF 22


6 Calycopterisfloribunda. Combretaceae


LF 26
7  Chloroxylon swietenia


Rutaceae LF 27
8 Colebrookeaoppositifolia


Lamiaceae LF 22
9  Ficus racemosa L.


Moraceae BK,  LF &


10 Piper betel L. Piperacea LF 29


11 Acacia catechu Mimosaceae BK 30


12 Ficus bengalensis L., Moraceae LF 31


13 Datura stramonium L. Solanaceae LF 30


14 Ficus religiosa L. Moraceae BK 31



LF- Leaf, BK- Bark and FR- Fruit



Plant Name                      Ficus hispidaLinn.

Kingdom                          Plantae

Division Magnoliopsida
Class Magnoliopsida
Subclass  Dilleniidae
Order Rosales
Family Moraceae
Genus Ficus
Spcies hispida

Botanicalname              Ficus hispida Linn.



Vernacular names

Hindi –             Global, Kasha, Kala Umbar, Katgularia & Phalgu.

Sanskrit-          Kakodumbarika, Malayuhu, Phalgu & Phanika.

Gujarati-        Umbar English

Malayalam –    Kaattaththi, Paarakam


ficus hispida

Photograph of the Ficus hispida Linn.

PLANT DESCRIPTION:  A moderate sized tree grows up to 5 meters in height. Leaves opposite, long, with scrubby surfaces, pubescent; receptacles fascicled in the stem, obovoid, hispid, and green turns yellow when ripe.

Distribution: Throughout India growing wild in evergreen forests and waste lands.
Traditional Uses: According to Ayurveda, it is astringent to bowels; useful in treatment of biliousness, ulcers, erysipelas, vomiting, vaginal complains, fever, inflammations, leukoderma, psoriasis, hemorrhoids, ulcers and leprosy. [32]

Chemical constituents: Oleanolic acid, β-sitosterol, triterpenoids, flavonoids,

Pharmacological Uses[33-38]:

  • Ghosh R et al., Hypoglycemic activity of ficus hispida (bark) in normal and diabetic albino rats. Indian J Pharmacol 2004; 36: 222-225.
  • Shanmugarajan TS, et al., Cardioprotective effect of ficus hispida linn: On cyclophosphamide provoked oxidative myocardial injury in a rat model. Int J Pharmacol 2008; 1:1-10.
  • Sivaraman D et al., Sedative and anticonvulsant activities of the methanol leaf extract of ficus hispida linn. Drug Invent Today 2009; 1: 23-27.
  • Huong VN et al., A strong anticancer agent isolated from the leaves of Ficus hispida L. Tap Chi Hoa Hoc 2006; 44: 345-9.
  • Vishnoi SP et al., Evaluation of anti-inflammatory activity of leaf extracts of Ficus hispida. Indian J Nat Prod 2004; 20: 27-9.
  • Mandal SC et al., Studies on antidiarrhoeal activity of ficus hispida. Leaf extract in rats. Fitoterapia 2002; 73: 663-667.



