Bicruciate ligament avulsions, lateral meniscus dual root avulsions - "Tibial Avulsion Tetrad"- with menisco- capsular injury - Floating meniscus in innocuous looking proximal tibia fracture.

Calvarial thinning refers to progressive loss of thickness of the upper, dome-shaped portion of the skull, including the frontal, parietal, and occipital bones. Calvarial thinning may arise from congenital syndromes or as a secondary manifestation of systemic disease, including primary and metastatic tumors, Gorham–Stout disease, hyperparathyroidism, systemic mastocytosis, granulomatosis with polyangiitis, diabetes mellitus, osteomyelitis, cystic angiomatosis, chronic steroid use, and bone aneurysm. When these etiologies are excluded, the process is termed idiopathic calvarial thinning, a rare, acquired, and indolently progressive reduction in calvarial thickness without antecedent trauma, systemic disorder, congenital syndrome, or surgical intervention. Radiographically, idiopathic calvarial thinning often presents as localized attenuation, classically with bilateral, symmetric involvement of the parietal bones in older women. Only approximately 150 cases have been reported to date. The disease pathogenesis, etiology, and optimal treatment guidelines are largely unknown. Given the rarity of this condition, idiopathic calvarial thinning may be mistaken for morphea, or localized scleroderma, a sclerosing inflammatory skin disease. Morphea is typically categorized into 5 subtypes: linear, circumscribed (plaque), generalized, pan-sclerotic, and mixed forms. When linear morphea involves the head and neck, it is termed “” (ECDS) or Parry-Romberg syndrome, typically presenting as atrophic and hyperpigmented plaques with a characteristic saber-cut depression or progressive hemifacial atrophy, respectively. Here, we describe a rare case of idiopathic calvarial thinning mimicking ECDS. A 66-year-old female presented to the dermatology clinic for a routine skin screening with a clinical depression on the right forehead that had progressed over 3 years (). The patient denied any associated pain, pruritus, or skin tightness. There was no extracutaneous involvement, such as fatigue, arthralgia, myalgia, or Raynaud’s phenomenon. Her past medical history of osteoporosis, subclinical hyperthyroidism, verruca, herpes viral breakout on the buttock and lip, actinic keratosis, and recession of the frontal hairline was noncontributory. The patient had no history of local procedures or prior bisphosphonate use. Her physical examination revealed a single, rounded 2 cm long depression along the right forehead with slight thinning of the associated hairline and concave skull lesions over the bilateral parietal skull (, ). These foci were anatomically separate and noncontiguous. Cutaneous examination demonstrated a faint, linear hypopigmented scar along the midline forehead, corresponding to a skating injury in 2020 that primarily resulted in a surgical neck fracture of the right humerus; a brain magnetic resonance imaging (MRI) at that time and subsequent evaluations to date revealed no calvarial abnormality in the scar region. The patient did not demonstrate any limb length discrepancy, joint contractures, or decreased range of motion. Her facial muscle strength and neurologic function were preserved.