 The usual norm is to not judge a person by his face, but today we will see why it is important to judge a fetus by its face and multiple genotypes of a phenotype. I am Anjali Bhuvir from St. G. S. Medical College and KEM Hospital, a 30-year-old Graviratu Para-1 lady with third-degree consanguinous marriage, resented at 23 weeks of gestation for a routine abnormally scan. She has a two-and-half-year-old daughter who is developmentally normal. She has no relevant medical obstetric or family history. There was no history of warfare and exposure, alcohol abuse, or vitamin K deficiency during her pregnancy. The ultrasonogram was performed in this lady. The sagittal section of the fetal phase at 23 weeks of gestation showed an abnormal profile with verticalised nasal bone, increased frontal nasal angle, and relative prognathism. The 3D surface rendering ultrasound view of the fetal phase shows flat mid-phase. Auscification is seen in the sacral vertebrae in the fetus. Normally, only the S1 and S2 vertebrae are expected to be ossified at 23 weeks of gestation. The image on your right shows premature ossification of the cossics. The cossics normally does not ossify till term. The image on your left shows simple femoral head epiphyasis. And the image on your right shows the foot of the fetus with ossified talus, calcaneum, and cuboid at 23 weeks of gestation. A photograph of the abortus shaken with parents' proper consent confirmed binders' feces. These are the radiographs of the abortus which show calcific shippling in the proximal femoral epiphyasis, ossified talus, calcaneum, and cuboid. The right lateral radiograph of the fetus shows verticalised nasal bone, maximally hypoklasea and ossified S1 to S5 vertebrae. These are the zoomed radiographs which show verticalised nasal bone with increased fronto-nasal angle. The shippling of the cervical vertebrae, the shippling of proximal femoral epiphyasis, and premature ossification of the ankle bones. The diagnosis was chondrodysplasia punctata with binder's feces. Identifying a normal fetal profile by ultrasound during second trimester screening is important in the exclusion of facial anomalies. This is the case of chondrodysplasia punctata with binder's feces diagnosed at 23 weeks of gestation. In our case, the fetal nose was flat with long bones and vertebrae showing shippled epiphyasis. There was premature ossification in the lumbar vertebrae, caustics, and ankle bones, seriously of chondrodysplasia punctata. Chondrodysplasia punctata is a spectrum of skeletal dysplasias. Characterised by punctate calcification in the cartilage, known as calcivic shippling. In some cases, there might be short-lame morphisms, spinal anomalies, facial dysmorphisms, joint contractures, skin lesions, and even heart defects. Premature calcification in the joints and shortening of the appendicular bone is also seen. Chondrodysplasia punctata presents in a variety of forms and exhibits significant locus and early leak variation. Binder's facelies. Sir Binder in 1962 described a condition known as maxillofasial dyshostosis, chitrized by short nose, flat nasal bridge with a short columnella, acute nasolabial angle, convex upper lip, high arch palate, and dental malocclusions. A low flat nasal bridge is associated with more than 15 unital syndromes. The parents in this case had a familial profile that was not consistent with expected phenotype and findings on ultrasound. Hence, they requested for medical termination of pregnancy. The kaio type of the abortus was normal. This is how we calculate the frontal nasal angle. A line is drawn parallel to the frontal bone, and another line is drawn along the nasal bone. And the angle between them is the naso-frontal angle. The nasal frontal angle from 14 weeks to 39 weeks of gestation is normally 126 plus minus 7 degrees. And we call it as, and we call the nasal bone as verticalized if it ranges from 135 to 162 degrees. Binder facelies can be associated or associated with multiple meteorologies. Some of them are as follows. Isolated binder type nasomaxillary dysplasia, which can be autosomal dominant or autosomal resistive. The second is chondrodysplasia punctata, which may be X-linked or rhizomalic type. X-linked chondrodysplasia punctata is characterized by scoliosis and asymmetrical shortening of the limbs. Rhizomalic type is characterized by epifysial shippling, talips, and short limbs. Phenitone or Wolfen exposure can be characterized by mild shippling. Robino syndrome presents with mesomalia, clenodactyly, and macrocephaly. Arxoc syndrome presents with brachydactyly and clenodactyly. Cruzon or upper syndrome presents with craniosynosis and chondroplasia presents with short tubular bones and megaloccephaly. Ideologies of chondrodysplasia punctata. There are four main classes in which we can describe the ideologies versus paroxysmal and lysosomal storage diseases, which include rhizomalic chondrodysplasia punctata, which is autosomal resistive and characterized by generalized shippling. Another cause is Zelvega syndrome, characterized by peripatela shippling, and gangliocytosis and galactocytosis. The cholesterol biosynthesis disorders include CDP-X2 chondrading hoonarmen syndrome, which is X-link dominant and is characterized by sensorine ureal hearing loss. This Greenberg dysplasia and Smith-Lemley opid syndrome. Chromosomal anomalies resulting from chondrodysplasia punctata are trisomy-13, trisomy-21, and Turner syndrome. Disrupted vitamin K metabolism also result in chondrodysplasia punctata, and the causes are autoimmune diseases like SLE, mixed-connective tissue disorders, and scleroderma, exposure to warfare infinitoin alcohol, rubella, hypoglycemic nail, maternal vitamin K deficiency, and brachy filifalongic chondrodysplasia punctata X1, and cutal syndrome. Pathogenesis of chondrodysplasia is that there is fragmentation of epiphysis of the long bones due to mycoid degeneration, and these fragments undergo ossification, giving shippled appearance. These punctate foci of calcification disappear after first year of life, which makes it important to diagnose it early. The clinical perspective in cases of chondrodysplasia punctata, the typical or usual clinical presentation, is that anti-natally the mothers are asymptomatic and have no risk factors of comorbidities. Some of them might give positive family history. The clinical problem and need for imaging are that in anti-natal ultras, anti-natal ultras plays a very important role in identifying mesomaxillary, hypoglycea and epiphyzine shippling. Some types of chondrodysplasia punctata manifest with intellectual delay, hearing loss and spinal abnormalities, resulting in poor quality of life. Communicating the findings with obstetrician and mother helps them decide regarding further course of pregnancy. These are my references. Thank you.