1.          Sachdev Yadav, Mayank Kulshreshtha, Mradul Goswami, Chandana V.Rao and Veena SharmaJournal of Applied Pharmaceutical Science 01 (01); 2011: 38-41
2.           Perumal SR, Ignacimuthu S, Patric RD, Preliminary screening of ethnomedicinal plants from India, Eur Rev Med Pharmacol Sci, 12, 2008, 1-7
3.          Fabricant DS, Farnsworth NR, The value of plants used in traditional medicine for drug discovery, Environ Health Pers, 109 (Suppl 1), 2001, 69-75.
4.          Priya KS, Gnanamani A, Radhakrishnan N, Babu, Healing potential of Datura alba on burn wounds in albino rats, J. Ethnopharmacol., 83, 2002, 193-199.
5.          Steenkamp V, Mathivha E, Gouws MC, Rensburg CEJ, Studies on antibacterial, antioxidant and fibroblast growth stimulation of wound healing remedies from South Afr. J. Ethnopharmacol., 95, 2004, 353–357.
6.          Principe P, Monetising the pharmacological benefits of  plants. US Environmental protection Agency,Washington, D.C. 2005, 1991
7.          Strodtbeck F, Physiology of wound healing, Newborn InfantNurs. Rev, 1, 2001, 43-45.
8.          Kumar B, Vinaykumar M, Govindarajan R, Pushpangadan P, Ethanopharmacological approaches to wound healingexploring medicinal plants of India, J.Ethanopharmacol., 114, 2007, 103-113.
 9.          Roberts PR, Black KW, Santamauo JT, Zaloga GP, Dietry peptides improve wound healing following surgery,Nutrition, 14, 1998, 266-269
10.      Li J, Chen J, Kirsener R, Pathophysiology of acute wound healing, Clin. Dermatol., 25,   2007, 9-18
11.      Stadelmalmann WK, Digenis AG, Tobin GR, Physiology and healing dynamics of chronic cutaneous wounds, Am. J.Surg. 176, 1998, 26S-38S
12.      Dr. Tamara et al. 2008, 12 book of pathophysiology basis for phase of wound healing.
13.      Romanian Biotechnological Letters  Copyright © 2008 Bucharest University. . Romanian Society of Biological Sciences Vol. 14, No. 4, 2009, pp. 4597-4605 Printed in Romania. All rights reserved.
14.       Clark RAF: Biology of dermal repair. Dermatol Clin 11:647-666, 1993
15.      Darby I, Skalli O, Gabbiani G: _-Smooth muscle actin is transiently expressed by myofibroblasts   during experimental wound healing. Lab Invest 63:21-29, 1990
16.      Jacobs KA, Leach DH, Fretz PB, et al: Comparative aspects of the healing of excisional wounds on the leg and body of horses. Vet Surg 13:83-90, 198
17.      Wilmink JM, van Weeren PR, Stolk PWT, et al: Differences in second intention wound healing between horses and ponies: Histological aspects. Equine Vet J 31:61-67, 1999
18.       Wilmink JM, Nederbragt H, van Weeren PR, et al: Differences in wound contraction between horses and ponies: the in vitro contraction capacity of fibroblasts. Equine Vet J 33:499-505, 2001
19.      Madden JW, Peacock EE, Studies on the biology of collagen during wound healing. I. Rate of collagen synthesis and deposition in cutaneous wounds of the rat, Surgery, 64, 1968, 288-294.
20.      Prockop DJ, Kivirikko KI, Tuderman L, Guzman NA, The biosynthesis of collagen and its disorders, N.Engl. J. Med.,301, 1979, 13-23.
21.      Purna SK, Babu M, Collagen based dressings/a review.  Burns 26, 2000, 54-62.
22.      Upadhyaya, O.P et al. (1998). Skin treatments of Bihar plants. Pharmaceutical Biology 36, 20–24
23.       Dash, S.S., Misra, M.K., 1999. Taxonomic survey and systematic census of
economic plants of Narayana Patna Hills of Koraput Dist., Orissa. Journal
of Economic and Taxonomic Botany 23, 473–498.
24.       Bhandary, M.J., Chandrasekhar, K.R., 2003. Herbal treatments for veterinary
diseases from the coastal districts of Karnataka, India. Journal of Economic
and Taxonomic Botany 27, 648–655
25.      Begum, D., Nath, S.C., 2000. Ethnobotanical reviewof medicinal plants used for
skin diseases and related problems in Northeastern India, Journal of Herbs.
Spices and Medicinal Plants 7, 55–93
26.      Bhandary, M.J., Chandrasekhar, K.R., 2002. Glimpses of ethnic herbal medicine
of coastal Karnataka. Ethnobotany 14, 1–12.
27.      Girach, R.D., Ahmed, A., 1998. Medical ethnobotany of Sundargarh, Orissa,
India. Pharmaceutical Biology 36, 20–24
28.      Punjani, B.L., 2002. Ethnobotanical aspects of some plants of Aravali Hills in
North Gujarat. Ancient Science of Life 21, 268–280.
29.      Sarma, S.K., Bhattacharya, B.K., Devi, B., 2002. Traditional use of herbal  medicine by Modahi tribe of Nalabari district of Assam. Ethnobotany 14, 103–111.
30.      Patil SB, Naikwade NS, Kondawar MS, Magdum CS, Awale  VB, Traditional uses of plants for wound healing in the  Sangli district, Maharashtra, International Journal of Pharm Tech Research, 1(3), 2009, 876-878
31.      Ayyanar M, Ignacimuthu S, Herbal medicines for wound  healing among tribal people in Southern India  Ethnobotanical and Scientific evidences, International Journal of Applied Research in Natural Products, 2(3), 2009,29-42
32.      Kirtikar KR, Basu BD. Indian Medicinal Plants. Periodical Experts, New Delhi, 1975; 2:  2338.
33.      Ghosh R et al., Hypoglycemic activity of ficus hispida (bark) in normal and diabetic albino rats. Indian J Pharmacol 2004; 36: 222-225.
34.      Shanmugarajan TS, et al., Cardioprotective effect of ficus hispida linn: On cyclophosphamide provoked oxidative myocardial injury in a rat model. Int J Pharmacol 2008; 1:1-10.
35.      Sivaraman D et al., Sedative and anticonvulsant activities of the methanol leaf extract of ficus hispida linn. Drug Invent Today 2009; 1: 23-27.
36.      Huong VN et al., A strong anticancer agent isolated from the leaves of Ficus hispida L. Tap Chi Hoa Hoc 2006; 44: 345-9.
37.      Vishnoi SP et al., Evaluation of anti-inflammatory activity of leaf extracts of Ficus hispida. Indian J Nat Prod 2004; 20: 27-9.
38.      Mandal SC et al., Studies on antidiarrhoeal activity of ficus hispida. Leaf extract in rats. Fitoterapia 2002; 73: 663-667.

Author Information:

Ramandeep Singh*

Dept of Pharmacology, Himachal Institute of Pharmacy,  Rampurghat Road, Paonta

Sahib -173025, Himachal Pradesh, INDIA

*Corresponding Author’s Email:

 Address for Correspondences:

Mr. Ramandeep Singh, Assistant Prof.(Pharmacology) Himachal Institute of Pharmacy,  Rampur ghat Road, Paonta Sahib -173025, Himachal Pradesh, INDIA, Email-

Mob- +919736922900,  +919017138383

Health Risks Associated with Type 2 Diabetes

20 Jul

From hearing loss to foot numbness, the complications that result from type 2 diabetes vary as much as the patients. Whether you are a man or a woman, Caucasian or African-American, there are subtle differences in the way the disease progresses. Type 2 diabetes is known to quietly attack various groups of people in slightly different ways.

Type 2 diabetes is the most common form of diabetes, affecting millions of people each year. Some groups have a higher risk for developing the disease, including Native Americans, Asian-Americans and Latinos. However, it is India that has developed the world’s largest diabetes population with over 50.8 million people living with diabetes. While India’s government continues to raise awareness to its public, many other countries are facing the widespread epidemic.  Scientists are not completely sure what mechanism causes the disease; they do know that it causes the body’s cells to either not produce or ignore insulin, a naturally occurring hormone made by the pancreas. Without insulin, glucose in the body does not properly break down. That leads to diabetes complications. The list of type 2 diabetes complications is a long one and covers all parts of the body, from head to toe:

  • Eye complications – Type 2 patients are more at risk for developing glaucoma, cataracts and retina dysfunction.
  • Heart disease – This very real risk is especially prevalent in men with diabetes. Type 2 patients are also at a higher risk for a stroke.
  • Mental health problems – Many patients go through stages of anger, denial and depression, especially when initially diagnosed.
  • Skin disorders – Having diabetes puts patients at an increased risk of getting bacterial and fungal infections, as well as other diabetes-related skin conditions.
  • Sexual dysfunction – Men with diabetes are more likely to suffer from erectile dysfunction and low testosterone.
  • Foot problems – Also called neuropathy, diabetic nerve damage can lessen the ability to feel pain, cold or heat. Neuropathy causes poor blood flow.

From the list, it’s easy to see why it is so important for type 2 patients to be vigilant about their health care. At the initial diagnosis, most doctors will recommend a strict diet, a steady exercise regime and medication to stabilize insulin levels. While a new diet and exercise routine might be difficult to establish, the medication aspect of the process could prove to be even more challenging. That’s because of the lingering safety questions surrounding the most popular type 2 diabetes drug, Actos.

Also known as pioglitazone, Actos has been linked to a variety of life threatening side effects, including congestive heart failure and bladder cancer. The drug is known to cause edema, or swelling, which increases the risk for heart failure. Worse yet, recent studies show that those taking the drug for longer than two years have a more than 80 percent chance of developing bladder cancer. It seems that this drug puts already compromised bodily functions at risk for even more damage. In fact, many users of this medication have filed an Actos lawsuit against the drug manufacturer, Takeda.

Today, many doctors are steering their patients to more trusted medications, such as metformin, as a means to control blood sugar levels. Many feel that the risks that Actos presents are far too great for patients who are already struggling with a life-threatening disease.

Surgery is Better than Medical Management for Non-Alcoholic Fatty Liver Disease

22 Jun


About the Author:

Dr.Abeezar Sarela

Abeezar Sarela specialises in surgery for diseases of the oesophagus and stomach (often referred to as Upper Gastrointestinal Surgery or Upper GI Surgery or Foregut Surgery). There are three areas of sub-specialisation in this area: (1) surgery for obesity & related diseases such as diabetes (Bariatric & Metabolic Surgery);(2) surgery for cancer of the oesophagus and stomach (Surgical Oncology) & (3) surgery for benign disorders, such as gastro-oesophageal reflux disease, hiatus hernia, achalasia cardia and gastroparesis.

He practices in UK at: St James’s University Hospital, Nuffield Hospital, and Spire Hospital. He also operates in India at Hinduja Hospital, Mumbai


Website: (Powered by Websites For Doctors)

Congenital deficiency of the proximal femur

7 Jun

Congenital deficiency of the proximal femur, literature review with a case report

Congenital anomalies of the femur are very uncommon, it is of extreme importance that every case of rare congenital deformity coming under the care of the surgeon should be  reported, as it may be helpful in further investigations both of an embryological and an anatomical nature.  Here by we are presenting a rarity of congenital deficiency of the proximal femur in a child of 3 months.



 Congenital anomalies of the femur and fibular aplasia/hypoplasia are considered as the main anomalies involved in congenital asymmetry of the lower limbs. Congenital anomalies of the femur is a rare anomaly, occurring with a frequency of approximately 0.2/10,000 live births. Congenital anomalies of the femur is described as an outbreak of femoral hypoplasia or aplasia, isolated or associated with fibular and/or ulnar anomalies. It is an uncommon congenital defect that involves the femur and acetabulum in varying degrees. It can either be isolated or in combination with other defects of the lower limbs including absence or hypoplasia of the patella, fibular a/hypoplasia and absence of lateral foot rays.  1-3 


Case report

The female infant of 12 weeks was brought to the hospital with complains of shortening of left lower limb and unable to move that limb, this was the first child, pregnancy and labor being without difficulty. Both parents were 30 years old. Family history and pregnancy were unremarkable. There was no history of maternal diabetes or exposure to any teratogenic agent during the pregnancy. The baby was delivered spontaneously at 39 weeks of gestation. Birth weight was 3500 g (50th centile), length was 50 cm (50th-75th centile), and occipitofrontal head circumference was 34 cm (25th-50th centile). Baby was well nourished for her age, the left lower extremity which is much shorter than the right, In the supine position the child held the left lower extremity in the frog position. Upon standing on the right leg, the left was held in ninety degrees’ external rotation. The child could stand on the left leg by flexing the right knee. Strength of the muscles was good. There is a congenital abnormality of the left femur with a complete absence of the upper half of the femur. The lower portion of the shaft gradually tapers to a point, and ends five centimeters above the epiphyseal line. The upper extremity of this rudimentary bone found in external and superior to the site of the acetabulum, which was undeveloped. The knee joint was clear and normal. The right femur was normal in development and measures sixteen centimeters from the upper to the lower epiphyseal line. The right hip and knee joints were normal. There was no pathology on chest roentgenograms and abdominal ultrasonography. Routine laboratory tests and ophthalmological examination were also normal. Peripheral blood chromosomal analysis showed normal male karyotype (46, XY). The physical examination of the parents including their limbs was normal.



Proximal femoral focal deficiency is a rare malformation of the lower limbs that involves the femur and acetabulum in varying degrees. It may occur with or without fibular hemimelia and can be unilateral or bilateral in presentation. 4 Fibular a/hypoplasia covers a spectrum of malformations including variable degrees of fibular a/hypoplasia ,shortening of the tibia and femur, genu valgum and lateral femoral condyle hypoplasia, knee ligament laxity, tibial bowing, ball and socket ankle joint, tarsal coalitions and missing lateral rays of the foot . 5 It has long been suggested that the basis of such anomalies may involve an alteration of limb “developmental fields”, i.e., tibial and fibular fields 6. However, a specific genetic cause, such as mutations involving a specific gene family, etc., has not been elaborated yet. One such affected putative gene family may be the Hox gene family involved in skeletogenesis both axial and appendicular, as well as in other systems such as the urogenital system 7. The etiology of proximal femoral focal deficiency is unknown. It is known that the development of the limb buds takes place early in fetal life, beginning at about four weeks’ gestation. Various factors act upon the developing limb, resulting in rotation, segmentation, longitudinal growth, and differentiation of elements. The most proximal elements of the limb develop first 8, 9   and the hand and foot follow, being fully formed by the seventh week. Chemical toxicity,radiation,enzyme alterations, viral infections,   and mechanical trauma 10 have produced limb anomalies in humans and experimental animals. Ring has stated that the primary problem is in the enchondral ossification of defective cartilage. Gardner 9 pointed out that failure of skeletal elements to form may be due to factors operating during the period of differentiation. This critical period-at four to eight weeks of fetal life-was defined by studies of thalidomide babies. It is apparent from these and other studies that as the severity of the defect increases, so does the incidence of associated anomalies. The theory advanced by Morgan and Somerville 10. that mechanical trauma to the advancing growth plate interferes with the development of normal infantile valgus, may be appropriate for simple coxa vara, but it does not explain the wide dissociation of fragments seen in the typical case of Proximal femoral focal deficiency.

Congenital deficiency of the proximal femur

Fig 1: Radiographic images of the lower extremities and pelvis showing Normal right lower extremity and   Affected left extremity



1. Hamanishi C. Congenital short femur. Clinical, genetic, and epidemiological comparison of the naturally occurring condition with that caused by thalidomide. J Bone Joint Surg Br 1980; 62: 307-320.

2. Sorge G, Ardito S, Genuardi M, et al. Proximal femoral focal deficiency (PFFD) and fibular a/hypoplasia (FA/H): a model of a developmental field defect. Am J Med Genet 1995; 55: 427-432.

3. Ashkenazy M, Lurie S, Ben-Itzhak I, Appelman Z, Casbi B. Unilateral congenital short femur: a case report. Prenatal Diagn 1990; 10: 67-70.

4. Stormer SV. Proximal femoral focal deficiency. Orthop Nurs 1997; 16(5): 25-31.
5. Caskey PM, Lester EL. Association of fibular hemimelia and clubfoot. J Pediatr Orthop 2002; 22: 522-525.

6. Lewin SO, Opitz JM. Fibular a/hypoplasia: review and documentation of the fibular developmental field. Am J Med Genet 1986; 91: 347-356.

7. Goodman FR. Limb malformation and the human Hox genes. Am J Med Genet 2002; 112: 256-265.s been suggested that   1938 and 1948).

8. Borggreve, J., Kniegelenksersatz dutch das in der Beinlangsachse um 180′ gedrehte Fussgelenk. Arch. Orthopad. Chir. 28:175-178. 1930.

9. Gardner, E. D. The development and growth of bones and joints. A.A.O.S. Instructional Course Lecture. J. Bone Joint Sure. 45A(4):856-862, 1963.

10. Morgan, J. D., and E. W. Somerville. Normal and abnormal growth at the upper end of the femur. J. Bone Joint Surg. 42B:264-272, 1960.


About the Author:
Dr Ramji lal Sahu

Associate professor, Department Of Orthopaedics, SMS and RI, Sharda University.

Greater Noida, U. P., India

Contact: Mobile no. 09871120703, Email



Understanding Female Sexual Response: An overview

10 May

About the Author:
Dr. Anand Shinde, M.D., Gyn

IVF Consultant & Director of Andrology At“IVF Pune”, 7th floor Deenanath Mangeshkar Hospital Pune-4
Phone : +91 20 26876396 / 40151777
Mobile : +91 9822012166
Email :

Dr Anand Shinde is Trained in High Risk Pregnancy Management & also in A. R. T. at Birmingham. He currently practices with Nirmiti Clinic and IVF Pune.

Website: (Powered by Websites For Doctors)

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